Links to Exploration step
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Advancements in Host-Based Interventions for Influenza Treatment</title><author><name sortKey="Yip, Tsz Fung" sort="Yip, Tsz Fung" uniqKey="Yip T" first="Tsz-Fung" last="Yip">Tsz-Fung Yip</name><affiliation><nlm:aff id="aff1"><institution>HKU-Pasteur Research Pole, School of Public Health, The University of Hong Kong</institution>,<addr-line>Hong Kong</addr-line>,<country>Hong Kong</country></nlm:aff></affiliation></author><author><name sortKey="Selim, Aisha Sami Mohammed" sort="Selim, Aisha Sami Mohammed" uniqKey="Selim A" first="Aisha Sami Mohammed" last="Selim">Aisha Sami Mohammed Selim</name><affiliation><nlm:aff id="aff1"><institution>HKU-Pasteur Research Pole, School of Public Health, The University of Hong Kong</institution>,<addr-line>Hong Kong</addr-line>,<country>Hong Kong</country></nlm:aff></affiliation></author><author><name sortKey="Lian, Ida" sort="Lian, Ida" uniqKey="Lian I" first="Ida" last="Lian">Ida Lian</name><affiliation><nlm:aff id="aff2"><institution>School of Life Sciences and Chemical Technology, Ngee Ann Polytechnic</institution>,<addr-line>Singapore</addr-line>,<country>Singapore</country></nlm:aff></affiliation></author><author><name sortKey="Lee, Suki Man Yan" sort="Lee, Suki Man Yan" uniqKey="Lee S" first="Suki Man-Yan" last="Lee">Suki Man-Yan Lee</name><affiliation><nlm:aff id="aff1"><institution>HKU-Pasteur Research Pole, School of Public Health, The University of Hong Kong</institution>,<addr-line>Hong Kong</addr-line>,<country>Hong Kong</country></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">30042762</idno><idno type="pmc">6048202</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6048202</idno><idno type="RBID">PMC:6048202</idno><idno type="doi">10.3389/fimmu.2018.01547</idno><date when="2018">2018</date><idno type="wicri:Area/Pmc/Corpus">000D50</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000D50</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Advancements in Host-Based Interventions for Influenza Treatment</title><author><name sortKey="Yip, Tsz Fung" sort="Yip, Tsz Fung" uniqKey="Yip T" first="Tsz-Fung" last="Yip">Tsz-Fung Yip</name><affiliation><nlm:aff id="aff1"><institution>HKU-Pasteur Research Pole, School of Public Health, The University of Hong Kong</institution>,<addr-line>Hong Kong</addr-line>,<country>Hong Kong</country></nlm:aff></affiliation></author><author><name sortKey="Selim, Aisha Sami Mohammed" sort="Selim, Aisha Sami Mohammed" uniqKey="Selim A" first="Aisha Sami Mohammed" last="Selim">Aisha Sami Mohammed Selim</name><affiliation><nlm:aff id="aff1"><institution>HKU-Pasteur Research Pole, School of Public Health, The University of Hong Kong</institution>,<addr-line>Hong Kong</addr-line>,<country>Hong Kong</country></nlm:aff></affiliation></author><author><name sortKey="Lian, Ida" sort="Lian, Ida" uniqKey="Lian I" first="Ida" last="Lian">Ida Lian</name><affiliation><nlm:aff id="aff2"><institution>School of Life Sciences and Chemical Technology, Ngee Ann Polytechnic</institution>,<addr-line>Singapore</addr-line>,<country>Singapore</country></nlm:aff></affiliation></author><author><name sortKey="Lee, Suki Man Yan" sort="Lee, Suki Man Yan" uniqKey="Lee S" first="Suki Man-Yan" last="Lee">Suki Man-Yan Lee</name><affiliation><nlm:aff id="aff1"><institution>HKU-Pasteur Research Pole, School of Public Health, The University of Hong Kong</institution>,<addr-line>Hong Kong</addr-line>,<country>Hong Kong</country></nlm:aff></affiliation></author></analytic><series><title level="j">Frontiers in Immunology</title><idno type="eISSN">1664-3224</idno><imprint><date when="2018">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Influenza is a major acute respiratory infection that causes mortality and morbidity worldwide. Two classes of conventional antivirals, M2 ion channel blockers and neuraminidase inhibitors, are mainstays in managing influenza disease to lessen symptoms while minimizing hospitalization and death in patients with severe influenza. However, the development of viral resistance to both drug classes has become a major public health concern. Vaccines are prophylaxis mainstays but are limited in efficacy due to the difficulty in matching predicted dominant viral strains to circulating strains. As such, other potential interventions are being explored. Since viruses rely on host cellular functions to replicate, recent therapeutic developments focus on targeting host factors involved in virus replication. Besides controlling virus replication, potential targets for drug development include controlling virus-induced host immune responses such as the recently suggested involvement of innate lymphoid cells and NADPH oxidases in influenza virus pathogenesis and immune cell metabolism. In this review, we will discuss the advancements in novel host-based interventions for treating influenza disease.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Gurav, Yk" uniqKey="Gurav Y">YK Gurav</name></author><author><name sortKey="Chadha, Ms" uniqKey="Chadha M">MS Chadha</name></author><author><name sortKey="Tandale, Bv" uniqKey="Tandale B">BV Tandale</name></author><author><name sortKey="Potdar, Va" uniqKey="Potdar V">VA Potdar</name></author><author><name sortKey="Pawar, Sd" uniqKey="Pawar S">SD Pawar</name></author><author><name sortKey="Shil, P" uniqKey="Shil P">P Shil</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hui, Dsc" uniqKey="Hui D">DSC Hui</name></author><author><name sortKey="Lee, N" uniqKey="Lee N">N Lee</name></author><author><name sortKey="Chan, Pks" uniqKey="Chan P">PKS Chan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Olafsdottir, Ta" uniqKey="Olafsdottir T">TA Olafsdottir</name></author><author><name sortKey="Alexandersson, Kf" uniqKey="Alexandersson K">KF Alexandersson</name></author><author><name sortKey="Sveinbjornsson, G" uniqKey="Sveinbjornsson G">G Sveinbjornsson</name></author><author><name sortKey="Lapini, G" uniqKey="Lapini G">G Lapini</name></author><author><name sortKey="Palladino, L" uniqKey="Palladino L">L Palladino</name></author><author><name sortKey="Montomoli, E" uniqKey="Montomoli E">E Montomoli</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Moscona, A" uniqKey="Moscona A">A Moscona</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Takashita, E" uniqKey="Takashita E">E Takashita</name></author><author><name sortKey="Fujisaki, S" uniqKey="Fujisaki S">S Fujisaki</name></author><author><name sortKey="Shirakura, M" uniqKey="Shirakura M">M Shirakura</name></author><author><name sortKey="Nakamura, K" uniqKey="Nakamura K">K Nakamura</name></author><author><name sortKey="Kishida, N" uniqKey="Kishida N">N Kishida</name></author><author><name sortKey="Kuwahara, T" uniqKey="Kuwahara T">T Kuwahara</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Schaduangrat, N" uniqKey="Schaduangrat N">N Schaduangrat</name></author><author><name sortKey="Phanich, J" uniqKey="Phanich J">J Phanich</name></author><author><name sortKey="Rungrotmongkol, T" uniqKey="Rungrotmongkol T">T Rungrotmongkol</name></author><author><name sortKey="Lerdsamran, H" uniqKey="Lerdsamran H">H Lerdsamran</name></author><author><name sortKey="Puthavathana, P" uniqKey="Puthavathana P">P Puthavathana</name></author><author><name sortKey="Ubol, S" uniqKey="Ubol S">S Ubol</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lina, B" uniqKey="Lina B">B Lina</name></author><author><name sortKey="Boucher, C" uniqKey="Boucher C">C Boucher</name></author><author><name sortKey="Osterhaus, A" uniqKey="Osterhaus A">A Osterhaus</name></author><author><name sortKey="Monto, As" uniqKey="Monto A">AS Monto</name></author><author><name sortKey="Schutten, M" uniqKey="Schutten M">M Schutten</name></author><author><name sortKey="Whitley, Rj" uniqKey="Whitley R">RJ Whitley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tandel, K" uniqKey="Tandel K">K Tandel</name></author><author><name sortKey="Sharma, S" uniqKey="Sharma S">S Sharma</name></author><author><name sortKey="Dash, Pk" uniqKey="Dash P">PK Dash</name></author><author><name sortKey="Parida, M" uniqKey="Parida M">M Parida</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Szretter, Kj" uniqKey="Szretter K">KJ Szretter</name></author><author><name sortKey="Gangappa, S" uniqKey="Gangappa S">S Gangappa</name></author><author><name sortKey="Lu, X" uniqKey="Lu X">X Lu</name></author><author><name sortKey="Smith, C" uniqKey="Smith C">C Smith</name></author><author><name sortKey="Shieh, Wj" uniqKey="Shieh W">WJ Shieh</name></author><author><name sortKey="Zaki, Sr" uniqKey="Zaki S">SR Zaki</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Short, Kr" uniqKey="Short K">KR Short</name></author><author><name sortKey="Veeris, R" uniqKey="Veeris R">R Veeris</name></author><author><name sortKey="Leijten, Lm" uniqKey="Leijten L">LM Leijten</name></author><author><name sortKey="Van Den Brand, Jm" uniqKey="Van Den Brand J">JM van den Brand</name></author><author><name sortKey="Jong, Vl" uniqKey="Jong V">VL Jong</name></author><author><name sortKey="Stittelaar, K" uniqKey="Stittelaar K">K Stittelaar</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chi, Y" uniqKey="Chi Y">Y Chi</name></author><author><name sortKey="Zhu, Y" uniqKey="Zhu Y">Y Zhu</name></author><author><name sortKey="Wen, T" uniqKey="Wen T">T Wen</name></author><author><name sortKey="Cui, L" uniqKey="Cui L">L Cui</name></author><author><name sortKey="Ge, Y" uniqKey="Ge Y">Y Ge</name></author><author><name sortKey="Jiao, Y" uniqKey="Jiao Y">Y Jiao</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lee, Sm" uniqKey="Lee S">SM Lee</name></author><author><name sortKey="Yen, Hl" uniqKey="Yen H">HL Yen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Konig, R" uniqKey="Konig R">R Konig</name></author><author><name sortKey="Stertz, S" uniqKey="Stertz S">S Stertz</name></author><author><name sortKey="Zhou, Y" uniqKey="Zhou Y">Y Zhou</name></author><author><name sortKey="Inoue, A" uniqKey="Inoue A">A Inoue</name></author><author><name sortKey="Hoffmann, Hh" uniqKey="Hoffmann H">HH Hoffmann</name></author><author><name sortKey="Bhattacharyya, S" uniqKey="Bhattacharyya S">S Bhattacharyya</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Karlas, A" uniqKey="Karlas A">A Karlas</name></author><author><name sortKey="Machuy, N" uniqKey="Machuy N">N Machuy</name></author><author><name sortKey="Shin, Y" uniqKey="Shin Y">Y Shin</name></author><author><name sortKey="Pleissner, Kp" uniqKey="Pleissner K">KP Pleissner</name></author><author><name sortKey="Artarini, A" uniqKey="Artarini A">A Artarini</name></author><author><name sortKey="Heuer, D" uniqKey="Heuer D">D Heuer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Edinger, To" uniqKey="Edinger T">TO Edinger</name></author><author><name sortKey="Pohl, Mo" uniqKey="Pohl M">MO Pohl</name></author><author><name sortKey="Stertz, S" uniqKey="Stertz S">S Stertz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Luo, M" uniqKey="Luo M">M Luo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rust, Mj" uniqKey="Rust M">MJ Rust</name></author><author><name sortKey="Lakadamyali, M" uniqKey="Lakadamyali M">M Lakadamyali</name></author><author><name sortKey="Zhang, F" uniqKey="Zhang F">F Zhang</name></author><author><name sortKey="Zhuang, X" uniqKey="Zhuang X">X Zhuang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="De Vries, E" uniqKey="De Vries E">E de Vries</name></author><author><name sortKey="Tscherne, Dm" uniqKey="Tscherne D">DM Tscherne</name></author><author><name sortKey="Wienholts, Mj" uniqKey="Wienholts M">MJ Wienholts</name></author><author><name sortKey="Cobos Jimenez, V" uniqKey="Cobos Jimenez V">V Cobos-Jimenez</name></author><author><name sortKey="Scholte, F" uniqKey="Scholte F">F Scholte</name></author><author><name sortKey="Garcia Sastre, A" uniqKey="Garcia Sastre A">A Garcia-Sastre</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yasuda, S" uniqKey="Yasuda S">S Yasuda</name></author><author><name sortKey="Morishita, S" uniqKey="Morishita S">S Morishita</name></author><author><name sortKey="Fujita, A" uniqKey="Fujita A">A Fujita</name></author><author><name sortKey="Nanao, T" uniqKey="Nanao T">T Nanao</name></author><author><name sortKey="Wada, N" uniqKey="Wada N">N Wada</name></author><author><name sortKey="Waguri, S" uniqKey="Waguri S">S Waguri</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rossman, Js" uniqKey="Rossman J">JS Rossman</name></author><author><name sortKey="Leser, Gp" uniqKey="Leser G">GP Leser</name></author><author><name sortKey="Lamb, Ra" uniqKey="Lamb R">RA Lamb</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Huotari, J" uniqKey="Huotari J">J Huotari</name></author><author><name sortKey="Helenius, A" uniqKey="Helenius A">A Helenius</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hu, Yb" uniqKey="Hu Y">YB Hu</name></author><author><name sortKey="Dammer, Eb" uniqKey="Dammer E">EB Dammer</name></author><author><name sortKey="Ren, Rj" uniqKey="Ren R">RJ Ren</name></author><author><name sortKey="Wang, G" uniqKey="Wang G">G Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, S" uniqKey="Li S">S Li</name></author><author><name sortKey="Sieben, C" uniqKey="Sieben C">C Sieben</name></author><author><name sortKey="Ludwig, K" uniqKey="Ludwig K">K Ludwig</name></author><author><name sortKey="Hofer, Ct" uniqKey="Hofer C">CT Hofer</name></author><author><name sortKey="Chiantia, S" uniqKey="Chiantia S">S Chiantia</name></author><author><name sortKey="Herrmann, A" uniqKey="Herrmann A">A Herrmann</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Steinhauer, Da" uniqKey="Steinhauer D">DA Steinhauer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhirnov, Op" uniqKey="Zhirnov O">OP Zhirnov</name></author><author><name sortKey="Ikizler, Mr" uniqKey="Ikizler M">MR Ikizler</name></author><author><name sortKey="Wright, Pf" uniqKey="Wright P">PF Wright</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pielak, Rm" uniqKey="Pielak R">RM Pielak</name></author><author><name sortKey="Chou, Jj" uniqKey="Chou J">JJ Chou</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ye, Z" uniqKey="Ye Z">Z Ye</name></author><author><name sortKey="Liu, T" uniqKey="Liu T">T Liu</name></author><author><name sortKey="Offringa, Dp" uniqKey="Offringa D">DP Offringa</name></author><author><name sortKey="Mcinnis, J" uniqKey="Mcinnis J">J McInnis</name></author><author><name sortKey="Levandowski, Ra" uniqKey="Levandowski R">RA Levandowski</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Byrd Leotis, L" uniqKey="Byrd Leotis L">L Byrd-Leotis</name></author><author><name sortKey="Galloway, Se" uniqKey="Galloway S">SE Galloway</name></author><author><name sortKey="Agbogu, E" uniqKey="Agbogu E">E Agbogu</name></author><author><name sortKey="Steinhauer, Da" uniqKey="Steinhauer D">DA Steinhauer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lu, X" uniqKey="Lu X">X Lu</name></author><author><name sortKey="Shi, Y" uniqKey="Shi Y">Y Shi</name></author><author><name sortKey="Gao, F" uniqKey="Gao F">F Gao</name></author><author><name sortKey="Xiao, H" uniqKey="Xiao H">H Xiao</name></author><author><name sortKey="Wang, M" uniqKey="Wang M">M Wang</name></author><author><name sortKey="Qi, J" uniqKey="Qi J">J Qi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bottcher, E" uniqKey="Bottcher E">E Bottcher</name></author><author><name sortKey="Matrosovich, T" uniqKey="Matrosovich T">T Matrosovich</name></author><author><name sortKey="Beyerle, M" uniqKey="Beyerle M">M Beyerle</name></author><author><name sortKey="Klenk, Hd" uniqKey="Klenk H">HD Klenk</name></author><author><name sortKey="Garten, W" uniqKey="Garten W">W Garten</name></author><author><name sortKey="Matrosovich, M" uniqKey="Matrosovich M">M Matrosovich</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xin, Y" uniqKey="Xin Y">Y Xin</name></author><author><name sortKey="Liu, L" uniqKey="Liu L">L Liu</name></author><author><name sortKey="Chen, B" uniqKey="Chen B">B Chen</name></author><author><name sortKey="Zhang, L" uniqKey="Zhang L">L Zhang</name></author><author><name sortKey="Tong, Y" uniqKey="Tong Y">Y Tong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Swaminathan, M" uniqKey="Swaminathan M">M Swaminathan</name></author><author><name sortKey="Stuart, M" uniqKey="Stuart M">M Stuart</name></author><author><name sortKey="Hughes, Gc" uniqKey="Hughes G">GC Hughes</name></author><author><name sortKey="Jaggers, J" uniqKey="Jaggers J">J Jaggers</name></author><author><name sortKey="Hill, Se" uniqKey="Hill S">SE Hill</name></author><author><name sortKey="Milano, Ca" uniqKey="Milano C">CA Milano</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ovcharenko, Av" uniqKey="Ovcharenko A">AV Ovcharenko</name></author><author><name sortKey="Zhirnov, Op" uniqKey="Zhirnov O">OP Zhirnov</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yamaya, M" uniqKey="Yamaya M">M Yamaya</name></author><author><name sortKey="Shimotai, Y" uniqKey="Shimotai Y">Y Shimotai</name></author><author><name sortKey="Hatachi, Y" uniqKey="Hatachi Y">Y Hatachi</name></author><author><name sortKey="Lusamba Kalonji, N" uniqKey="Lusamba Kalonji N">N Lusamba Kalonji</name></author><author><name sortKey="Tando, Y" uniqKey="Tando Y">Y Tando</name></author><author><name sortKey="Kitajima, Y" uniqKey="Kitajima Y">Y Kitajima</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhirnov, Op" uniqKey="Zhirnov O">OP Zhirnov</name></author><author><name sortKey="Klenk, Hd" uniqKey="Klenk H">HD Klenk</name></author><author><name sortKey="Wright, Pf" uniqKey="Wright P">PF Wright</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lee, Mg" uniqKey="Lee M">MG Lee</name></author><author><name sortKey="Kim, Kh" uniqKey="Kim K">KH Kim</name></author><author><name sortKey="Park, Ky" uniqKey="Park K">KY Park</name></author><author><name sortKey="Kim, Js" uniqKey="Kim J">JS Kim</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ota, S" uniqKey="Ota S">S Ota</name></author><author><name sortKey="Hara, Y" uniqKey="Hara Y">Y Hara</name></author><author><name sortKey="Kanoh, S" uniqKey="Kanoh S">S Kanoh</name></author><author><name sortKey="Shinoda, M" uniqKey="Shinoda M">M Shinoda</name></author><author><name sortKey="Kawano, S" uniqKey="Kawano S">S Kawano</name></author><author><name sortKey="Fujikura, Y" uniqKey="Fujikura Y">Y Fujikura</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shen, Lw" uniqKey="Shen L">LW Shen</name></author><author><name sortKey="Mao, Hj" uniqKey="Mao H">HJ Mao</name></author><author><name sortKey="Wu, Yl" uniqKey="Wu Y">YL Wu</name></author><author><name sortKey="Tanaka, Y" uniqKey="Tanaka Y">Y Tanaka</name></author><author><name sortKey="Zhang, W" uniqKey="Zhang W">W Zhang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stieneke Grober, A" uniqKey="Stieneke Grober A">A Stieneke-Grober</name></author><author><name sortKey="Vey, M" uniqKey="Vey M">M Vey</name></author><author><name sortKey="Angliker, H" uniqKey="Angliker H">H Angliker</name></author><author><name sortKey="Shaw, E" uniqKey="Shaw E">E Shaw</name></author><author><name sortKey="Thomas, G" uniqKey="Thomas G">G Thomas</name></author><author><name sortKey="Roberts, C" uniqKey="Roberts C">C Roberts</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bahgat, Mm" uniqKey="Bahgat M">MM Bahgat</name></author><author><name sortKey="Blazejewska, P" uniqKey="Blazejewska P">P Blazejewska</name></author><author><name sortKey="Schughart, K" uniqKey="Schughart K">K Schughart</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Matlin, Ks" uniqKey="Matlin K">KS Matlin</name></author><author><name sortKey="Reggio, H" uniqKey="Reggio H">H Reggio</name></author><author><name sortKey="Helenius, A" uniqKey="Helenius A">A Helenius</name></author><author><name sortKey="Simons, K" uniqKey="Simons K">K Simons</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ochiai, H" uniqKey="Ochiai H">H Ochiai</name></author><author><name sortKey="Sakai, S" uniqKey="Sakai S">S Sakai</name></author><author><name sortKey="Hirabayashi, T" uniqKey="Hirabayashi T">T Hirabayashi</name></author><author><name sortKey="Shimizu, Y" uniqKey="Shimizu Y">Y Shimizu</name></author><author><name sortKey="Terasawa, K" uniqKey="Terasawa K">K Terasawa</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yeganeh, B" uniqKey="Yeganeh B">B Yeganeh</name></author><author><name sortKey="Ghavami, S" uniqKey="Ghavami S">S Ghavami</name></author><author><name sortKey="Kroeker, Al" uniqKey="Kroeker A">AL Kroeker</name></author><author><name sortKey="Mahood, Th" uniqKey="Mahood T">TH Mahood</name></author><author><name sortKey="Stelmack, Gl" uniqKey="Stelmack G">GL Stelmack</name></author><author><name sortKey="Klonisch, T" uniqKey="Klonisch T">T Klonisch</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sorensen, Mg" uniqKey="Sorensen M">MG Sorensen</name></author><author><name sortKey="Henriksen, K" uniqKey="Henriksen K">K Henriksen</name></author><author><name sortKey="Neutzsky Wulff, Av" uniqKey="Neutzsky Wulff A">AV Neutzsky-Wulff</name></author><author><name sortKey="Dziegiel, Mh" uniqKey="Dziegiel M">MH Dziegiel</name></author><author><name sortKey="Karsdal, Ma" uniqKey="Karsdal M">MA Karsdal</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chen, Hw" uniqKey="Chen H">HW Chen</name></author><author><name sortKey="Cheng, Jx" uniqKey="Cheng J">JX Cheng</name></author><author><name sortKey="Liu, Mt" uniqKey="Liu M">MT Liu</name></author><author><name sortKey="King, K" uniqKey="King K">K King</name></author><author><name sortKey="Peng, Jy" uniqKey="Peng J">JY Peng</name></author><author><name sortKey="Zhang, Xq" uniqKey="Zhang X">XQ Zhang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Diamond, Ms" uniqKey="Diamond M">MS Diamond</name></author><author><name sortKey="Farzan, M" uniqKey="Farzan M">M Farzan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shi, G" uniqKey="Shi G">G Shi</name></author><author><name sortKey="Schwartz, O" uniqKey="Schwartz O">O Schwartz</name></author><author><name sortKey="Compton, Aa" uniqKey="Compton A">AA Compton</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Perreira, Jm" uniqKey="Perreira J">JM Perreira</name></author><author><name sortKey="Chin, Cr" uniqKey="Chin C">CR Chin</name></author><author><name sortKey="Feeley, Em" uniqKey="Feeley E">EM Feeley</name></author><author><name sortKey="Brass, Al" uniqKey="Brass A">AL Brass</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, K" uniqKey="Li K">K Li</name></author><author><name sortKey="Markosyan, Rm" uniqKey="Markosyan R">RM Markosyan</name></author><author><name sortKey="Zheng, Ym" uniqKey="Zheng Y">YM Zheng</name></author><author><name sortKey="Golfetto, O" uniqKey="Golfetto O">O Golfetto</name></author><author><name sortKey="Bungart, B" uniqKey="Bungart B">B Bungart</name></author><author><name sortKey="Li, M" uniqKey="Li M">M Li</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Amini Bavil Olyaee, S" uniqKey="Amini Bavil Olyaee S">S Amini-Bavil-Olyaee</name></author><author><name sortKey="Choi, Yj" uniqKey="Choi Y">YJ Choi</name></author><author><name sortKey="Lee, Jh" uniqKey="Lee J">JH Lee</name></author><author><name sortKey="Shi, M" uniqKey="Shi M">M Shi</name></author><author><name sortKey="Huang, Ic" uniqKey="Huang I">IC Huang</name></author><author><name sortKey="Farzan, M" uniqKey="Farzan M">M Farzan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lee, J" uniqKey="Lee J">J Lee</name></author><author><name sortKey="Kim, J" uniqKey="Kim J">J Kim</name></author><author><name sortKey="Son, K" uniqKey="Son K">K Son</name></author><author><name sortKey="D Lexandry D Rengiani, Ap" uniqKey="D Lexandry D Rengiani A">AP d’Alexandry d’Orengiani</name></author><author><name sortKey="Min, Jy" uniqKey="Min J">JY Min</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Desai, Tm" uniqKey="Desai T">TM Desai</name></author><author><name sortKey="Marin, M" uniqKey="Marin M">M Marin</name></author><author><name sortKey="Chin, Cr" uniqKey="Chin C">CR Chin</name></author><author><name sortKey="Savidis, G" uniqKey="Savidis G">G Savidis</name></author><author><name sortKey="Brass, Al" uniqKey="Brass A">AL Brass</name></author><author><name sortKey="Melikyan, Gb" uniqKey="Melikyan G">GB Melikyan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ma, H" uniqKey="Ma H">H Ma</name></author><author><name sortKey="Kien, F" uniqKey="Kien F">F Kien</name></author><author><name sortKey="Maniere, M" uniqKey="Maniere M">M Maniere</name></author><author><name sortKey="Zhang, Y" uniqKey="Zhang Y">Y Zhang</name></author><author><name sortKey="Lagarde, N" uniqKey="Lagarde N">N Lagarde</name></author><author><name sortKey="Tse, Ks" uniqKey="Tse K">KS Tse</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Musiol, A" uniqKey="Musiol A">A Musiol</name></author><author><name sortKey="Gran, S" uniqKey="Gran S">S Gran</name></author><author><name sortKey="Ehrhardt, C" uniqKey="Ehrhardt C">C Ehrhardt</name></author><author><name sortKey="Ludwig, S" uniqKey="Ludwig S">S Ludwig</name></author><author><name sortKey="Grewal, T" uniqKey="Grewal T">T Grewal</name></author><author><name sortKey="Gerke, V" uniqKey="Gerke V">V Gerke</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hu, Y" uniqKey="Hu Y">Y Hu</name></author><author><name sortKey="Jiang, L" uniqKey="Jiang L">L Jiang</name></author><author><name sortKey="Lai, W" uniqKey="Lai W">W Lai</name></author><author><name sortKey="Qin, Y" uniqKey="Qin Y">Y Qin</name></author><author><name sortKey="Zhang, T" uniqKey="Zhang T">T Zhang</name></author><author><name sortKey="Wang, S" uniqKey="Wang S">S Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xu, X" uniqKey="Xu X">X Xu</name></author><author><name sortKey="Kedlaya, R" uniqKey="Kedlaya R">R Kedlaya</name></author><author><name sortKey="Higuchi, H" uniqKey="Higuchi H">H Higuchi</name></author><author><name sortKey="Ikeda, S" uniqKey="Ikeda S">S Ikeda</name></author><author><name sortKey="Justice, Mj" uniqKey="Justice M">MJ Justice</name></author><author><name sortKey="Setaluri, V" uniqKey="Setaluri V">V Setaluri</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sun, E" uniqKey="Sun E">E Sun</name></author><author><name sortKey="He, J" uniqKey="He J">J He</name></author><author><name sortKey="Zhuang, X" uniqKey="Zhuang X">X Zhuang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Eisfeld, Aj" uniqKey="Eisfeld A">AJ Eisfeld</name></author><author><name sortKey="Neumann, G" uniqKey="Neumann G">G Neumann</name></author><author><name sortKey="Kawaoka, Y" uniqKey="Kawaoka Y">Y Kawaoka</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Babcock, Hp" uniqKey="Babcock H">HP Babcock</name></author><author><name sortKey="Chen, C" uniqKey="Chen C">C Chen</name></author><author><name sortKey="Zhuang, X" uniqKey="Zhuang X">X Zhuang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Resa Infante, P" uniqKey="Resa Infante P">P Resa-Infante</name></author><author><name sortKey="Paterson, D" uniqKey="Paterson D">D Paterson</name></author><author><name sortKey="Bonet, J" uniqKey="Bonet J">J Bonet</name></author><author><name sortKey="Otte, A" uniqKey="Otte A">A Otte</name></author><author><name sortKey="Oliva, B" uniqKey="Oliva B">B Oliva</name></author><author><name sortKey="Fodor, E" uniqKey="Fodor E">E Fodor</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gabriel, G" uniqKey="Gabriel G">G Gabriel</name></author><author><name sortKey="Klingel, K" uniqKey="Klingel K">K Klingel</name></author><author><name sortKey="Otte, A" uniqKey="Otte A">A Otte</name></author><author><name sortKey="Thiele, S" uniqKey="Thiele S">S Thiele</name></author><author><name sortKey="Hudjetz, B" uniqKey="Hudjetz B">B Hudjetz</name></author><author><name sortKey="Arman Kalcek, G" uniqKey="Arman Kalcek G">G Arman-Kalcek</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rosenblatt, Je" uniqKey="Rosenblatt J">JE Rosenblatt</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wagstaff, Km" uniqKey="Wagstaff K">KM Wagstaff</name></author><author><name sortKey="Sivakumaran, H" uniqKey="Sivakumaran H">H Sivakumaran</name></author><author><name sortKey="Heaton, Sm" uniqKey="Heaton S">SM Heaton</name></author><author><name sortKey="Harrich, D" uniqKey="Harrich D">D Harrich</name></author><author><name sortKey="Jans, Da" uniqKey="Jans D">DA Jans</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gotz, V" uniqKey="Gotz V">V Gotz</name></author><author><name sortKey="Magar, L" uniqKey="Magar L">L Magar</name></author><author><name sortKey="Dornfeld, D" uniqKey="Dornfeld D">D Dornfeld</name></author><author><name sortKey="Giese, S" uniqKey="Giese S">S Giese</name></author><author><name sortKey="Pohlmann, A" uniqKey="Pohlmann A">A Pohlmann</name></author><author><name sortKey="Hoper, D" uniqKey="Hoper D">D Hoper</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mor, A" uniqKey="Mor A">A Mor</name></author><author><name sortKey="White, A" uniqKey="White A">A White</name></author><author><name sortKey="Zhang, K" uniqKey="Zhang K">K Zhang</name></author><author><name sortKey="Thompson, M" uniqKey="Thompson M">M Thompson</name></author><author><name sortKey="Esparza, M" uniqKey="Esparza M">M Esparza</name></author><author><name sortKey="Munoz Moreno, R" uniqKey="Munoz Moreno R">R Munoz-Moreno</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dubois, J" uniqKey="Dubois J">J Dubois</name></author><author><name sortKey="Terrier, O" uniqKey="Terrier O">O Terrier</name></author><author><name sortKey="Rosa Calatrava, M" uniqKey="Rosa Calatrava M">M Rosa-Calatrava</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bullock, An" uniqKey="Bullock A">AN Bullock</name></author><author><name sortKey="Das, S" uniqKey="Das S">S Das</name></author><author><name sortKey="Debreczeni, Je" uniqKey="Debreczeni J">JE Debreczeni</name></author><author><name sortKey="Rellos, P" uniqKey="Rellos P">P Rellos</name></author><author><name sortKey="Fedorov, O" uniqKey="Fedorov O">O Fedorov</name></author><author><name sortKey="Niesen, Fh" uniqKey="Niesen F">FH Niesen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zu, M" uniqKey="Zu M">M Zu</name></author><author><name sortKey="Li, C" uniqKey="Li C">C Li</name></author><author><name sortKey="Fang, Js" uniqKey="Fang J">JS Fang</name></author><author><name sortKey="Lian, Ww" uniqKey="Lian W">WW Lian</name></author><author><name sortKey="Liu, Al" uniqKey="Liu A">AL Liu</name></author><author><name sortKey="Zheng, Ls" uniqKey="Zheng L">LS Zheng</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Amorim, Mj" uniqKey="Amorim M">MJ Amorim</name></author><author><name sortKey="Read, Ek" uniqKey="Read E">EK Read</name></author><author><name sortKey="Dalton, Rm" uniqKey="Dalton R">RM Dalton</name></author><author><name sortKey="Medcalf, L" uniqKey="Medcalf L">L Medcalf</name></author><author><name sortKey="Digard, P" uniqKey="Digard P">P Digard</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Utine, Ca" uniqKey="Utine C">CA Utine</name></author><author><name sortKey="Stern, M" uniqKey="Stern M">M Stern</name></author><author><name sortKey="Akpek, Ek" uniqKey="Akpek E">EK Akpek</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, X" uniqKey="Liu X">X Liu</name></author><author><name sortKey="Zhao, Z" uniqKey="Zhao Z">Z Zhao</name></author><author><name sortKey="Li, Z" uniqKey="Li Z">Z Li</name></author><author><name sortKey="Xu, C" uniqKey="Xu C">C Xu</name></author><author><name sortKey="Sun, L" uniqKey="Sun L">L Sun</name></author><author><name sortKey="Chen, J" uniqKey="Chen J">J Chen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ma, C" uniqKey="Ma C">C Ma</name></author><author><name sortKey="Li, F" uniqKey="Li F">F Li</name></author><author><name sortKey="Musharrafieh, Rg" uniqKey="Musharrafieh R">RG Musharrafieh</name></author><author><name sortKey="Wang, J" uniqKey="Wang J">J Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Read, Ek" uniqKey="Read E">EK Read</name></author><author><name sortKey="Digard, P" uniqKey="Digard P">P Digard</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Morita, M" uniqKey="Morita M">M Morita</name></author><author><name sortKey="Kuba, K" uniqKey="Kuba K">K Kuba</name></author><author><name sortKey="Ichikawa, A" uniqKey="Ichikawa A">A Ichikawa</name></author><author><name sortKey="Nakayama, M" uniqKey="Nakayama M">M Nakayama</name></author><author><name sortKey="Katahira, J" uniqKey="Katahira J">J Katahira</name></author><author><name sortKey="Iwamoto, R" uniqKey="Iwamoto R">R Iwamoto</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cencic, R" uniqKey="Cencic R">R Cencic</name></author><author><name sortKey="Pelletier, J" uniqKey="Pelletier J">J Pelletier</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sokabe, M" uniqKey="Sokabe M">M Sokabe</name></author><author><name sortKey="Fraser, Cs" uniqKey="Fraser C">CS Fraser</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Muller, C" uniqKey="Muller C">C Muller</name></author><author><name sortKey="Schulte, Fw" uniqKey="Schulte F">FW Schulte</name></author><author><name sortKey="Lange Grunweller, K" uniqKey="Lange Grunweller K">K Lange-Grunweller</name></author><author><name sortKey="Obermann, W" uniqKey="Obermann W">W Obermann</name></author><author><name sortKey="Madhugiri, R" uniqKey="Madhugiri R">R Madhugiri</name></author><author><name sortKey="Pleschka, S" uniqKey="Pleschka S">S Pleschka</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yanguez, E" uniqKey="Yanguez E">E Yanguez</name></author><author><name sortKey="Castello, A" uniqKey="Castello A">A Castello</name></author><author><name sortKey="Welnowska, E" uniqKey="Welnowska E">E Welnowska</name></author><author><name sortKey="Carrasco, L" uniqKey="Carrasco L">L Carrasco</name></author><author><name sortKey="Goodfellow, I" uniqKey="Goodfellow I">I Goodfellow</name></author><author><name sortKey="Nieto, A" uniqKey="Nieto A">A Nieto</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Slaine, Pd" uniqKey="Slaine P">PD Slaine</name></author><author><name sortKey="Kleer, M" uniqKey="Kleer M">M Kleer</name></author><author><name sortKey="Smith, Nk" uniqKey="Smith N">NK Smith</name></author><author><name sortKey="Khaperskyy, Da" uniqKey="Khaperskyy D">DA Khaperskyy</name></author><author><name sortKey="Mccormick, C" uniqKey="Mccormick C">C McCormick</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Malina, A" uniqKey="Malina A">A Malina</name></author><author><name sortKey="Mills, Jr" uniqKey="Mills J">JR Mills</name></author><author><name sortKey="Pelletier, J" uniqKey="Pelletier J">J Pelletier</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rossignol, Jf" uniqKey="Rossignol J">JF Rossignol</name></author><author><name sortKey="La Frazia, S" uniqKey="La Frazia S">S La Frazia</name></author><author><name sortKey="Chiappa, L" uniqKey="Chiappa L">L Chiappa</name></author><author><name sortKey="Ciucci, A" uniqKey="Ciucci A">A Ciucci</name></author><author><name sortKey="Santoro, Mg" uniqKey="Santoro M">MG Santoro</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rossignol, Jf" uniqKey="Rossignol J">JF Rossignol</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tilmanis, D" uniqKey="Tilmanis D">D Tilmanis</name></author><author><name sortKey="Van Baalen, C" uniqKey="Van Baalen C">C van Baalen</name></author><author><name sortKey="Oh, Dy" uniqKey="Oh D">DY Oh</name></author><author><name sortKey="Rossignol, Jf" uniqKey="Rossignol J">JF Rossignol</name></author><author><name sortKey="Hurt, Ac" uniqKey="Hurt A">AC Hurt</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Belardo, G" uniqKey="Belardo G">G Belardo</name></author><author><name sortKey="Cenciarelli, O" uniqKey="Cenciarelli O">O Cenciarelli</name></author><author><name sortKey="La Frazia, S" uniqKey="La Frazia S">S La Frazia</name></author><author><name sortKey="Rossignol, Jf" uniqKey="Rossignol J">JF Rossignol</name></author><author><name sortKey="Santoro, Mg" uniqKey="Santoro M">MG Santoro</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lakdawala, Ss" uniqKey="Lakdawala S">SS Lakdawala</name></author><author><name sortKey="Wu, Y" uniqKey="Wu Y">Y Wu</name></author><author><name sortKey="Wawrzusin, P" uniqKey="Wawrzusin P">P Wawrzusin</name></author><author><name sortKey="Kabat, J" uniqKey="Kabat J">J Kabat</name></author><author><name sortKey="Broadbent, Aj" uniqKey="Broadbent A">AJ Broadbent</name></author><author><name sortKey="Lamirande, Ew" uniqKey="Lamirande E">EW Lamirande</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Momose, F" uniqKey="Momose F">F Momose</name></author><author><name sortKey="Sekimoto, T" uniqKey="Sekimoto T">T Sekimoto</name></author><author><name sortKey="Ohkura, T" uniqKey="Ohkura T">T Ohkura</name></author><author><name sortKey="Jo, S" uniqKey="Jo S">S Jo</name></author><author><name sortKey="Kawaguchi, A" uniqKey="Kawaguchi A">A Kawaguchi</name></author><author><name sortKey="Nagata, K" uniqKey="Nagata K">K Nagata</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kudo, N" uniqKey="Kudo N">N Kudo</name></author><author><name sortKey="Khochbin, S" uniqKey="Khochbin S">S Khochbin</name></author><author><name sortKey="Nishi, K" uniqKey="Nishi K">K Nishi</name></author><author><name sortKey="Kitano, K" uniqKey="Kitano K">K Kitano</name></author><author><name sortKey="Yanagida, M" uniqKey="Yanagida M">M Yanagida</name></author><author><name sortKey="Yoshida, M" uniqKey="Yoshida M">M Yoshida</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kohler, A" uniqKey="Kohler A">A Kohler</name></author><author><name sortKey="Hurt, E" uniqKey="Hurt E">E Hurt</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fischer, U" uniqKey="Fischer U">U Fischer</name></author><author><name sortKey="Huber, J" uniqKey="Huber J">J Huber</name></author><author><name sortKey="Boelens, Wc" uniqKey="Boelens W">WC Boelens</name></author><author><name sortKey="Mattaj, Iw" uniqKey="Mattaj I">IW Mattaj</name></author><author><name sortKey="Luhrmann, R" uniqKey="Luhrmann R">R Luhrmann</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Brunotte, L" uniqKey="Brunotte L">L Brunotte</name></author><author><name sortKey="Flies, J" uniqKey="Flies J">J Flies</name></author><author><name sortKey="Bolte, H" uniqKey="Bolte H">H Bolte</name></author><author><name sortKey="Reuther, P" uniqKey="Reuther P">P Reuther</name></author><author><name sortKey="Vreede, F" uniqKey="Vreede F">F Vreede</name></author><author><name sortKey="Schwemmle, M" uniqKey="Schwemmle M">M Schwemmle</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Elton, D" uniqKey="Elton D">D Elton</name></author><author><name sortKey="Simpson Holley, M" uniqKey="Simpson Holley M">M Simpson-Holley</name></author><author><name sortKey="Archer, K" uniqKey="Archer K">K Archer</name></author><author><name sortKey="Medcalf, L" uniqKey="Medcalf L">L Medcalf</name></author><author><name sortKey="Hallam, R" uniqKey="Hallam R">R Hallam</name></author><author><name sortKey="Mccauley, J" uniqKey="Mccauley J">J McCauley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Watanabe, K" uniqKey="Watanabe K">K Watanabe</name></author><author><name sortKey="Takizawa, N" uniqKey="Takizawa N">N Takizawa</name></author><author><name sortKey="Katoh, M" uniqKey="Katoh M">M Katoh</name></author><author><name sortKey="Hoshida, K" uniqKey="Hoshida K">K Hoshida</name></author><author><name sortKey="Kobayashi, N" uniqKey="Kobayashi N">N Kobayashi</name></author><author><name sortKey="Nagata, K" uniqKey="Nagata K">K Nagata</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Newlands, Es" uniqKey="Newlands E">ES Newlands</name></author><author><name sortKey="Rustin, Gj" uniqKey="Rustin G">GJ Rustin</name></author><author><name sortKey="Brampton, Mh" uniqKey="Brampton M">MH Brampton</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Perwitasari, O" uniqKey="Perwitasari O">O Perwitasari</name></author><author><name sortKey="Johnson, S" uniqKey="Johnson S">S Johnson</name></author><author><name sortKey="Yan, X" uniqKey="Yan X">X Yan</name></author><author><name sortKey="Howerth, E" uniqKey="Howerth E">E Howerth</name></author><author><name sortKey="Shacham, S" uniqKey="Shacham S">S Shacham</name></author><author><name sortKey="Landesman, Y" uniqKey="Landesman Y">Y Landesman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Perwitasari, O" uniqKey="Perwitasari O">O Perwitasari</name></author><author><name sortKey="Johnson, S" uniqKey="Johnson S">S Johnson</name></author><author><name sortKey="Yan, X" uniqKey="Yan X">X Yan</name></author><author><name sortKey="Register, E" uniqKey="Register E">E Register</name></author><author><name sortKey="Crabtree, J" uniqKey="Crabtree J">J Crabtree</name></author><author><name sortKey="Gabbard, J" uniqKey="Gabbard J">J Gabbard</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Muthuri, Sg" uniqKey="Muthuri S">SG Muthuri</name></author><author><name sortKey="Venkatesan, S" uniqKey="Venkatesan S">S Venkatesan</name></author><author><name sortKey="Myles, Pr" uniqKey="Myles P">PR Myles</name></author><author><name sortKey="Leonardi Bee, J" uniqKey="Leonardi Bee J">J Leonardi-Bee</name></author><author><name sortKey="Al Khuwaitir, Ts" uniqKey="Al Khuwaitir T">TS Al Khuwaitir</name></author><author><name sortKey="Al Mamun, A" uniqKey="Al Mamun A">A Al Mamun</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chutiwitoonchai, N" uniqKey="Chutiwitoonchai N">N Chutiwitoonchai</name></author><author><name sortKey="Mano, T" uniqKey="Mano T">T Mano</name></author><author><name sortKey="Kakisaka, M" uniqKey="Kakisaka M">M Kakisaka</name></author><author><name sortKey="Sato, H" uniqKey="Sato H">H Sato</name></author><author><name sortKey="Kondoh, Y" uniqKey="Kondoh Y">Y Kondoh</name></author><author><name sortKey="Osada, H" uniqKey="Osada H">H Osada</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, J" uniqKey="Li J">J Li</name></author><author><name sortKey="Chen, C" uniqKey="Chen C">C Chen</name></author><author><name sortKey="Wong, G" uniqKey="Wong G">G Wong</name></author><author><name sortKey="Dong, W" uniqKey="Dong W">W Dong</name></author><author><name sortKey="Zheng, W" uniqKey="Zheng W">W Zheng</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y Li</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, X" uniqKey="Liu X">X Liu</name></author><author><name sortKey="Sun, L" uniqKey="Sun L">L Sun</name></author><author><name sortKey="Yu, M" uniqKey="Yu M">M Yu</name></author><author><name sortKey="Wang, Z" uniqKey="Wang Z">Z Wang</name></author><author><name sortKey="Xu, C" uniqKey="Xu C">C Xu</name></author><author><name sortKey="Xue, Q" uniqKey="Xue Q">Q Xue</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, X" uniqKey="Liu X">X Liu</name></author><author><name sortKey="Zhao, Z" uniqKey="Zhao Z">Z Zhao</name></author><author><name sortKey="Xu, C" uniqKey="Xu C">C Xu</name></author><author><name sortKey="Sun, L" uniqKey="Sun L">L Sun</name></author><author><name sortKey="Chen, J" uniqKey="Chen J">J Chen</name></author><author><name sortKey="Zhang, L" uniqKey="Zhang L">L Zhang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Qiao, Y" uniqKey="Qiao Y">Y Qiao</name></author><author><name sortKey="Yan, Y" uniqKey="Yan Y">Y Yan</name></author><author><name sortKey="Tan, Ks" uniqKey="Tan K">KS Tan</name></author><author><name sortKey="Tan, Ss" uniqKey="Tan S">SS Tan</name></author><author><name sortKey="Seet, Je" uniqKey="Seet J">JE Seet</name></author><author><name sortKey="Arumugam, Tv" uniqKey="Arumugam T">TV Arumugam</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gavara, Mm" uniqKey="Gavara M">MM Gavara</name></author><author><name sortKey="Zaveri, K" uniqKey="Zaveri K">K Zaveri</name></author><author><name sortKey="Badana, Ak" uniqKey="Badana A">AK Badana</name></author><author><name sortKey="Gugalavath, S" uniqKey="Gugalavath S">S Gugalavath</name></author><author><name sortKey="Amajala, Kc" uniqKey="Amajala K">KC Amajala</name></author><author><name sortKey="Patnala, K" uniqKey="Patnala K">K Patnala</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Haidari, M" uniqKey="Haidari M">M Haidari</name></author><author><name sortKey="Zhang, W" uniqKey="Zhang W">W Zhang</name></author><author><name sortKey="Ganjehei, L" uniqKey="Ganjehei L">L Ganjehei</name></author><author><name sortKey="Ali, M" uniqKey="Ali M">M Ali</name></author><author><name sortKey="Chen, Z" uniqKey="Chen Z">Z Chen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pleschka, S" uniqKey="Pleschka S">S Pleschka</name></author><author><name sortKey="Wolff, T" uniqKey="Wolff T">T Wolff</name></author><author><name sortKey="Ehrhardt, C" uniqKey="Ehrhardt C">C Ehrhardt</name></author><author><name sortKey="Hobom, G" uniqKey="Hobom G">G Hobom</name></author><author><name sortKey="Planz, O" uniqKey="Planz O">O Planz</name></author><author><name sortKey="Rapp, Ur" uniqKey="Rapp U">UR Rapp</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Droebner, K" uniqKey="Droebner K">K Droebner</name></author><author><name sortKey="Pleschka, S" uniqKey="Pleschka S">S Pleschka</name></author><author><name sortKey="Ludwig, S" uniqKey="Ludwig S">S Ludwig</name></author><author><name sortKey="Planz, O" uniqKey="Planz O">O Planz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ludwig, S" uniqKey="Ludwig S">S Ludwig</name></author><author><name sortKey="Wolff, T" uniqKey="Wolff T">T Wolff</name></author><author><name sortKey="Ehrhardt, C" uniqKey="Ehrhardt C">C Ehrhardt</name></author><author><name sortKey="Wurzer, Wj" uniqKey="Wurzer W">WJ Wurzer</name></author><author><name sortKey="Reinhardt, J" uniqKey="Reinhardt J">J Reinhardt</name></author><author><name sortKey="Planz, O" uniqKey="Planz O">O Planz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Planz, O" uniqKey="Planz O">O Planz</name></author><author><name sortKey="Pleschka, S" uniqKey="Pleschka S">S Pleschka</name></author><author><name sortKey="Ludwig, S" uniqKey="Ludwig S">S Ludwig</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Haasbach, E" uniqKey="Haasbach E">E Haasbach</name></author><author><name sortKey="Muller, C" uniqKey="Muller C">C Muller</name></author><author><name sortKey="Ehrhardt, C" uniqKey="Ehrhardt C">C Ehrhardt</name></author><author><name sortKey="Schreiber, A" uniqKey="Schreiber A">A Schreiber</name></author><author><name sortKey="Pleschka, S" uniqKey="Pleschka S">S Pleschka</name></author><author><name sortKey="Ludwig, S" uniqKey="Ludwig S">S Ludwig</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tcherniuk, S" uniqKey="Tcherniuk S">S Tcherniuk</name></author><author><name sortKey="Cenac, N" uniqKey="Cenac N">N Cenac</name></author><author><name sortKey="Comte, M" uniqKey="Comte M">M Comte</name></author><author><name sortKey="Frouard, J" uniqKey="Frouard J">J Frouard</name></author><author><name sortKey="Errazuriz Cerda, E" uniqKey="Errazuriz Cerda E">E Errazuriz-Cerda</name></author><author><name sortKey="Galabov, A" uniqKey="Galabov A">A Galabov</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Courtin, N" uniqKey="Courtin N">N Courtin</name></author><author><name sortKey="Fotso, Af" uniqKey="Fotso A">AF Fotso</name></author><author><name sortKey="Fautrad, P" uniqKey="Fautrad P">P Fautrad</name></author><author><name sortKey="Mas, F" uniqKey="Mas F">F Mas</name></author><author><name sortKey="Alessi, Mc" uniqKey="Alessi M">MC Alessi</name></author><author><name sortKey="Riteau, B" uniqKey="Riteau B">B Riteau</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Grant, Bd" uniqKey="Grant B">BD Grant</name></author><author><name sortKey="Donaldson, Jg" uniqKey="Donaldson J">JG Donaldson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bruce, Ea" uniqKey="Bruce E">EA Bruce</name></author><author><name sortKey="Stuart, A" uniqKey="Stuart A">A Stuart</name></author><author><name sortKey="Mccaffrey, Mw" uniqKey="Mccaffrey M">MW McCaffrey</name></author><author><name sortKey="Digard, P" uniqKey="Digard P">P Digard</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Amorim, Mj" uniqKey="Amorim M">MJ Amorim</name></author><author><name sortKey="Bruce, Ea" uniqKey="Bruce E">EA Bruce</name></author><author><name sortKey="Read, Ek" uniqKey="Read E">EK Read</name></author><author><name sortKey="Foeglein, A" uniqKey="Foeglein A">A Foeglein</name></author><author><name sortKey="Mahen, R" uniqKey="Mahen R">R Mahen</name></author><author><name sortKey="Stuart, Ad" uniqKey="Stuart A">AD Stuart</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Eisfeld, Aj" uniqKey="Eisfeld A">AJ Eisfeld</name></author><author><name sortKey="Kawakami, E" uniqKey="Kawakami E">E Kawakami</name></author><author><name sortKey="Watanabe, T" uniqKey="Watanabe T">T Watanabe</name></author><author><name sortKey="Neumann, G" uniqKey="Neumann G">G Neumann</name></author><author><name sortKey="Kawaoka, Y" uniqKey="Kawaoka Y">Y Kawaoka</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bruce, Ea" uniqKey="Bruce E">EA Bruce</name></author><author><name sortKey="Digard, P" uniqKey="Digard P">P Digard</name></author><author><name sortKey="Stuart, Ad" uniqKey="Stuart A">AD Stuart</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ramos Nascimento, A" uniqKey="Ramos Nascimento A">A Ramos-Nascimento</name></author><author><name sortKey="Kellen, B" uniqKey="Kellen B">B Kellen</name></author><author><name sortKey="Ferreira, F" uniqKey="Ferreira F">F Ferreira</name></author><author><name sortKey="Alenquer, M" uniqKey="Alenquer M">M Alenquer</name></author><author><name sortKey="Vale Costa, S" uniqKey="Vale Costa S">S Vale-Costa</name></author><author><name sortKey="Raposo, G" uniqKey="Raposo G">G Raposo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Portran, D" uniqKey="Portran D">D Portran</name></author><author><name sortKey="Schaedel, L" uniqKey="Schaedel L">L Schaedel</name></author><author><name sortKey="Xu, Z" uniqKey="Xu Z">Z Xu</name></author><author><name sortKey="Thery, M" uniqKey="Thery M">M Thery</name></author><author><name sortKey="Nachury, Mv" uniqKey="Nachury M">MV Nachury</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hubbert, C" uniqKey="Hubbert C">C Hubbert</name></author><author><name sortKey="Guardiola, A" uniqKey="Guardiola A">A Guardiola</name></author><author><name sortKey="Shao, R" uniqKey="Shao R">R Shao</name></author><author><name sortKey="Kawaguchi, Y" uniqKey="Kawaguchi Y">Y Kawaguchi</name></author><author><name sortKey="Ito, A" uniqKey="Ito A">A Ito</name></author><author><name sortKey="Nixon, A" uniqKey="Nixon A">A Nixon</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Husain, M" uniqKey="Husain M">M Husain</name></author><author><name sortKey="Cheung, Cy" uniqKey="Cheung C">CY Cheung</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mori, K" uniqKey="Mori K">K Mori</name></author><author><name sortKey="Haruyama, T" uniqKey="Haruyama T">T Haruyama</name></author><author><name sortKey="Nagata, K" uniqKey="Nagata K">K Nagata</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Roberts, Kl" uniqKey="Roberts K">KL Roberts</name></author><author><name sortKey="Manicassamy, B" uniqKey="Manicassamy B">B Manicassamy</name></author><author><name sortKey="Lamb, Ra" uniqKey="Lamb R">RA Lamb</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rossman, Js" uniqKey="Rossman J">JS Rossman</name></author><author><name sortKey="Lamb, Ra" uniqKey="Lamb R">RA Lamb</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Martyna, A" uniqKey="Martyna A">A Martyna</name></author><author><name sortKey="Rossman, J" uniqKey="Rossman J">J Rossman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Elkins, Mr" uniqKey="Elkins M">MR Elkins</name></author><author><name sortKey="Williams, Jk" uniqKey="Williams J">JK Williams</name></author><author><name sortKey="Gelenter, Md" uniqKey="Gelenter M">MD Gelenter</name></author><author><name sortKey="Dai, P" uniqKey="Dai P">P Dai</name></author><author><name sortKey="Kwon, B" uniqKey="Kwon B">B Kwon</name></author><author><name sortKey="Sergeyev, Iv" uniqKey="Sergeyev I">IV Sergeyev</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bajimaya, S" uniqKey="Bajimaya S">S Bajimaya</name></author><author><name sortKey="Frankl, T" uniqKey="Frankl T">T Frankl</name></author><author><name sortKey="Hayashi, T" uniqKey="Hayashi T">T Hayashi</name></author><author><name sortKey="Takimoto, T" uniqKey="Takimoto T">T Takimoto</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Matsui, K" uniqKey="Matsui K">K Matsui</name></author><author><name sortKey="Ozawa, M" uniqKey="Ozawa M">M Ozawa</name></author><author><name sortKey="Kiso, M" uniqKey="Kiso M">M Kiso</name></author><author><name sortKey="Yamashita, M" uniqKey="Yamashita M">M Yamashita</name></author><author><name sortKey="Maekawa, T" uniqKey="Maekawa T">T Maekawa</name></author><author><name sortKey="Kubota, M" uniqKey="Kubota M">M Kubota</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Herold, S" uniqKey="Herold S">S Herold</name></author><author><name sortKey="Becker, C" uniqKey="Becker C">C Becker</name></author><author><name sortKey="Ridge, Km" uniqKey="Ridge K">KM Ridge</name></author><author><name sortKey="Budinger, Gr" uniqKey="Budinger G">GR Budinger</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pulendran, B" uniqKey="Pulendran B">B Pulendran</name></author><author><name sortKey="Maddur, Ms" uniqKey="Maddur M">MS Maddur</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chen, X" uniqKey="Chen X">X Chen</name></author><author><name sortKey="Liu, S" uniqKey="Liu S">S Liu</name></author><author><name sortKey="Goraya, Mu" uniqKey="Goraya M">MU Goraya</name></author><author><name sortKey="Maarouf, M" uniqKey="Maarouf M">M Maarouf</name></author><author><name sortKey="Huang, S" uniqKey="Huang S">S Huang</name></author><author><name sortKey="Chen, Jl" uniqKey="Chen J">JL Chen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kruger, P" uniqKey="Kruger P">P Kruger</name></author><author><name sortKey="Saffarzadeh, M" uniqKey="Saffarzadeh M">M Saffarzadeh</name></author><author><name sortKey="Weber, An" uniqKey="Weber A">AN Weber</name></author><author><name sortKey="Rieber, N" uniqKey="Rieber N">N Rieber</name></author><author><name sortKey="Radsak, M" uniqKey="Radsak M">M Radsak</name></author><author><name sortKey="Von Bernuth, H" uniqKey="Von Bernuth H">H von Bernuth</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tate, Md" uniqKey="Tate M">MD Tate</name></author><author><name sortKey="Brooks, Ag" uniqKey="Brooks A">AG Brooks</name></author><author><name sortKey="Reading, Pc" uniqKey="Reading P">PC Reading</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tate, Md" uniqKey="Tate M">MD Tate</name></author><author><name sortKey="Ioannidis, Lj" uniqKey="Ioannidis L">LJ Ioannidis</name></author><author><name sortKey="Croker, B" uniqKey="Croker B">B Croker</name></author><author><name sortKey="Brown, Le" uniqKey="Brown L">LE Brown</name></author><author><name sortKey="Brooks, Ag" uniqKey="Brooks A">AG Brooks</name></author><author><name sortKey="Reading, Pc" uniqKey="Reading P">PC Reading</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lim, K" uniqKey="Lim K">K Lim</name></author><author><name sortKey="Hyun, Ym" uniqKey="Hyun Y">YM Hyun</name></author><author><name sortKey="Lambert Emo, K" uniqKey="Lambert Emo K">K Lambert-Emo</name></author><author><name sortKey="Capece, T" uniqKey="Capece T">T Capece</name></author><author><name sortKey="Bae, S" uniqKey="Bae S">S Bae</name></author><author><name sortKey="Miller, R" uniqKey="Miller R">R Miller</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Van Riel, D" uniqKey="Van Riel D">D van Riel</name></author><author><name sortKey="Leijten, Lm" uniqKey="Leijten L">LM Leijten</name></author><author><name sortKey="Van Der Eerden, M" uniqKey="Van Der Eerden M">M van der Eerden</name></author><author><name sortKey="Hoogsteden, Hc" uniqKey="Hoogsteden H">HC Hoogsteden</name></author><author><name sortKey="Boven, La" uniqKey="Boven L">LA Boven</name></author><author><name sortKey="Lambrecht, Bn" uniqKey="Lambrecht B">BN Lambrecht</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Seth, S" uniqKey="Seth S">S Seth</name></author><author><name sortKey="Oberdorfer, L" uniqKey="Oberdorfer L">L Oberdorfer</name></author><author><name sortKey="Hyde, R" uniqKey="Hyde R">R Hyde</name></author><author><name sortKey="Hoff, K" uniqKey="Hoff K">K Hoff</name></author><author><name sortKey="Thies, V" uniqKey="Thies V">V Thies</name></author><author><name sortKey="Worbs, T" uniqKey="Worbs T">T Worbs</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Qu, C" uniqKey="Qu C">C Qu</name></author><author><name sortKey="Nguyen, Va" uniqKey="Nguyen V">VA Nguyen</name></author><author><name sortKey="Merad, M" uniqKey="Merad M">M Merad</name></author><author><name sortKey="Randolph, Gj" uniqKey="Randolph G">GJ Randolph</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Allan, Rs" uniqKey="Allan R">RS Allan</name></author><author><name sortKey="Waithman, J" uniqKey="Waithman J">J Waithman</name></author><author><name sortKey="Bedoui, S" uniqKey="Bedoui S">S Bedoui</name></author><author><name sortKey="Jones, Cm" uniqKey="Jones C">CM Jones</name></author><author><name sortKey="Villadangos, Ja" uniqKey="Villadangos J">JA Villadangos</name></author><author><name sortKey="Zhan, Y" uniqKey="Zhan Y">Y Zhan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Leon, B" uniqKey="Leon B">B Leon</name></author><author><name sortKey="Ardavin, C" uniqKey="Ardavin C">C Ardavin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Qu, C" uniqKey="Qu C">C Qu</name></author><author><name sortKey="Brinck Jensen, Ns" uniqKey="Brinck Jensen N">NS Brinck-Jensen</name></author><author><name sortKey="Zang, M" uniqKey="Zang M">M Zang</name></author><author><name sortKey="Chen, K" uniqKey="Chen K">K Chen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Swiecki, M" uniqKey="Swiecki M">M Swiecki</name></author><author><name sortKey="Gilfillan, S" uniqKey="Gilfillan S">S Gilfillan</name></author><author><name sortKey="Vermi, W" uniqKey="Vermi W">W Vermi</name></author><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y Wang</name></author><author><name sortKey="Colonna, M" uniqKey="Colonna M">M Colonna</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hochrein, H" uniqKey="Hochrein H">H Hochrein</name></author><author><name sortKey="Shortman, K" uniqKey="Shortman K">K Shortman</name></author><author><name sortKey="Vremec, D" uniqKey="Vremec D">D Vremec</name></author><author><name sortKey="Scott, B" uniqKey="Scott B">B Scott</name></author><author><name sortKey="Hertzog, P" uniqKey="Hertzog P">P Hertzog</name></author><author><name sortKey="O Eeffe, M" uniqKey="O Eeffe M">M O’Keeffe</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pipkin, Me" uniqKey="Pipkin M">ME Pipkin</name></author><author><name sortKey="Sacks, Ja" uniqKey="Sacks J">JA Sacks</name></author><author><name sortKey="Cruz Guilloty, F" uniqKey="Cruz Guilloty F">F Cruz-Guilloty</name></author><author><name sortKey="Lichtenheld, Mg" uniqKey="Lichtenheld M">MG Lichtenheld</name></author><author><name sortKey="Bevan, Mj" uniqKey="Bevan M">MJ Bevan</name></author><author><name sortKey="Rao, A" uniqKey="Rao A">A Rao</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Luckheeram, Rv" uniqKey="Luckheeram R">RV Luckheeram</name></author><author><name sortKey="Zhou, R" uniqKey="Zhou R">R Zhou</name></author><author><name sortKey="Verma, Ad" uniqKey="Verma A">AD Verma</name></author><author><name sortKey="Xia, B" uniqKey="Xia B">B Xia</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Crotty, S" uniqKey="Crotty S">S Crotty</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kurosaki, T" uniqKey="Kurosaki T">T Kurosaki</name></author><author><name sortKey="Kometani, K" uniqKey="Kometani K">K Kometani</name></author><author><name sortKey="Ise, W" uniqKey="Ise W">W Ise</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jameson, Sc" uniqKey="Jameson S">SC Jameson</name></author><author><name sortKey="Masopust, D" uniqKey="Masopust D">D Masopust</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Obar, Jj" uniqKey="Obar J">JJ Obar</name></author><author><name sortKey="Lefrancois, L" uniqKey="Lefrancois L">L Lefrancois</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Macleod, Mk" uniqKey="Macleod M">MK MacLeod</name></author><author><name sortKey="Kappler, Jw" uniqKey="Kappler J">JW Kappler</name></author><author><name sortKey="Marrack, P" uniqKey="Marrack P">P Marrack</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kong, Kf" uniqKey="Kong K">KF Kong</name></author><author><name sortKey="Delroux, K" uniqKey="Delroux K">K Delroux</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X Wang</name></author><author><name sortKey="Qian, F" uniqKey="Qian F">F Qian</name></author><author><name sortKey="Arjona, A" uniqKey="Arjona A">A Arjona</name></author><author><name sortKey="Malawista, Se" uniqKey="Malawista S">SE Malawista</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Openshaw, Pj" uniqKey="Openshaw P">PJ Openshaw</name></author><author><name sortKey="Chiu, C" uniqKey="Chiu C">C Chiu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hendrickson, Cm" uniqKey="Hendrickson C">CM Hendrickson</name></author><author><name sortKey="Matthay, Ma" uniqKey="Matthay M">MA Matthay</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cheung, Cy" uniqKey="Cheung C">CY Cheung</name></author><author><name sortKey="Poon, Ll" uniqKey="Poon L">LL Poon</name></author><author><name sortKey="Lau, As" uniqKey="Lau A">AS Lau</name></author><author><name sortKey="Luk, W" uniqKey="Luk W">W Luk</name></author><author><name sortKey="Lau, Yl" uniqKey="Lau Y">YL Lau</name></author><author><name sortKey="Shortridge, Kf" uniqKey="Shortridge K">KF Shortridge</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ye, S" uniqKey="Ye S">S Ye</name></author><author><name sortKey="Lowther, S" uniqKey="Lowther S">S Lowther</name></author><author><name sortKey="Stambas, J" uniqKey="Stambas J">J Stambas</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pauli, Ek" uniqKey="Pauli E">EK Pauli</name></author><author><name sortKey="Schmolke, M" uniqKey="Schmolke M">M Schmolke</name></author><author><name sortKey="Wolff, T" uniqKey="Wolff T">T Wolff</name></author><author><name sortKey="Viemann, D" uniqKey="Viemann D">D Viemann</name></author><author><name sortKey="Roth, J" uniqKey="Roth J">J Roth</name></author><author><name sortKey="Bode, Jg" uniqKey="Bode J">JG Bode</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tumpey, Tm" uniqKey="Tumpey T">TM Tumpey</name></author><author><name sortKey="Basler, Cf" uniqKey="Basler C">CF Basler</name></author><author><name sortKey="Aguilar, Pv" uniqKey="Aguilar P">PV Aguilar</name></author><author><name sortKey="Zeng, H" uniqKey="Zeng H">H Zeng</name></author><author><name sortKey="Solorzano, A" uniqKey="Solorzano A">A Solorzano</name></author><author><name sortKey="Swayne, De" uniqKey="Swayne D">DE Swayne</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Saffarzadeh, M" uniqKey="Saffarzadeh M">M Saffarzadeh</name></author><author><name sortKey="Juenemann, C" uniqKey="Juenemann C">C Juenemann</name></author><author><name sortKey="Queisser, Ma" uniqKey="Queisser M">MA Queisser</name></author><author><name sortKey="Lochnit, G" uniqKey="Lochnit G">G Lochnit</name></author><author><name sortKey="Barreto, G" uniqKey="Barreto G">G Barreto</name></author><author><name sortKey="Galuska, Sp" uniqKey="Galuska S">SP Galuska</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tate, Md" uniqKey="Tate M">MD Tate</name></author><author><name sortKey="Deng, Ym" uniqKey="Deng Y">YM Deng</name></author><author><name sortKey="Jones, Je" uniqKey="Jones J">JE Jones</name></author><author><name sortKey="Anderson, Gp" uniqKey="Anderson G">GP Anderson</name></author><author><name sortKey="Brooks, Ag" uniqKey="Brooks A">AG Brooks</name></author><author><name sortKey="Reading, Pc" uniqKey="Reading P">PC Reading</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Narasaraju, T" uniqKey="Narasaraju T">T Narasaraju</name></author><author><name sortKey="Yang, E" uniqKey="Yang E">E Yang</name></author><author><name sortKey="Samy, Rp" uniqKey="Samy R">RP Samy</name></author><author><name sortKey="Ng, Hh" uniqKey="Ng H">HH Ng</name></author><author><name sortKey="Poh, Wp" uniqKey="Poh W">WP Poh</name></author><author><name sortKey="Liew, Aa" uniqKey="Liew A">AA Liew</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hoeksema, M" uniqKey="Hoeksema M">M Hoeksema</name></author><author><name sortKey="Tripathi, S" uniqKey="Tripathi S">S Tripathi</name></author><author><name sortKey="White, M" uniqKey="White M">M White</name></author><author><name sortKey="Qi, L" uniqKey="Qi L">L Qi</name></author><author><name sortKey="Taubenberger, J" uniqKey="Taubenberger J">J Taubenberger</name></author><author><name sortKey="Van Eijk, M" uniqKey="Van Eijk M">M van Eijk</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ashar, Hk" uniqKey="Ashar H">HK Ashar</name></author><author><name sortKey="Mueller, Nc" uniqKey="Mueller N">NC Mueller</name></author><author><name sortKey="Rudd, Jm" uniqKey="Rudd J">JM Rudd</name></author><author><name sortKey="Snider, Ta" uniqKey="Snider T">TA Snider</name></author><author><name sortKey="Achanta, M" uniqKey="Achanta M">M Achanta</name></author><author><name sortKey="Prasanthi, M" uniqKey="Prasanthi M">M Prasanthi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhu, L" uniqKey="Zhu L">L Zhu</name></author><author><name sortKey="Liu, L" uniqKey="Liu L">L Liu</name></author><author><name sortKey="Zhang, Y" uniqKey="Zhang Y">Y Zhang</name></author><author><name sortKey="Pu, L" uniqKey="Pu L">L Pu</name></author><author><name sortKey="Liu, J" uniqKey="Liu J">J Liu</name></author><author><name sortKey="Li, X" uniqKey="Li X">X Li</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Martinez, Ne" uniqKey="Martinez N">NE Martinez</name></author><author><name sortKey="Zimmermann, Tj" uniqKey="Zimmermann T">TJ Zimmermann</name></author><author><name sortKey="Goosmann, C" uniqKey="Goosmann C">C Goosmann</name></author><author><name sortKey="Alexander, T" uniqKey="Alexander T">T Alexander</name></author><author><name sortKey="Hedberg, C" uniqKey="Hedberg C">C Hedberg</name></author><author><name sortKey="Ziegler, S" uniqKey="Ziegler S">S Ziegler</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kusunoki, Y" uniqKey="Kusunoki Y">Y Kusunoki</name></author><author><name sortKey="Nakazawa, D" uniqKey="Nakazawa D">D Nakazawa</name></author><author><name sortKey="Shida, H" uniqKey="Shida H">H Shida</name></author><author><name sortKey="Hattanda, F" uniqKey="Hattanda F">F Hattanda</name></author><author><name sortKey="Miyoshi, A" uniqKey="Miyoshi A">A Miyoshi</name></author><author><name sortKey="Masuda, S" uniqKey="Masuda S">S Masuda</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hemmers, S" uniqKey="Hemmers S">S Hemmers</name></author><author><name sortKey="Teijaro, Jr" uniqKey="Teijaro J">JR Teijaro</name></author><author><name sortKey="Arandjelovic, S" uniqKey="Arandjelovic S">S Arandjelovic</name></author><author><name sortKey="Mowen, Ka" uniqKey="Mowen K">KA Mowen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kim, Hy" uniqKey="Kim H">HY Kim</name></author><author><name sortKey="Umetsu, Dt" uniqKey="Umetsu D">DT Umetsu</name></author><author><name sortKey="Dekruyff, Rh" uniqKey="Dekruyff R">RH Dekruyff</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Monticelli, La" uniqKey="Monticelli L">LA Monticelli</name></author><author><name sortKey="Sonnenberg, Gf" uniqKey="Sonnenberg G">GF Sonnenberg</name></author><author><name sortKey="Artis, D" uniqKey="Artis D">D Artis</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Monticelli, La" uniqKey="Monticelli L">LA Monticelli</name></author><author><name sortKey="Sonnenberg, Gf" uniqKey="Sonnenberg G">GF Sonnenberg</name></author><author><name sortKey="Abt, Mc" uniqKey="Abt M">MC Abt</name></author><author><name sortKey="Alenghat, T" uniqKey="Alenghat T">T Alenghat</name></author><author><name sortKey="Ziegler, Cg" uniqKey="Ziegler C">CG Ziegler</name></author><author><name sortKey="Doering, Ta" uniqKey="Doering T">TA Doering</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jiao, Y" uniqKey="Jiao Y">Y Jiao</name></author><author><name sortKey="Huntington, Nd" uniqKey="Huntington N">ND Huntington</name></author><author><name sortKey="Belz, Gt" uniqKey="Belz G">GT Belz</name></author><author><name sortKey="Seillet, C" uniqKey="Seillet C">C Seillet</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Weizman, Oe" uniqKey="Weizman O">OE Weizman</name></author><author><name sortKey="Adams, Nm" uniqKey="Adams N">NM Adams</name></author><author><name sortKey="Schuster, Is" uniqKey="Schuster I">IS Schuster</name></author><author><name sortKey="Krishna, C" uniqKey="Krishna C">C Krishna</name></author><author><name sortKey="Pritykin, Y" uniqKey="Pritykin Y">Y Pritykin</name></author><author><name sortKey="Lau, C" uniqKey="Lau C">C Lau</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Califano, D" uniqKey="Califano D">D Califano</name></author><author><name sortKey="Furuya, Y" uniqKey="Furuya Y">Y Furuya</name></author><author><name sortKey="Roberts, S" uniqKey="Roberts S">S Roberts</name></author><author><name sortKey="Avram, D" uniqKey="Avram D">D Avram</name></author><author><name sortKey="Mckenzie, Anj" uniqKey="Mckenzie A">ANJ McKenzie</name></author><author><name sortKey="Metzger, Dw" uniqKey="Metzger D">DW Metzger</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cephus, Jy" uniqKey="Cephus J">JY Cephus</name></author><author><name sortKey="Stier, Mt" uniqKey="Stier M">MT Stier</name></author><author><name sortKey="Fuseini, H" uniqKey="Fuseini H">H Fuseini</name></author><author><name sortKey="Yung, Ja" uniqKey="Yung J">JA Yung</name></author><author><name sortKey="Toki, S" uniqKey="Toki S">S Toki</name></author><author><name sortKey="Bloodworth, Mh" uniqKey="Bloodworth M">MH Bloodworth</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Doherty, Ta" uniqKey="Doherty T">TA Doherty</name></author><author><name sortKey="Broide, Dh" uniqKey="Broide D">DH Broide</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Vlahos, R" uniqKey="Vlahos R">R Vlahos</name></author><author><name sortKey="Selemidis, S" uniqKey="Selemidis S">S Selemidis</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Strengert, M" uniqKey="Strengert M">M Strengert</name></author><author><name sortKey="Jennings, R" uniqKey="Jennings R">R Jennings</name></author><author><name sortKey="Davanture, S" uniqKey="Davanture S">S Davanture</name></author><author><name sortKey="Hayes, P" uniqKey="Hayes P">P Hayes</name></author><author><name sortKey="Gabriel, G" uniqKey="Gabriel G">G Gabriel</name></author><author><name sortKey="Knaus, Ug" uniqKey="Knaus U">UG Knaus</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kim, Hj" uniqKey="Kim H">HJ Kim</name></author><author><name sortKey="Kim, Ch" uniqKey="Kim C">CH Kim</name></author><author><name sortKey="Ryu, Jh" uniqKey="Ryu J">JH Ryu</name></author><author><name sortKey="Kim, Mj" uniqKey="Kim M">MJ Kim</name></author><author><name sortKey="Park, Cy" uniqKey="Park C">CY Park</name></author><author><name sortKey="Lee, Jm" uniqKey="Lee J">JM Lee</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="To, Ee" uniqKey="To E">EE To</name></author><author><name sortKey="Vlahos, R" uniqKey="Vlahos R">R Vlahos</name></author><author><name sortKey="Luong, R" uniqKey="Luong R">R Luong</name></author><author><name sortKey="Halls, Ml" uniqKey="Halls M">ML Halls</name></author><author><name sortKey="Reading, Pc" uniqKey="Reading P">PC Reading</name></author><author><name sortKey="King, Pt" uniqKey="King P">PT King</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Amatore, D" uniqKey="Amatore D">D Amatore</name></author><author><name sortKey="Sgarbanti, R" uniqKey="Sgarbanti R">R Sgarbanti</name></author><author><name sortKey="Aquilano, K" uniqKey="Aquilano K">K Aquilano</name></author><author><name sortKey="Baldelli, S" uniqKey="Baldelli S">S Baldelli</name></author><author><name sortKey="Limongi, D" uniqKey="Limongi D">D Limongi</name></author><author><name sortKey="Civitelli, L" uniqKey="Civitelli L">L Civitelli</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lejal, N" uniqKey="Lejal N">N Lejal</name></author><author><name sortKey="Truchet, S" uniqKey="Truchet S">S Truchet</name></author><author><name sortKey="Bechor, E" uniqKey="Bechor E">E Bechor</name></author><author><name sortKey="Bouguyon, E" uniqKey="Bouguyon E">E Bouguyon</name></author><author><name sortKey="Khedkar, V" uniqKey="Khedkar V">V Khedkar</name></author><author><name sortKey="Bertho, N" uniqKey="Bertho N">N Bertho</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wind, S" uniqKey="Wind S">S Wind</name></author><author><name sortKey="Beuerlein, K" uniqKey="Beuerlein K">K Beuerlein</name></author><author><name sortKey="Eucker, T" uniqKey="Eucker T">T Eucker</name></author><author><name sortKey="Muller, H" uniqKey="Muller H">H Muller</name></author><author><name sortKey="Scheurer, P" uniqKey="Scheurer P">P Scheurer</name></author><author><name sortKey="Armitage, Me" uniqKey="Armitage M">ME Armitage</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Altenhofer, S" uniqKey="Altenhofer S">S Altenhofer</name></author><author><name sortKey="Kleikers, Pw" uniqKey="Kleikers P">PW Kleikers</name></author><author><name sortKey="Radermacher, Ka" uniqKey="Radermacher K">KA Radermacher</name></author><author><name sortKey="Scheurer, P" uniqKey="Scheurer P">P Scheurer</name></author><author><name sortKey="Rob Hermans, Jj" uniqKey="Rob Hermans J">JJ Rob Hermans</name></author><author><name sortKey="Schiffers, P" uniqKey="Schiffers P">P Schiffers</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Heumuller, S" uniqKey="Heumuller S">S Heumuller</name></author><author><name sortKey="Wind, S" uniqKey="Wind S">S Wind</name></author><author><name sortKey="Barbosa Sicard, E" uniqKey="Barbosa Sicard E">E Barbosa-Sicard</name></author><author><name sortKey="Schmidt, Hh" uniqKey="Schmidt H">HH Schmidt</name></author><author><name sortKey="Busse, R" uniqKey="Busse R">R Busse</name></author><author><name sortKey="Schroder, K" uniqKey="Schroder K">K Schroder</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Vlahos, R" uniqKey="Vlahos R">R Vlahos</name></author><author><name sortKey="Stambas, J" uniqKey="Stambas J">J Stambas</name></author><author><name sortKey="Bozinovski, S" uniqKey="Bozinovski S">S Bozinovski</name></author><author><name sortKey="Broughton, Br" uniqKey="Broughton B">BR Broughton</name></author><author><name sortKey="Drummond, Gr" uniqKey="Drummond G">GR Drummond</name></author><author><name sortKey="Selemidis, S" uniqKey="Selemidis S">S Selemidis</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Oostwoud, Lc" uniqKey="Oostwoud L">LC Oostwoud</name></author><author><name sortKey="Gunasinghe, P" uniqKey="Gunasinghe P">P Gunasinghe</name></author><author><name sortKey="Seow, Hj" uniqKey="Seow H">HJ Seow</name></author><author><name sortKey="Ye, Jm" uniqKey="Ye J">JM Ye</name></author><author><name sortKey="Selemidis, S" uniqKey="Selemidis S">S Selemidis</name></author><author><name sortKey="Bozinovski, S" uniqKey="Bozinovski S">S Bozinovski</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, Q" uniqKey="Liu Q">Q Liu</name></author><author><name sortKey="Zhou, Yh" uniqKey="Zhou Y">YH Zhou</name></author><author><name sortKey="Yang, Zq" uniqKey="Yang Z">ZQ Yang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Betakova, T" uniqKey="Betakova T">T Betakova</name></author><author><name sortKey="Kostrabova, A" uniqKey="Kostrabova A">A Kostrabova</name></author><author><name sortKey="Lachova, V" uniqKey="Lachova V">V Lachova</name></author><author><name sortKey="Turianova, L" uniqKey="Turianova L">L Turianova</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Julkunen, I" uniqKey="Julkunen I">I Julkunen</name></author><author><name sortKey="Sareneva, T" uniqKey="Sareneva T">T Sareneva</name></author><author><name sortKey="Pirhonen, J" uniqKey="Pirhonen J">J Pirhonen</name></author><author><name sortKey="Ronni, T" uniqKey="Ronni T">T Ronni</name></author><author><name sortKey="Melen, K" uniqKey="Melen K">K Melen</name></author><author><name sortKey="Matikainen, S" uniqKey="Matikainen S">S Matikainen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Iwai, A" uniqKey="Iwai A">A Iwai</name></author><author><name sortKey="Shiozaki, T" uniqKey="Shiozaki T">T Shiozaki</name></author><author><name sortKey="Miyazaki, T" uniqKey="Miyazaki T">T Miyazaki</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhou, X" uniqKey="Zhou X">X Zhou</name></author><author><name sortKey="Jiang, W" uniqKey="Jiang W">W Jiang</name></author><author><name sortKey="Liu, Z" uniqKey="Liu Z">Z Liu</name></author><author><name sortKey="Liu, S" uniqKey="Liu S">S Liu</name></author><author><name sortKey="Liang, X" uniqKey="Liang X">X Liang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="To, Kk" uniqKey="To K">KK To</name></author><author><name sortKey="Lau, Cc" uniqKey="Lau C">CC Lau</name></author><author><name sortKey="Woo, Pc" uniqKey="Woo P">PC Woo</name></author><author><name sortKey="Lau, Sk" uniqKey="Lau S">SK Lau</name></author><author><name sortKey="Chan, Jf" uniqKey="Chan J">JF Chan</name></author><author><name sortKey="Chan, Kh" uniqKey="Chan K">KH Chan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Quinn, Km" uniqKey="Quinn K">KM Quinn</name></author><author><name sortKey="Kan, Wt" uniqKey="Kan W">WT Kan</name></author><author><name sortKey="Watson, Ka" uniqKey="Watson K">KA Watson</name></author><author><name sortKey="Liddicoat, Bj" uniqKey="Liddicoat B">BJ Liddicoat</name></author><author><name sortKey="Swan, Ng" uniqKey="Swan N">NG Swan</name></author><author><name sortKey="Mcquilten, H" uniqKey="Mcquilten H">H McQuilten</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Deberge, Mp" uniqKey="Deberge M">MP DeBerge</name></author><author><name sortKey="Ely, Kh" uniqKey="Ely K">KH Ely</name></author><author><name sortKey="Enelow, Ri" uniqKey="Enelow R">RI Enelow</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Van De Sandt, Ce" uniqKey="Van De Sandt C">CE van de Sandt</name></author><author><name sortKey="Barcena, M" uniqKey="Barcena M">M Barcena</name></author><author><name sortKey="Koster, Aj" uniqKey="Koster A">AJ Koster</name></author><author><name sortKey="Kasper, J" uniqKey="Kasper J">J Kasper</name></author><author><name sortKey="Kirkpatrick, Cj" uniqKey="Kirkpatrick C">CJ Kirkpatrick</name></author><author><name sortKey="Scott, Dp" uniqKey="Scott D">DP Scott</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Brincks, El" uniqKey="Brincks E">EL Brincks</name></author><author><name sortKey="Woodland, Dl" uniqKey="Woodland D">DL Woodland</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gagnon, J" uniqKey="Gagnon J">J Gagnon</name></author><author><name sortKey="Ramanathan, S" uniqKey="Ramanathan S">S Ramanathan</name></author><author><name sortKey="Leblanc, C" uniqKey="Leblanc C">C Leblanc</name></author><author><name sortKey="Cloutier, A" uniqKey="Cloutier A">A Cloutier</name></author><author><name sortKey="Mcdonald, Pp" uniqKey="Mcdonald P">PP McDonald</name></author><author><name sortKey="Ilangumaran, S" uniqKey="Ilangumaran S">S Ilangumaran</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Damjanovic, D" uniqKey="Damjanovic D">D Damjanovic</name></author><author><name sortKey="Divangahi, M" uniqKey="Divangahi M">M Divangahi</name></author><author><name sortKey="Kugathasan, K" uniqKey="Kugathasan K">K Kugathasan</name></author><author><name sortKey="Small, Cl" uniqKey="Small C">CL Small</name></author><author><name sortKey="Zganiacz, A" uniqKey="Zganiacz A">A Zganiacz</name></author><author><name sortKey="Brown, Eg" uniqKey="Brown E">EG Brown</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, G" uniqKey="Yang G">G Yang</name></author><author><name sortKey="Hamacher, J" uniqKey="Hamacher J">J Hamacher</name></author><author><name sortKey="Gorshkov, B" uniqKey="Gorshkov B">B Gorshkov</name></author><author><name sortKey="White, R" uniqKey="White R">R White</name></author><author><name sortKey="Sridhar, S" uniqKey="Sridhar S">S Sridhar</name></author><author><name sortKey="Verin, A" uniqKey="Verin A">A Verin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Deberge, Mp" uniqKey="Deberge M">MP DeBerge</name></author><author><name sortKey="Ely, Kh" uniqKey="Ely K">KH Ely</name></author><author><name sortKey="Cheng, Gs" uniqKey="Cheng G">GS Cheng</name></author><author><name sortKey="Enelow, Ri" uniqKey="Enelow R">RI Enelow</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hasegawa, S" uniqKey="Hasegawa S">S Hasegawa</name></author><author><name sortKey="Matsushige, T" uniqKey="Matsushige T">T Matsushige</name></author><author><name sortKey="Inoue, H" uniqKey="Inoue H">H Inoue</name></author><author><name sortKey="Shirabe, K" uniqKey="Shirabe K">K Shirabe</name></author><author><name sortKey="Fukano, R" uniqKey="Fukano R">R Fukano</name></author><author><name sortKey="Ichiyama, T" uniqKey="Ichiyama T">T Ichiyama</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ichiyama, T" uniqKey="Ichiyama T">T Ichiyama</name></author><author><name sortKey="Nishikawa, M" uniqKey="Nishikawa M">M Nishikawa</name></author><author><name sortKey="Yoshitomi, T" uniqKey="Yoshitomi T">T Yoshitomi</name></author><author><name sortKey="Hayashi, T" uniqKey="Hayashi T">T Hayashi</name></author><author><name sortKey="Furukawa, S" uniqKey="Furukawa S">S Furukawa</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ito, Y" uniqKey="Ito Y">Y Ito</name></author><author><name sortKey="Ichiyama, T" uniqKey="Ichiyama T">T Ichiyama</name></author><author><name sortKey="Kimura, H" uniqKey="Kimura H">H Kimura</name></author><author><name sortKey="Shibata, M" uniqKey="Shibata M">M Shibata</name></author><author><name sortKey="Ishiwada, N" uniqKey="Ishiwada N">N Ishiwada</name></author><author><name sortKey="Kuroki, H" uniqKey="Kuroki H">H Kuroki</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lv, S" uniqKey="Lv S">S Lv</name></author><author><name sortKey="Song, Hl" uniqKey="Song H">HL Song</name></author><author><name sortKey="Zhou, Y" uniqKey="Zhou Y">Y Zhou</name></author><author><name sortKey="Li, Lx" uniqKey="Li L">LX Li</name></author><author><name sortKey="Cui, W" uniqKey="Cui W">W Cui</name></author><author><name sortKey="Wang, W" uniqKey="Wang W">W Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tsuge, M" uniqKey="Tsuge M">M Tsuge</name></author><author><name sortKey="Yasui, K" uniqKey="Yasui K">K Yasui</name></author><author><name sortKey="Ichiyawa, T" uniqKey="Ichiyawa T">T Ichiyawa</name></author><author><name sortKey="Saito, Y" uniqKey="Saito Y">Y Saito</name></author><author><name sortKey="Nagaoka, Y" uniqKey="Nagaoka Y">Y Nagaoka</name></author><author><name sortKey="Yashiro, M" uniqKey="Yashiro M">M Yashiro</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kuperberg, Sj" uniqKey="Kuperberg S">SJ Kuperberg</name></author><author><name sortKey="Wadgaonkar, R" uniqKey="Wadgaonkar R">R Wadgaonkar</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shi, X" uniqKey="Shi X">X Shi</name></author><author><name sortKey="Zhou, W" uniqKey="Zhou W">W Zhou</name></author><author><name sortKey="Huang, H" uniqKey="Huang H">H Huang</name></author><author><name sortKey="Zhu, H" uniqKey="Zhu H">H Zhu</name></author><author><name sortKey="Zhou, P" uniqKey="Zhou P">P Zhou</name></author><author><name sortKey="Zhu, H" uniqKey="Zhu H">H Zhu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dienz, O" uniqKey="Dienz O">O Dienz</name></author><author><name sortKey="Rud, Jg" uniqKey="Rud J">JG Rud</name></author><author><name sortKey="Eaton, Sm" uniqKey="Eaton S">SM Eaton</name></author><author><name sortKey="Lanthier, Pa" uniqKey="Lanthier P">PA Lanthier</name></author><author><name sortKey="Burg, E" uniqKey="Burg E">E Burg</name></author><author><name sortKey="Drew, A" uniqKey="Drew A">A Drew</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, Ml" uniqKey="Yang M">ML Yang</name></author><author><name sortKey="Wang, Ct" uniqKey="Wang C">CT Wang</name></author><author><name sortKey="Yang, Sj" uniqKey="Yang S">SJ Yang</name></author><author><name sortKey="Leu, Ch" uniqKey="Leu C">CH Leu</name></author><author><name sortKey="Chen, Sh" uniqKey="Chen S">SH Chen</name></author><author><name sortKey="Wu, Cl" uniqKey="Wu C">CL Wu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pyle, Cj" uniqKey="Pyle C">CJ Pyle</name></author><author><name sortKey="Uwadiae, Fi" uniqKey="Uwadiae F">FI Uwadiae</name></author><author><name sortKey="Swieboda, Dp" uniqKey="Swieboda D">DP Swieboda</name></author><author><name sortKey="Harker, Ja" uniqKey="Harker J">JA Harker</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Aiba, H" uniqKey="Aiba H">H Aiba</name></author><author><name sortKey="Mochizuki, M" uniqKey="Mochizuki M">M Mochizuki</name></author><author><name sortKey="Kimura, M" uniqKey="Kimura M">M Kimura</name></author><author><name sortKey="Hojo, H" uniqKey="Hojo H">H Hojo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fukumoto, Y" uniqKey="Fukumoto Y">Y Fukumoto</name></author><author><name sortKey="Okumura, A" uniqKey="Okumura A">A Okumura</name></author><author><name sortKey="Hayakawa, F" uniqKey="Hayakawa F">F Hayakawa</name></author><author><name sortKey="Suzuki, M" uniqKey="Suzuki M">M Suzuki</name></author><author><name sortKey="Kato, T" uniqKey="Kato T">T Kato</name></author><author><name sortKey="Watanabe, K" uniqKey="Watanabe K">K Watanabe</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cohen, Ss" uniqKey="Cohen S">SS Cohen</name></author><author><name sortKey="Min, M" uniqKey="Min M">M Min</name></author><author><name sortKey="Cummings, Ee" uniqKey="Cummings E">EE Cummings</name></author><author><name sortKey="Chen, X" uniqKey="Chen X">X Chen</name></author><author><name sortKey="Sadowska, Gb" uniqKey="Sadowska G">GB Sadowska</name></author><author><name sortKey="Sharma, S" uniqKey="Sharma S">S Sharma</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Song, M" uniqKey="Song M">M Song</name></author><author><name sortKey="Winchester, J" uniqKey="Winchester J">J Winchester</name></author><author><name sortKey="Albright, Rl" uniqKey="Albright R">RL Albright</name></author><author><name sortKey="Capponi, Vj" uniqKey="Capponi V">VJ Capponi</name></author><author><name sortKey="Choquette, Md" uniqKey="Choquette M">MD Choquette</name></author><author><name sortKey="Kellum, Ja" uniqKey="Kellum J">JA Kellum</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lees, Nj" uniqKey="Lees N">NJ Lees</name></author><author><name sortKey="Rosenberg, A" uniqKey="Rosenberg A">A Rosenberg</name></author><author><name sortKey="Hurtado Doce, Ai" uniqKey="Hurtado Doce A">AI Hurtado-Doce</name></author><author><name sortKey="Jones, J" uniqKey="Jones J">J Jones</name></author><author><name sortKey="Marczin, N" uniqKey="Marczin N">N Marczin</name></author><author><name sortKey="Zeriouh, M" uniqKey="Zeriouh M">M Zeriouh</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, Fd" uniqKey="Liu F">FD Liu</name></author><author><name sortKey="Kenngott, Ee" uniqKey="Kenngott E">EE Kenngott</name></author><author><name sortKey="Schroter, Mf" uniqKey="Schroter M">MF Schroter</name></author><author><name sortKey="Kuhl, A" uniqKey="Kuhl A">A Kuhl</name></author><author><name sortKey="Jennrich, S" uniqKey="Jennrich S">S Jennrich</name></author><author><name sortKey="Watzlawick, R" uniqKey="Watzlawick R">R Watzlawick</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Robinson, Km" uniqKey="Robinson K">KM Robinson</name></author><author><name sortKey="Lee, B" uniqKey="Lee B">B Lee</name></author><author><name sortKey="Scheller, Ev" uniqKey="Scheller E">EV Scheller</name></author><author><name sortKey="Mandalapu, S" uniqKey="Mandalapu S">S Mandalapu</name></author><author><name sortKey="Enelow, Ri" uniqKey="Enelow R">RI Enelow</name></author><author><name sortKey="Kolls, Jk" uniqKey="Kolls J">JK Kolls</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Krug, Rm" uniqKey="Krug R">RM Krug</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jureka, As" uniqKey="Jureka A">AS Jureka</name></author><author><name sortKey="Kleinpeter, Ab" uniqKey="Kleinpeter A">AB Kleinpeter</name></author><author><name sortKey="Cornilescu, G" uniqKey="Cornilescu G">G Cornilescu</name></author><author><name sortKey="Cornilescu, Cc" uniqKey="Cornilescu C">CC Cornilescu</name></author><author><name sortKey="Petit, Cm" uniqKey="Petit C">CM Petit</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ciancanelli, Mj" uniqKey="Ciancanelli M">MJ Ciancanelli</name></author><author><name sortKey="Huang, Sx" uniqKey="Huang S">SX Huang</name></author><author><name sortKey="Luthra, P" uniqKey="Luthra P">P Luthra</name></author><author><name sortKey="Garner, H" uniqKey="Garner H">H Garner</name></author><author><name sortKey="Itan, Y" uniqKey="Itan Y">Y Itan</name></author><author><name sortKey="Volpi, S" uniqKey="Volpi S">S Volpi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Davidson, S" uniqKey="Davidson S">S Davidson</name></author><author><name sortKey="Maini, Mk" uniqKey="Maini M">MK Maini</name></author><author><name sortKey="Wack, A" uniqKey="Wack A">A Wack</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Beilharz, Mw" uniqKey="Beilharz M">MW Beilharz</name></author><author><name sortKey="Cummins, Jm" uniqKey="Cummins J">JM Cummins</name></author><author><name sortKey="Bennett, Al" uniqKey="Bennett A">AL Bennett</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bennett, Al" uniqKey="Bennett A">AL Bennett</name></author><author><name sortKey="Smith, Dw" uniqKey="Smith D">DW Smith</name></author><author><name sortKey="Cummins, Mj" uniqKey="Cummins M">MJ Cummins</name></author><author><name sortKey="Jacoby, Pa" uniqKey="Jacoby P">PA Jacoby</name></author><author><name sortKey="Cummins, Jm" uniqKey="Cummins J">JM Cummins</name></author><author><name sortKey="Beilharz, Mw" uniqKey="Beilharz M">MW Beilharz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Davidson, S" uniqKey="Davidson S">S Davidson</name></author><author><name sortKey="Mccabe, Tm" uniqKey="Mccabe T">TM McCabe</name></author><author><name sortKey="Crotta, S" uniqKey="Crotta S">S Crotta</name></author><author><name sortKey="Gad, Hh" uniqKey="Gad H">HH Gad</name></author><author><name sortKey="Hessel, Em" uniqKey="Hessel E">EM Hessel</name></author><author><name sortKey="Beinke, S" uniqKey="Beinke S">S Beinke</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Davidson, S" uniqKey="Davidson S">S Davidson</name></author><author><name sortKey="Crotta, S" uniqKey="Crotta S">S Crotta</name></author><author><name sortKey="Mccabe, Tm" uniqKey="Mccabe T">TM McCabe</name></author><author><name sortKey="Wack, A" uniqKey="Wack A">A Wack</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kim, S" uniqKey="Kim S">S Kim</name></author><author><name sortKey="Kim, Mj" uniqKey="Kim M">MJ Kim</name></author><author><name sortKey="Kim, Ch" uniqKey="Kim C">CH Kim</name></author><author><name sortKey="Kang, Jw" uniqKey="Kang J">JW Kang</name></author><author><name sortKey="Shin, Hk" uniqKey="Shin H">HK Shin</name></author><author><name sortKey="Kim, Dy" uniqKey="Kim D">DY Kim</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, W" uniqKey="Li W">W Li</name></author><author><name sortKey="Moltedo, B" uniqKey="Moltedo B">B Moltedo</name></author><author><name sortKey="Moran, Tm" uniqKey="Moran T">TM Moran</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Galani, Ie" uniqKey="Galani I">IE Galani</name></author><author><name sortKey="Triantafyllia, V" uniqKey="Triantafyllia V">V Triantafyllia</name></author><author><name sortKey="Eleminiadou, Ee" uniqKey="Eleminiadou E">EE Eleminiadou</name></author><author><name sortKey="Koltsida, O" uniqKey="Koltsida O">O Koltsida</name></author><author><name sortKey="Stavropoulos, A" uniqKey="Stavropoulos A">A Stavropoulos</name></author><author><name sortKey="Manioudaki, M" uniqKey="Manioudaki M">M Manioudaki</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Coch, C" uniqKey="Coch C">C Coch</name></author><author><name sortKey="Stumpel, Jp" uniqKey="Stumpel J">JP Stumpel</name></author><author><name sortKey="Lilien Waldau, V" uniqKey="Lilien Waldau V">V Lilien-Waldau</name></author><author><name sortKey="Wohlleber, D" uniqKey="Wohlleber D">D Wohlleber</name></author><author><name sortKey="Kummerer, Bm" uniqKey="Kummerer B">BM Kummerer</name></author><author><name sortKey="Bekeredjian Ding, I" uniqKey="Bekeredjian Ding I">I Bekeredjian-Ding</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lee, Sm" uniqKey="Lee S">SM Lee</name></author><author><name sortKey="Gai, Ww" uniqKey="Gai W">WW Gai</name></author><author><name sortKey="Cheung, Tk" uniqKey="Cheung T">TK Cheung</name></author><author><name sortKey="Peiris, Js" uniqKey="Peiris J">JS Peiris</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, C" uniqKey="Li C">C Li</name></author><author><name sortKey="Li, C" uniqKey="Li C">C Li</name></author><author><name sortKey="Zhang, Aj" uniqKey="Zhang A">AJ Zhang</name></author><author><name sortKey="To, Kk" uniqKey="To K">KK To</name></author><author><name sortKey="Lee, Ac" uniqKey="Lee A">AC Lee</name></author><author><name sortKey="Zhu, H" uniqKey="Zhu H">H Zhu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lee, My" uniqKey="Lee M">MY Lee</name></author><author><name sortKey="Cheung, Cy" uniqKey="Cheung C">CY Cheung</name></author><author><name sortKey="Peiris, Js" uniqKey="Peiris J">JS Peiris</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Coulombe, F" uniqKey="Coulombe F">F Coulombe</name></author><author><name sortKey="Jaworska, J" uniqKey="Jaworska J">J Jaworska</name></author><author><name sortKey="Verway, M" uniqKey="Verway M">M Verway</name></author><author><name sortKey="Tzelepis, F" uniqKey="Tzelepis F">F Tzelepis</name></author><author><name sortKey="Massoud, A" uniqKey="Massoud A">A Massoud</name></author><author><name sortKey="Gillard, J" uniqKey="Gillard J">J Gillard</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chen, L" uniqKey="Chen L">L Chen</name></author><author><name sortKey="Fan, J" uniqKey="Fan J">J Fan</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y Li</name></author><author><name sortKey="Shi, X" uniqKey="Shi X">X Shi</name></author><author><name sortKey="Ju, D" uniqKey="Ju D">D Ju</name></author><author><name sortKey="Yan, Q" uniqKey="Yan Q">Q Yan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Takeuchi, O" uniqKey="Takeuchi O">O Takeuchi</name></author><author><name sortKey="Akira, S" uniqKey="Akira S">S Akira</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Le Goffic, R" uniqKey="Le Goffic R">R Le Goffic</name></author><author><name sortKey="Pothlichet, J" uniqKey="Pothlichet J">J Pothlichet</name></author><author><name sortKey="Vitour, D" uniqKey="Vitour D">D Vitour</name></author><author><name sortKey="Fujita, T" uniqKey="Fujita T">T Fujita</name></author><author><name sortKey="Meurs, E" uniqKey="Meurs E">E Meurs</name></author><author><name sortKey="Chignard, M" uniqKey="Chignard M">M Chignard</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lee, Sm" uniqKey="Lee S">SM Lee</name></author><author><name sortKey="Kok, Kh" uniqKey="Kok K">KH Kok</name></author><author><name sortKey="Jaume, M" uniqKey="Jaume M">M Jaume</name></author><author><name sortKey="Cheung, Tk" uniqKey="Cheung T">TK Cheung</name></author><author><name sortKey="Yip, Tf" uniqKey="Yip T">TF Yip</name></author><author><name sortKey="Lai, Jc" uniqKey="Lai J">JC Lai</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wu, W" uniqKey="Wu W">W Wu</name></author><author><name sortKey="Zhang, W" uniqKey="Zhang W">W Zhang</name></author><author><name sortKey="Duggan, Es" uniqKey="Duggan E">ES Duggan</name></author><author><name sortKey="Booth, Jl" uniqKey="Booth J">JL Booth</name></author><author><name sortKey="Zou, Mh" uniqKey="Zou M">MH Zou</name></author><author><name sortKey="Metcalf, Jp" uniqKey="Metcalf J">JP Metcalf</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Patel, Jr" uniqKey="Patel J">JR Patel</name></author><author><name sortKey="Garcia Sastre, A" uniqKey="Garcia Sastre A">A Garcia-Sastre</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Weber Gerlach, M" uniqKey="Weber Gerlach M">M Weber-Gerlach</name></author><author><name sortKey="Weber, F" uniqKey="Weber F">F Weber</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yoneyama, M" uniqKey="Yoneyama M">M Yoneyama</name></author><author><name sortKey="Onomoto, K" uniqKey="Onomoto K">K Onomoto</name></author><author><name sortKey="Jogi, M" uniqKey="Jogi M">M Jogi</name></author><author><name sortKey="Akaboshi, T" uniqKey="Akaboshi T">T Akaboshi</name></author><author><name sortKey="Fujita, T" uniqKey="Fujita T">T Fujita</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="De Nardo, D" uniqKey="De Nardo D">D De Nardo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kagan, Jc" uniqKey="Kagan J">JC Kagan</name></author><author><name sortKey="Su, T" uniqKey="Su T">T Su</name></author><author><name sortKey="Horng, T" uniqKey="Horng T">T Horng</name></author><author><name sortKey="Chow, A" uniqKey="Chow A">A Chow</name></author><author><name sortKey="Akira, S" uniqKey="Akira S">S Akira</name></author><author><name sortKey="Medzhitov, R" uniqKey="Medzhitov R">R Medzhitov</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Oosting, M" uniqKey="Oosting M">M Oosting</name></author><author><name sortKey="Cheng, Sc" uniqKey="Cheng S">SC Cheng</name></author><author><name sortKey="Bolscher, Jm" uniqKey="Bolscher J">JM Bolscher</name></author><author><name sortKey="Vestering Stenger, R" uniqKey="Vestering Stenger R">R Vestering-Stenger</name></author><author><name sortKey="Plantinga, Ts" uniqKey="Plantinga T">TS Plantinga</name></author><author><name sortKey="Verschueren, Ic" uniqKey="Verschueren I">IC Verschueren</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jiang, S" uniqKey="Jiang S">S Jiang</name></author><author><name sortKey="Li, X" uniqKey="Li X">X Li</name></author><author><name sortKey="Hess, Nj" uniqKey="Hess N">NJ Hess</name></author><author><name sortKey="Guan, Y" uniqKey="Guan Y">Y Guan</name></author><author><name sortKey="Tapping, Ri" uniqKey="Tapping R">RI Tapping</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lee, Smy" uniqKey="Lee S">SMY Lee</name></author><author><name sortKey="Yip, Tf" uniqKey="Yip T">TF Yip</name></author><author><name sortKey="Yan, S" uniqKey="Yan S">S Yan</name></author><author><name sortKey="Jin, Dy" uniqKey="Jin D">DY Jin</name></author><author><name sortKey="Wei, Hl" uniqKey="Wei H">HL Wei</name></author><author><name sortKey="Guo, Rt" uniqKey="Guo R">RT Guo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Imai, Y" uniqKey="Imai Y">Y Imai</name></author><author><name sortKey="Kuba, K" uniqKey="Kuba K">K Kuba</name></author><author><name sortKey="Neely, Gg" uniqKey="Neely G">GG Neely</name></author><author><name sortKey="Yaghubian Malhami, R" uniqKey="Yaghubian Malhami R">R Yaghubian-Malhami</name></author><author><name sortKey="Perkmann, T" uniqKey="Perkmann T">T Perkmann</name></author><author><name sortKey="Van Loo, G" uniqKey="Van Loo G">G van Loo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tsai, Sy" uniqKey="Tsai S">SY Tsai</name></author><author><name sortKey="Segovia, Ja" uniqKey="Segovia J">JA Segovia</name></author><author><name sortKey="Chang, Th" uniqKey="Chang T">TH Chang</name></author><author><name sortKey="Morris, Ir" uniqKey="Morris I">IR Morris</name></author><author><name sortKey="Berton, Mt" uniqKey="Berton M">MT Berton</name></author><author><name sortKey="Tessier, Pa" uniqKey="Tessier P">PA Tessier</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Opal, Sm" uniqKey="Opal S">SM Opal</name></author><author><name sortKey="Laterre, Pf" uniqKey="Laterre P">PF Laterre</name></author><author><name sortKey="Francois, B" uniqKey="Francois B">B Francois</name></author><author><name sortKey="Larosa, Sp" uniqKey="Larosa S">SP LaRosa</name></author><author><name sortKey="Angus, Dc" uniqKey="Angus D">DC Angus</name></author><author><name sortKey="Mira, Jp" uniqKey="Mira J">JP Mira</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shirey, Ka" uniqKey="Shirey K">KA Shirey</name></author><author><name sortKey="Lai, W" uniqKey="Lai W">W Lai</name></author><author><name sortKey="Scott, Aj" uniqKey="Scott A">AJ Scott</name></author><author><name sortKey="Lipsky, M" uniqKey="Lipsky M">M Lipsky</name></author><author><name sortKey="Mistry, P" uniqKey="Mistry P">P Mistry</name></author><author><name sortKey="Pletneva, Lm" uniqKey="Pletneva L">LM Pletneva</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Perrin Cocon, L" uniqKey="Perrin Cocon L">L Perrin-Cocon</name></author><author><name sortKey="Aublin Gex, A" uniqKey="Aublin Gex A">A Aublin-Gex</name></author><author><name sortKey="Sestito, Se" uniqKey="Sestito S">SE Sestito</name></author><author><name sortKey="Shirey, Ka" uniqKey="Shirey K">KA Shirey</name></author><author><name sortKey="Patel, Mc" uniqKey="Patel M">MC Patel</name></author><author><name sortKey="Andre, P" uniqKey="Andre P">P Andre</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Piao, W" uniqKey="Piao W">W Piao</name></author><author><name sortKey="Shirey, Ka" uniqKey="Shirey K">KA Shirey</name></author><author><name sortKey="Ru, Lw" uniqKey="Ru L">LW Ru</name></author><author><name sortKey="Lai, W" uniqKey="Lai W">W Lai</name></author><author><name sortKey="Szmacinski, H" uniqKey="Szmacinski H">H Szmacinski</name></author><author><name sortKey="Snyder, Ga" uniqKey="Snyder G">GA Snyder</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shirey, Ka" uniqKey="Shirey K">KA Shirey</name></author><author><name sortKey="Lai, W" uniqKey="Lai W">W Lai</name></author><author><name sortKey="Patel, Mc" uniqKey="Patel M">MC Patel</name></author><author><name sortKey="Pletneva, Lm" uniqKey="Pletneva L">LM Pletneva</name></author><author><name sortKey="Pang, C" uniqKey="Pang C">C Pang</name></author><author><name sortKey="Kurt Jones, E" uniqKey="Kurt Jones E">E Kurt-Jones</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Leung, Yh" uniqKey="Leung Y">YH Leung</name></author><author><name sortKey="Nicholls, Jm" uniqKey="Nicholls J">JM Nicholls</name></author><author><name sortKey="Ho, Ck" uniqKey="Ho C">CK Ho</name></author><author><name sortKey="Sia, Sf" uniqKey="Sia S">SF Sia</name></author><author><name sortKey="Mok, Ck" uniqKey="Mok C">CK Mok</name></author><author><name sortKey="Valkenburg, Sa" uniqKey="Valkenburg S">SA Valkenburg</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gao, W" uniqKey="Gao W">W Gao</name></author><author><name sortKey="Xiong, Y" uniqKey="Xiong Y">Y Xiong</name></author><author><name sortKey="Li, Q" uniqKey="Li Q">Q Li</name></author><author><name sortKey="Yang, H" uniqKey="Yang H">H Yang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cheng, K" uniqKey="Cheng K">K Cheng</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X Wang</name></author><author><name sortKey="Yin, H" uniqKey="Yin H">H Yin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, Z" uniqKey="Li Z">Z Li</name></author><author><name sortKey="Li, L" uniqKey="Li L">L Li</name></author><author><name sortKey="Zhou, H" uniqKey="Zhou H">H Zhou</name></author><author><name sortKey="Zeng, L" uniqKey="Zeng L">L Zeng</name></author><author><name sortKey="Chen, T" uniqKey="Chen T">T Chen</name></author><author><name sortKey="Chen, Q" uniqKey="Chen Q">Q Chen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tian, J" uniqKey="Tian J">J Tian</name></author><author><name sortKey="Jiao, X" uniqKey="Jiao X">X Jiao</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X Wang</name></author><author><name sortKey="Geng, J" uniqKey="Geng J">J Geng</name></author><author><name sortKey="Wang, R" uniqKey="Wang R">R Wang</name></author><author><name sortKey="Liu, N" uniqKey="Liu N">N Liu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hulme, Kd" uniqKey="Hulme K">KD Hulme</name></author><author><name sortKey="Gallo, La" uniqKey="Gallo L">LA Gallo</name></author><author><name sortKey="Short, Kr" uniqKey="Short K">KR Short</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kohio, Hp" uniqKey="Kohio H">HP Kohio</name></author><author><name sortKey="Adamson, Al" uniqKey="Adamson A">AL Adamson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Miyake Stoner, Sj" uniqKey="Miyake Stoner S">SJ Miyake-Stoner</name></author><author><name sortKey="O Hea, Cc" uniqKey="O Hea C">CC O’Shea</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Munger, J" uniqKey="Munger J">J Munger</name></author><author><name sortKey="Bajad, Su" uniqKey="Bajad S">SU Bajad</name></author><author><name sortKey="Coller, Ha" uniqKey="Coller H">HA Coller</name></author><author><name sortKey="Shenk, T" uniqKey="Shenk T">T Shenk</name></author><author><name sortKey="Rabinowitz, Jd" uniqKey="Rabinowitz J">JD Rabinowitz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Koyuncu, E" uniqKey="Koyuncu E">E Koyuncu</name></author><author><name sortKey="Purdy, Jg" uniqKey="Purdy J">JG Purdy</name></author><author><name sortKey="Rabinowitz, Jd" uniqKey="Rabinowitz J">JD Rabinowitz</name></author><author><name sortKey="Shenk, T" uniqKey="Shenk T">T Shenk</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Goodwin, Cm" uniqKey="Goodwin C">CM Goodwin</name></author><author><name sortKey="Xu, S" uniqKey="Xu S">S Xu</name></author><author><name sortKey="Munger, J" uniqKey="Munger J">J Munger</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sanchez, El" uniqKey="Sanchez E">EL Sanchez</name></author><author><name sortKey="Lagunoff, M" uniqKey="Lagunoff M">M Lagunoff</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Smallwood, Hs" uniqKey="Smallwood H">HS Smallwood</name></author><author><name sortKey="Duan, S" uniqKey="Duan S">S Duan</name></author><author><name sortKey="Morfouace, M" uniqKey="Morfouace M">M Morfouace</name></author><author><name sortKey="Rezinciuc, S" uniqKey="Rezinciuc S">S Rezinciuc</name></author><author><name sortKey="Shulkin, Bl" uniqKey="Shulkin B">BL Shulkin</name></author><author><name sortKey="Shelat, A" uniqKey="Shelat A">A Shelat</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ritter, Jb" uniqKey="Ritter J">JB Ritter</name></author><author><name sortKey="Wahl, As" uniqKey="Wahl A">AS Wahl</name></author><author><name sortKey="Freund, S" uniqKey="Freund S">S Freund</name></author><author><name sortKey="Genzel, Y" uniqKey="Genzel Y">Y Genzel</name></author><author><name sortKey="Reichl, U" uniqKey="Reichl U">U Reichl</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ryan, Dg" uniqKey="Ryan D">DG Ryan</name></author><author><name sortKey="O Eill, Laj" uniqKey="O Eill L">LAJ O’Neill</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tannahill, Gm" uniqKey="Tannahill G">GM Tannahill</name></author><author><name sortKey="Curtis, Am" uniqKey="Curtis A">AM Curtis</name></author><author><name sortKey="Adamik, J" uniqKey="Adamik J">J Adamik</name></author><author><name sortKey="Palsson Mcdermott, Em" uniqKey="Palsson Mcdermott E">EM Palsson-McDermott</name></author><author><name sortKey="Mcgettrick, Af" uniqKey="Mcgettrick A">AF McGettrick</name></author><author><name sortKey="Goel, G" uniqKey="Goel G">G Goel</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mills, El" uniqKey="Mills E">EL Mills</name></author><author><name sortKey="Ryan, Dg" uniqKey="Ryan D">DG Ryan</name></author><author><name sortKey="Prag, Ha" uniqKey="Prag H">HA Prag</name></author><author><name sortKey="Dikovskaya, D" uniqKey="Dikovskaya D">D Dikovskaya</name></author><author><name sortKey="Menon, D" uniqKey="Menon D">D Menon</name></author><author><name sortKey="Zaslona, Z" uniqKey="Zaslona Z">Z Zaslona</name></author></analytic></biblStruct></listBibl></div1></back></TEI><pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Immunol</journal-id><journal-id journal-id-type="iso-abbrev">Front Immunol</journal-id><journal-id journal-id-type="publisher-id">Front. Immunol.</journal-id><journal-title-group><journal-title>Frontiers in Immunology</journal-title></journal-title-group><issn pub-type="epub">1664-3224</issn><publisher><publisher-name>Frontiers Media S.A.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">30042762</article-id><article-id pub-id-type="pmc">6048202</article-id><article-id pub-id-type="doi">10.3389/fimmu.2018.01547</article-id><article-categories><subj-group subj-group-type="heading"><subject>Immunology</subject><subj-group><subject>Review</subject></subj-group></subj-group></article-categories><title-group><article-title>Advancements in Host-Based Interventions for Influenza Treatment</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Yip</surname><given-names>Tsz-Fung</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><uri xlink:type="simple" xlink:href="https://frontiersin.org/people/u/512497"></uri></contrib><contrib contrib-type="author"><name><surname>Selim</surname><given-names>Aisha Sami Mohammed</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><uri xlink:type="simple" xlink:href="https://frontiersin.org/people/u/568399"></uri></contrib><contrib contrib-type="author"><name><surname>Lian</surname><given-names>Ida</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref><uri xlink:type="simple" xlink:href="https://frontiersin.org/people/u/551388"></uri></contrib><contrib contrib-type="author"><name><surname>Lee</surname><given-names>Suki Man-Yan</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="corresp" rid="fn001">*</xref><uri xlink:type="simple" xlink:href="https://frontiersin.org/people/u/487283"></uri></contrib></contrib-group><aff id="aff1"><sup>1</sup><institution>HKU-Pasteur Research Pole, School of Public Health, The University of Hong Kong</institution>,<addr-line>Hong Kong</addr-line>,<country>Hong Kong</country></aff><aff id="aff2"><sup>2</sup><institution>School of Life Sciences and Chemical Technology, Ngee Ann Polytechnic</institution>,<addr-line>Singapore</addr-line>,<country>Singapore</country></aff><author-notes><fn fn-type="edited-by"><p>Edited by: Alan Chen-Yu Hsu, University of Newcastle, Australia</p></fn><fn fn-type="edited-by"><p>Reviewed by: Stavros Selemidis, Monash University, Australia; Anastasia N. Vlasova, The Ohio State University, United States</p></fn><corresp id="fn001">*Correspondence: Suki Man-Yan Lee, <email>suki@hku.hk</email>, <email>myleesuki01@gmail.com</email></corresp><fn fn-type="other" id="fn002"><p>Specialty section: This article was submitted to Microbial Immunology, a section of the journal Frontiers in Immunology</p></fn></author-notes><pub-date pub-type="epub"><day>10</day><month>7</month><year>2018</year></pub-date><pub-date pub-type="collection"><year>2018</year></pub-date><volume>9</volume><elocation-id>1547</elocation-id><history><date date-type="received"><day>13</day><month>4</month><year>2018</year></date><date date-type="accepted"><day>22</day><month>6</month><year>2018</year></date></history><permissions><copyright-statement>Copyright © 2018 Yip, Selim, Lian and Lee.</copyright-statement><copyright-year>2018</copyright-year><copyright-holder>Yip, Selim, Lian and Lee</copyright-holder><license xlink:href="https://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p></license></permissions><abstract><p>Influenza is a major acute respiratory infection that causes mortality and morbidity worldwide. Two classes of conventional antivirals, M2 ion channel blockers and neuraminidase inhibitors, are mainstays in managing influenza disease to lessen symptoms while minimizing hospitalization and death in patients with severe influenza. However, the development of viral resistance to both drug classes has become a major public health concern. Vaccines are prophylaxis mainstays but are limited in efficacy due to the difficulty in matching predicted dominant viral strains to circulating strains. As such, other potential interventions are being explored. Since viruses rely on host cellular functions to replicate, recent therapeutic developments focus on targeting host factors involved in virus replication. Besides controlling virus replication, potential targets for drug development include controlling virus-induced host immune responses such as the recently suggested involvement of innate lymphoid cells and NADPH oxidases in influenza virus pathogenesis and immune cell metabolism. In this review, we will discuss the advancements in novel host-based interventions for treating influenza disease.</p></abstract><kwd-group><kwd>host factors</kwd><kwd>influenza</kwd><kwd>cytokines</kwd><kwd>metabolism</kwd><kwd>immunomodulation</kwd></kwd-group><funding-group><award-group><funding-source id="cn01">Research Grants Council, University Grants Committee<named-content content-type="fundref-id">10.13039/501100002920</named-content></funding-source><award-id rid="cn01">17111714, T11-705/14-N</award-id></award-group><award-group><funding-source id="cn02">Health and Medical Research Fund<named-content content-type="fundref-id">10.13039/501100005847</named-content></funding-source><award-id rid="cn02">12111822, 14130662</award-id></award-group></funding-group><counts><fig-count count="1"></fig-count><table-count count="2"></table-count><equation-count count="0"></equation-count><ref-count count="268"></ref-count><page-count count="21"></page-count><word-count count="19638"></word-count></counts></article-meta></front><body><sec sec-type="introduction" id="S1"><title>Introduction</title><p>Influenza remains a source of public health concern. Influenza A virus (IAV) has been the cause of historical noxious pandemics, such as the Spanish flu 1918 H1N1, Asian flu H2N2 1957, Hong Kong H3N2 flu 1968, and more recently the pandemic of H1N1 2009 (Swine flu). Influenza also causes seasonal epidemics and outbreaks with high morbidity and mortality rates such as the 2015 H1N1 outbreak in India (<xref rid="B1" ref-type="bibr">1</xref>, <xref rid="B2" ref-type="bibr">2</xref>). The error-prone nature of the viral RNA polymerase (RdRP) and virus’ capacity for genetic re-assortment (antigenic drift and shift) result in the viral components’ susceptibility to mutations, allowing the viruses to evade the immune system and increases their resistance to control strategies.</p><p>Currently, influenza vaccination and two classes of antiviral drugs—M2 ion channel blockers (amantadine and rimantadine) and neuraminidase (NA) inhibitor (oseltamivir, zanamivir, and peramivir)—and the novel treatment option using polymerase inhibitor (favipiravir) are considered as mainstays in influenza infection treatment and control. The use of influenza vaccinations remains challenging due to antigenic drifts and shifts, with seasonal variation of new circulating species. Production of vaccine is time consuming with efficacy concerns, especially in the case of pandemic. Variations in vaccine efficacy caused by age should be aware, with studies suggesting that vaccine-conferred protection may not be optimal in certain age groups (<xref rid="B3" ref-type="bibr">3</xref>).</p><p>The disadvantages of using the conventional antiviral drugs have also been a concern. Significant levels of resistance to both classes of drugs have been repeatedly reported (<xref rid="B4" ref-type="bibr">4</xref>, <xref rid="B5" ref-type="bibr">5</xref>). High level of resistance (up to 91%) to M2 blockers has been reported in H3N2 virus strain in American isolates (<xref rid="B6" ref-type="bibr">6</xref>). Resistance has also been reported in H5N1 virus (<xref rid="B7" ref-type="bibr">7</xref>). IAV resistance to NA inhibitors has also become an increasingly prevalent concern, with the recent highly fatal outbreak of influenza A(H1N1)pdm09 in India 2015 associated with oseltamivir drug resistance (<xref rid="B8" ref-type="bibr">8</xref>, <xref rid="B9" ref-type="bibr">9</xref>). In addition, a large cluster of influenza A(H1N1)pdm09 viruses in Japan was found to have increased oseltamivir and peramivir drug resistance (<xref rid="B5" ref-type="bibr">5</xref>). There is an urgent need to search for alternative targets to treat influenza virus infections, including non-viral targets such as host cellular factors; which are promising as viruses rely on the host machinery for replication. While host immune response is intended to confer a degree of protection against the infection, an impaired or exaggerated host immune response could be detrimental—IAV H5N1 and H7N9 virus infection was reported to exaggerate aberrant cytokine release, resulting in a cytokine storm that caused accelerated host death (<xref rid="B10" ref-type="bibr">10</xref>–<xref rid="B12" ref-type="bibr">12</xref>).</p><p>Many recent studies have focused on the investigation of targeting host factors to control virus replication as well as modulate immune response, which we have previously evaluated (<xref rid="B13" ref-type="bibr">13</xref>). In this review, we will discuss the latest studies (in the past 5 years) on the investigation of novel host-based approaches with potential for influenza treatment.</p></sec><sec id="S2"><title>Strategies Targeting Host Cell Machinery</title><p>The replication cycle of IAV can be grossly divided into four different stages: (1) entry, (2) genome nuclear import, (3) replication and protein synthesis, and (4) genome nuclear export, apical transport, assembly, and budding. As an obligate intracellular pathogen, IAVs are heavily dependent on host machinery for replication and propagation. To this extent, studies employing genome-wide RNA interference (RNAi) to screen for host factors involved in IAV replication cycle have been performed (<xref rid="B14" ref-type="bibr">14</xref>, <xref rid="B15" ref-type="bibr">15</xref>) and an increasing number of approaches targeting these host factors to control IAV replication have been investigated.</p><sec id="S2-1"><title>Entry of IAV</title><p>Entry of IAV into the host cell is divided into several steps (<xref rid="B16" ref-type="bibr">16</xref>, <xref rid="B17" ref-type="bibr">17</xref>). First, hemagglutinin (HA) on the surface of IAV binds to the terminal α-sialic acid on the host cell receptor. This induces the internalization of the viral particle by clathrin-dependent, caveolin-, and clathrin-independent endocytosis (<xref rid="B18" ref-type="bibr">18</xref>). Macropinocytosis was revealed as an alternative entry pathway for IAV (<xref rid="B19" ref-type="bibr">19</xref>), which subsequently enters the canonical endocytic pathway (<xref rid="B20" ref-type="bibr">20</xref>, <xref rid="B21" ref-type="bibr">21</xref>). The vesicle-containing viral particle forms an early endosome (also known as sorting endosome), which matures into a late endosome as the endocytic pathway progresses. A gradual decrease in intraluminal pH from pH 6.5 to 5.0, mediated by V-ATPase proton pump (<xref rid="B22" ref-type="bibr">22</xref>), takes place as the endosome matures (<xref rid="B23" ref-type="bibr">23</xref>, <xref rid="B24" ref-type="bibr">24</xref>). This pH drop in the endosomal lumen induces a conformational change in HA, which is activated by proteolytic cleavage to generate HA1 and HA2 from precursor molecule HA0 (<xref rid="B25" ref-type="bibr">25</xref>, <xref rid="B26" ref-type="bibr">26</xref>). This conformational change triggers the fusion of the viral envelope with the endosomal membrane, releasing the viral genome into the cytoplasm.</p><p>Acidification of the endosome causes the subsequent acidification of viral lumen <italic>via</italic> the IAV M2 proton channel (<xref rid="B27" ref-type="bibr">27</xref>), which in turn promotes the dissociation of M1 layer from both the viral envelope (<xref rid="B24" ref-type="bibr">24</xref>) and the viral ribonucleoprotein (vRNP) complex (<xref rid="B28" ref-type="bibr">28</xref>). Interestingly, a sharp decrease in pH from neutral to an acidic pH of 5.0 as utilized by acid bypass has been observed to be sub-optimal for viral replication. It is hence proposed that a gradual decrease in endosomal pH is necessary for sequential reduction in viral stiffness, dissociation of M1 from the NP in the vRNP complex, destabilization of M1 layer from the viral envelope, and the eventual conformational change of the HA for the release of viral genome and proteins to the cytoplasm from late endosome (<xref rid="B24" ref-type="bibr">24</xref>).</p><sec id="S2-1-1"><title>Inhibition of Proteolytic Cleavage of HA</title><p>Proteolytic cleavage of HA0 to HA1/HA2 is an important step in IAV replication. This cleavage relocates HA2, converting previously uncleaved HA0 to a metastable conformation that induces membrane fusion at acidic pH (<xref rid="B29" ref-type="bibr">29</xref>). Inefficient cleavage and activation of HA leads to low infectivity (<xref rid="B30" ref-type="bibr">30</xref>). As identified proteins encoded by the viral genome do not possess proteolytic properties, the virus is dependent on host protease for the cleavage of HA. This provides a potential target to control IAV infection. HA is commonly cleaved by trypsin-like proteases at the single arginine residue at position 329. Human airway epithelium serine proteases HAT and TMPRSS2 were identified as the host factors for cleavage at this residue (<xref rid="B31" ref-type="bibr">31</xref>).</p><p>Aprotinin, purified from bovine lung (<xref rid="B32" ref-type="bibr">32</xref>), is a protease inhibitor with a long history of clinical use as an antifibrinolytic agent in cardiac surgery (<xref rid="B33" ref-type="bibr">33</xref>). Its potential as an anti-IAV drug has been recognized for over a decade (<xref rid="B34" ref-type="bibr">34</xref>) and has been shown to reduce the infectivity of a broad spectrum of IAV strains (<xref rid="B34" ref-type="bibr">34</xref>, <xref rid="B35" ref-type="bibr">35</xref>) both <italic>in vitro</italic> (<xref rid="B26" ref-type="bibr">26</xref>) and <italic>in vivo</italic> (<xref rid="B36" ref-type="bibr">36</xref>). Once withdrawn from the Western drug market due to its association with mortality (<xref rid="B33" ref-type="bibr">33</xref>), aprotinin has been approved as a locally administered, small-particle aerosol drug for the treatment of IAV infection in Russia (<xref rid="B36" ref-type="bibr">36</xref>). However, side-effects associated with the systemic administration of aprotinin raises the need for an alternative protease inhibitor for use in treatment of IAV infections.</p><p>Camostat, a serine protease inhibitor, was reported to demonstrate anti-IAV potential in mice dating back to 1996 (<xref rid="B37" ref-type="bibr">37</xref>), but little to no research has been conducted to develop it into an anti-IAV treatment. It was revisited and proven to be one of the most efficient serine protease inhibitors for the inhibition of IAV replication in primary human tracheal epithelial cells <italic>in vitro</italic> when tested compounds were used at similar molarities (<xref rid="B35" ref-type="bibr">35</xref>). At present, camostat is widely administered for the treatment of liver fibrosis, chronic pancreatitis, and cancer (<xref rid="B38" ref-type="bibr">38</xref>, <xref rid="B39" ref-type="bibr">39</xref>), making it a highly promising candidate for drug repurposing. Despite the lack of association between camostat and increased mortality (as with aprotinin), reports of camostat potentially inducing acute eosinophilic pneumonia (<xref rid="B38" ref-type="bibr">38</xref>) warrants the need for careful consideration and further research into the repositioning of drugs from the same class.</p><p>Highly pathogenic IAV, such as the H5 and H7 subtypes, are reported to have HA cleavage sites rich in basic residues (<xref rid="B30" ref-type="bibr">30</xref>). The polybasic nature of the cleavage sites provides multiple targets for a broad spectrum of proteases, including the more ubiquitously expressed intracellular proteases such as furin (<xref rid="B40" ref-type="bibr">40</xref>). This increased protease spectrum could be utilized by these viruses for the activation of HA prior to viral budding, allowing for evasion of potential inhibition by exogenously administered serine protease inhibitors. Furthermore, an <italic>in vivo</italic> study utilizing mice treated with a single protease inhibitor prior to infection with H7 virus bearing a polybasic cleavage site showed poor efficacy despite good results were obtained for infection with H1N1 virus bearing single cleavage site (<xref rid="B41" ref-type="bibr">41</xref>), suggesting strain specificity in using serine protease inhibitors to treat IAV infections.</p></sec><sec id="S2-1-2"><title>Inhibition of Endosomal Acidification</title><p>Endosomal acidification is required for the release of IAV genome (in the form of a vRNP complex) into the cytoplasm (<xref rid="B24" ref-type="bibr">24</xref>). Research has shown that an increase in endosomal pH during the early phases of infection could inhibit IAV infection <italic>in vitro</italic> (<xref rid="B42" ref-type="bibr">42</xref>), bringing to light the possibility of controlling IAV infection through the prevention of endosomal acidification.</p><p>The V-ATPase inhibitor bafilomycin A1, when used at high concentrations (10–100 nM) has been proven to inhibit IAV replication through the efficient suppression of V-ATPase (<xref rid="B43" ref-type="bibr">43</xref>, <xref rid="B44" ref-type="bibr">44</xref>). However, prominent cytotoxicity to host cells was also observed at such concentrations (<xref rid="B44" ref-type="bibr">44</xref>). Interestingly, lower concentrations (0.1 nM) of bafilomycin A1 lack inhibitory effects on V-ATPase attenuated IAV replication due to disruption of endosomal trafficking. Thus, bafilomycin A1 is suggested to exert its antiviral function <italic>via</italic> distinct mechanisms at differing concentrations.</p><p>Diphyllin, isolated from the plant <italic>Cleistanthus collinus</italic>, is a natural compound able to induce a V-ATPase inhibitory effect (<xref rid="B45" ref-type="bibr">45</xref>). In contrast to bafilomycin A1, diphyllin is well-tolerated <italic>in vitro</italic> without inducing obvious cytotoxic effects (<xref rid="B46" ref-type="bibr">46</xref>). Most notably, diphyllin is found to effectively inhibit replication of viral strains resistant to amantadine and/or oseltamivir (<xref rid="B46" ref-type="bibr">46</xref>). Since drug resistance to these widely administered antivirals is of major public health concern (<xref rid="B13" ref-type="bibr">13</xref>), diphyllin is regarded as a promising antiviral against drug-resistant IAV strains.</p></sec><sec id="S2-1-3"><title>Controlling Cholesterol Homeostasis</title><p>The release of IAV genomic material during replication requires the fusion of the endosomal membrane with the viral envelope. Since cholesterol plays a major role in controlling the fluidity of the lipid bilayer in cells, it is hence suspected to have a role in the infection cycle of IAV.</p><p>Interferon-induced transmembrane proteins (IFITMs) are proteins expressed in many vertebrates (including humans) and are found on the plasma membrane, the membranes of early and late endosomes, as well as on lysosomes (<xref rid="B47" ref-type="bibr">47</xref>, <xref rid="B48" ref-type="bibr">48</xref>). While humans express IFITM1, IFITM2, IFITM3, IFITM5, and IFITM10, only IFITM 1, 2, and 3 are both immune-related as well as interferon (IFN)-inducible (<xref rid="B48" ref-type="bibr">48</xref>), and have been observed to restrict the replication of different viruses, including IAV (<xref rid="B49" ref-type="bibr">49</xref>). Studies suggest that IFITMs limit viral infection by reducing membrane fluidity and hence restrict the hemifusion (the mixing of lipid bilayer without the release of viral content) of viral and endosomal membranes (<xref rid="B50" ref-type="bibr">50</xref>), probably <italic>via</italic> the disruption of cholesterol homeostasis of late endosomes, where viral fusion and genome release conventionally take place (<xref rid="B51" ref-type="bibr">51</xref>). A recent study using RNAi also demonstrated that cholesterol homeostasis can be regulated <italic>via</italic> acid phosphatase 2 (ACP2)-mediated Niemann–Pick C2 activity and impaired the membrane fusion of IAV and influenza B virus (IBV) (<xref rid="B52" ref-type="bibr">52</xref>), further suggesting the importance of controlling cholesterol homeostasis in the release of viral genome to cytoplasm.</p><p>On the contrary, later studies suggest that IFITM3 exerts its antiviral activity in a cholesterol-independent manner, showing that an increase in cholesterol composition of late endosomal membranes fail to inhibit viral membrane fusion (<xref rid="B53" ref-type="bibr">53</xref>). In addition, studies suggested the accumulation of cholesterol level in the late endosome does not inhibit the IAV genome release into cytoplasm (<xref rid="B54" ref-type="bibr">54</xref>, <xref rid="B55" ref-type="bibr">55</xref>).</p><p>With the modulation of cholesterol levels in host endosomal membrane as a mean to inhibit IAV host cell entry is still under debate, further studies are required before clear conclusions can be drawn.</p></sec><sec id="S2-1-4"><title>Other Possible Targets for IAV Entry Inhibition</title><p>By comparing the miRNA profiles of the IAV-permissive HEK 293T cells and (less permissive) HeLa cells, miRNA-33a has been identified as a negative regulator for IAV infection <italic>via</italic> the inhibition of archain 1 (ARCN1, also known as δ-COPI) (<xref rid="B56" ref-type="bibr">56</xref>). ARCN1 is a subunit of the COPI complex that is required for intracellular trafficking and endosome function (<xref rid="B57" ref-type="bibr">57</xref>), depletion of which has been reported to inhibit IAV infection (<xref rid="B14" ref-type="bibr">14</xref>). Despite impaired IAV internalization caused by ARCN1 depletion <italic>via</italic> siRNA (<xref rid="B56" ref-type="bibr">56</xref>, <xref rid="B58" ref-type="bibr">58</xref>), it was not able to recapitulate through acute inhibition of COPI complex by pharmaceutical means (<xref rid="B58" ref-type="bibr">58</xref>). It is hypothesized that the long-term (lasting days) perturbation on ARCN1 by RNAi affected the general endosomal trafficking network, a phenomena which cannot be recapitulated by acute pharmaceutical inhibition to block IAV infection (<xref rid="B58" ref-type="bibr">58</xref>). The potential of targeting ARCN1 for IAV treatment deserves further investigation, despite the favorable results from RNAi studies.</p></sec></sec><sec id="S2-2"><title>Blocking the Nuclear Import of vRNP Complex</title><p>Nuclear import of vRNP complexes from the cytoplasm following fusion of the viral and the endosomal membrane is required for replication to take place (<xref rid="B59" ref-type="bibr">59</xref>). An early study suggested that vRNP complexes could be transported to the periphery of the nucleus (<xref rid="B60" ref-type="bibr">60</xref>), while recent studies report that vRNP complexes utilize the importin-α-importin-β1 (IMPα-IMPβ1) system for nuclear import (<xref rid="B59" ref-type="bibr">59</xref>, <xref rid="B61" ref-type="bibr">61</xref>) and lacking of importin-α7, in an importin-α7 knockout mouse model were found to be resistant to IAV infection (<xref rid="B62" ref-type="bibr">62</xref>).</p><p>Ivermectin has long been clinically administered for the treatment of parasitosis (<xref rid="B63" ref-type="bibr">63</xref>), but has recently come to attention as a potential inhibitor of IMPα/β (<xref rid="B64" ref-type="bibr">64</xref>). Ivermectin inhibition of IMPα/β has shown to inhibit the replication of RNA viruses such as dengue virus and HIV-1 (<xref rid="B64" ref-type="bibr">64</xref>). Ivermectin was recently tested for the inhibition of IAV <italic>in vitro</italic>, with nuclear import of vRNP complex (of both wild-type and antiviral MxA escape mutant) efficiently inhibited (<xref rid="B65" ref-type="bibr">65</xref>). Given ivermectin’s longstanding record of clinical applications and FDA-approved status, repurposing of this drug for the treatment of IAV should be considered, especially while under threat of pandemic IAV outbreak.</p></sec><sec id="S2-3"><title>Genomic Replication and Protein Synthesis</title><p>Following the import of the vRNP complex into the nucleus of the host cell, RdRP uses the vRNA as a template to synthesize mRNA or cRNA. Synthesized cRNA remains in the nucleus for new vRNA generation, while mRNA is exported out of the nucleus for translation. Viral protein products are either transported to the cell surface <italic>via</italic> Golgi (in case of HA and NA) or imported back into the nucleus to bind with vRNA, forming new vRNP complex (<xref rid="B59" ref-type="bibr">59</xref>). Numerous host factors are involved in this process and hence could be possible targets for therapeutic intervention.</p><sec id="S2-3-1"><title>Regulation of the Splicing of Pre-mRNA</title><p>Out of the eight genome segments of IAV, the M and NS segments are well known for undergoing splicing to generate at least two different mRNAs per individual segment (<xref rid="B66" ref-type="bibr">66</xref>, <xref rid="B67" ref-type="bibr">67</xref>). Cdc2-like kinase 1 (CLK1) is a kinase which regulates alternative splicing of pre-mRNA (<xref rid="B68" ref-type="bibr">68</xref>). Inhibition of CLK1 by the chemical TG003 or knockdown of CLK1 is shown to cause a decrease in M2 mRNA generation and disrupt downstream M2 protein expression, prominently reduced IAV propagation (<xref rid="B15" ref-type="bibr">15</xref>).</p><p>Clypearin and corilagin were both found to be potent anti-IAV compounds, with a higher therapeutic index than TG003 <italic>in vitro</italic> (<xref rid="B69" ref-type="bibr">69</xref>). Clypearin is isolated from herbs used by Chinese medicine practitioners for treating respiratory tract diseases (<xref rid="B69" ref-type="bibr">69</xref>), while corilagin is isolated from medicinal plants and herbs. The identification of effective compounds and the systemic investigation of the use of traditional Chinese medicine (TCM) in the treatment of IAV infection open new frontiers in research and therapeutics.</p></sec><sec id="S2-3-2"><title>Inhibition of mRNA Export</title><p>During replication, viral mRNA is exported from the nucleus to cytoplasm, where protein synthesis takes place. Human RNA polymerase II activity is found to be correlated with IAV replication through the inhibition of nuclear export of certain viral mRNAs, such as M1 mRNA (<xref rid="B70" ref-type="bibr">70</xref>).</p><p>Cyclosporine A (CsA) is a FDA-approved drug with immunomodulatory functions (<xref rid="B71" ref-type="bibr">71</xref>) that has been found to have an anti-IAV effect in both cyclophilin A (CypA)-dependent and -independent manners (<xref rid="B72" ref-type="bibr">72</xref>). The CypA-dependent effect was found to correlate with nuclear export of vRNP complex (see <xref ref-type="sec" rid="S2-4-1-1">Targeting Nuclear Export Complex</xref>). The CypA-independent effect caused inhibition of host RNA polymerase II. CsA is a prospective drug candidate for treatment of IAV infections with a relatively high barrier for development of intrinsic drug resistance, as opposed to commonly used antivirals (<xref rid="B73" ref-type="bibr">73</xref>).</p><p>Nuclear RNA export factor 1 (NXF1) is a host factor that has been identified to be involved in the nuclear export of IAV mRNA. The knockdown of NXF1 in HEK 293T cells revealed prominent viral mRNA nuclear retention in host cell nucleus (<xref rid="B74" ref-type="bibr">74</xref>). Protectin D1 (PD1), an endogenously produced lipid in the respiratory tract, has been identified to have potent anti-inflammatory and antiviral effects (<xref rid="B75" ref-type="bibr">75</xref>). PD1 production was notably found to be reduced in the lungs of IAV-infected mice. Therapeutic administration of PD1 was shown to significantly reduce IAV mRNA expression, lower lung viral titer, as well as improve survival of IAV-infected mice. Mechanistic studies revealed attenuated cytoplasmic translocation of viral mRNA with such treatment. A decrease in recruitment of viral transcripts to NXF1 was observed while nuclear export of host RNA remained largely unaffected, suggesting a role of PD1 in regulating NXF1 in nuclear export of viral RNA. Natural PD1 expression in the human airway makes this an ideal candidate for novel therapeutics in the treatment of IAV infection.</p></sec><sec id="S2-3-3"><title>Inhibition of mRNA Translation</title><p>The eukaryotic initiation factor-4A (eIF4A) family plays an important role in protein translation (<xref rid="B76" ref-type="bibr">76</xref>, <xref rid="B77" ref-type="bibr">77</xref>). eIF4A impairment has been proven to be related to antiviral activity in a broad spectrum of RNA viruses <italic>in vitro</italic> (<xref rid="B78" ref-type="bibr">78</xref>), with inhibition of IAV mRNA translation (<xref rid="B79" ref-type="bibr">79</xref>). The eIF4A inhibitors, silvestrol and pateamine A were demonstrated to arrest viral protein synthesis, thus blocking viral genome replication <italic>in vitro</italic> (<xref rid="B80" ref-type="bibr">80</xref>). Although both silvestrol and pateamine A caused high cytotoxicity at the concentration required effective for IAV inhibition, drugs targeting mRNA translation for various diseases have been approved by FDA or are under active development (<xref rid="B81" ref-type="bibr">81</xref>). As such, inhibition of IAV infections by disrupting mRNA translation may well be a therapeutic approach in the future.</p></sec><sec id="S2-3-4"><title>Inhibition of HA Maturation</title><p>Post-translational modifications during protein maturation ensure proper function of proteins, with proteins of IAV no exception. Nitazoxanide, a FDA-licensed drug used to treat enteritis, was found to be effective in controlling IAV infection by interfering with HA N-glycosylation as well as intracellular trafficking in host cell and eventually led to a reduction in viral budding (<xref rid="B82" ref-type="bibr">82</xref>). Despite the mechanism of nitazoxanide being presently unknown, its ability to inhibit replication of numerous viruses [IAV, respiratory syncytial virus, coronavirus, hepatitis B virus, and many others (<xref rid="B83" ref-type="bibr">83</xref>)] suggests that it may act on host machinery. The drug has also been proven <italic>in vitro</italic> to inhibit the propagation of many circulating strains of human IAV, including those resistant to oseltamivir or zanamivir (<xref rid="B84" ref-type="bibr">84</xref>). Nitazoxanide has a high barrier of resistance to IAV (<xref rid="B83" ref-type="bibr">83</xref>) and other viral strains resistance to neuraminidase inhibitors (<xref rid="B85" ref-type="bibr">85</xref>), making it a very promising therapeutic target for IAV treatment. The drug is currently under phase III clinical trials (<xref rid="B83" ref-type="bibr">83</xref>).</p></sec></sec><sec id="S2-4"><title>Nuclear Export, Assembly, Apical Transport, and Viral Budding</title><p>In the later stage of viral replication, viral RNAs of IAV packed with RdRP and NP (known as vRNP complexes) are exported from the nucleus (<xref rid="B59" ref-type="bibr">59</xref>), assembled (<xref rid="B86" ref-type="bibr">86</xref>), and transported to the plasma membrane [apical in polarized cells (<xref rid="B87" ref-type="bibr">87</xref>)] for budding.</p><sec id="S2-4-1"><title>Inhibition of Nuclear Export</title><sec id="S2-4-1-1"><title>Targeting Nuclear Export Complex</title><p>Exportin 1 (XPO1, also known as CRM1) is well known for its function in the nuclear export of protein (<xref rid="B88" ref-type="bibr">88</xref>) and RNA, including viral RNA (<xref rid="B89" ref-type="bibr">89</xref>). Similar to HIV (<xref rid="B89" ref-type="bibr">89</xref>, <xref rid="B90" ref-type="bibr">90</xref>), IAV viral RNA does not directly bind to XPO1 but is instead held together by several viral proteins. The viral nuclear export protein (NEP, or previously known as NS2) and the vRNP complex have been proposed as the nuclear export complex (<xref rid="B91" ref-type="bibr">91</xref>). Cellular XPO1 has been proven to be crucial in the nuclear export of the vRNP complex, with early studies using leptomycin B (LMB), a potent XPO1 inhibitor, revealing that <italic>in vitro</italic> inhibition of XPO1 led to nuclear retention of vRNP complex (<xref rid="B92" ref-type="bibr">92</xref>, <xref rid="B93" ref-type="bibr">93</xref>). However, LMB was deemed unsuitable for development as a potential drug in the phase I clinical trial due to observed cytotoxic effects (<xref rid="B94" ref-type="bibr">94</xref>).</p><p>Verdinexor (also known as KPT-355) is a new bioavailable selective inhibitor of XPO1. It has been shown to be effective against different strains of IAVs both <italic>in vitro</italic> and <italic>in vivo</italic> as prophylactic and therapeutic treatments (<xref rid="B95" ref-type="bibr">95</xref>, <xref rid="B96" ref-type="bibr">96</xref>). It is worth mentioning that delayed administration of verdinexor at day 4 post-infection was still deemed beneficial, with reduced viral load <italic>in vivo</italic> (<xref rid="B96" ref-type="bibr">96</xref>). This suggests a prolonged therapeutic time window when compared to the mainstay antiviral drugs such as oseltamivir, where recommended administration is at the early stage of infection (within 48 h of symptom onset) (<xref rid="B97" ref-type="bibr">97</xref>). Currently, verdinexor has passed the phase I clinical study trials, suggesting that it does not pose severe cytotoxic effects as LMB does.</p><p>In addition, a recent report demonstrated that a new drug, DP2392-E10, which binds and inhibits the function of XPO1, can suppress IAV replication <italic>in vitro</italic> (<xref rid="B98" ref-type="bibr">98</xref>) further strengthens the concept of IAV intervention by targeting XPO1.</p><p>Viral M1 protein is crucial in assisting the nuclear export of vRNP complex. It was commonly suggested that M1 protein links vRNP complex to viral nuclear export protein NEP which interacts with XPO1 for nuclear export (<xref rid="B59" ref-type="bibr">59</xref>). Thus, viral M1 protein may serve as a target to inhibit nuclear export of vRNP. As previously mentioned (see <xref ref-type="sec" rid="S2-3-2">Inhibition of mRNA Export</xref>), CsA inhibits IAV replication <italic>via</italic> both CypA-dependent and -independent mechanisms. A recent study using a transgenic mice over-expressing CypA showed greater resistance to IAV challenge (<xref rid="B99" ref-type="bibr">99</xref>). In the CypA-dependent mechanism, CsA enhances the binding of CypA to M1 protein (<xref rid="B72" ref-type="bibr">72</xref>), increases the self-association of M1, and hinders M1 nuclear import (<xref rid="B100" ref-type="bibr">100</xref>). CsA also promotes the CypA-dependent degradation of viral M1 protein (<xref rid="B72" ref-type="bibr">72</xref>, <xref rid="B101" ref-type="bibr">101</xref>). CsA seems to be a promising drug to inhibit the nuclear export of vRNP complex by inhibiting viral M1 protein stability and function.</p><p>Recently, CD151, a tetraspanin (defined by four transmembrane domains with conserved residues) that is expressed abundantly in lungs and interacts with integrins has been implicated in the regulation of IAV replication <italic>in vitro</italic> and <italic>in vivo</italic> (<xref rid="B102" ref-type="bibr">102</xref>). Knockdown of CD151 in primary human nasal epithelial cells resulted in the nuclear retention of host XPO1, viral NP, NEP, and M1 proteins, with an increased survival rate observed in IAV-infected CD151 knockout mice. Co-immunoprecipitation assays suggest that CD151 interacts with viral NP, M1, and NEP proteins (<xref rid="B102" ref-type="bibr">102</xref>); however, the exact domains involved in interaction and the mechanism of CD151 function in nuclear export remain unclear. Given that a small molecule inhibitor for CD151 is now under development (<xref rid="B103" ref-type="bibr">103</xref>), more data revealing the role of CD151 in IAV infection and subsequent use in targeting CD151 as anti-IAV therapy is anticipated.</p></sec><sec id="S2-4-1-2"><title>Targeting the Raf/MEK/ERK Pathway</title><p>During IAV infection, Raf/MEK/ERK signaling cascade is activated, while the inhibition of MEK by U0126, probably mediated <italic>via</italic> myosin (light chain) (<xref rid="B104" ref-type="bibr">104</xref>), a known motor protein, impairs the nuclear export of vRNP complexes (<xref rid="B105" ref-type="bibr">105</xref>). Suppressing IAV replication by inhibition of Raf/MEK/ERK signaling cascade has been illustrated both <italic>in vivo</italic> (<xref rid="B106" ref-type="bibr">106</xref>) and <italic>in vitro</italic> (<xref rid="B105" ref-type="bibr">105</xref>). The replication of IBV (<xref rid="B107" ref-type="bibr">107</xref>) as well as Borna disease virus (<xref rid="B108" ref-type="bibr">108</xref>) was shown to be inhibited by U0126, suggesting the versatility of this approach in controlling infection by different viruses. Despite being effective when administered locally to lungs <italic>via</italic> aerosol, U0126 has little effect when administered orally (<xref rid="B106" ref-type="bibr">106</xref>).</p><p>Another MEK inhibitor, CI-1040 (also known as PD184352) was shown to have high potency against IAV <italic>in vitro</italic> (<xref rid="B106" ref-type="bibr">106</xref>). CI-1040 has completed phase II clinical trials as an anti-tumor drug, with the application of CI-1040 as a potential anti-IAV drug candidate recently revisited. Unlike U0126, CI-1040 is orally bioavailable and oral administration of CI-1040 at 48 h post-infection protected 60% of the IAV-infected mice, while the oseltamivir-treated group experienced a 100% death rate (<xref rid="B109" ref-type="bibr">109</xref>). Oseltamivir is known to be effective only when administered in the early stages of IAV infection. This suggests the potential use of CI-1040 as an agent used in IAV treatment due to its potentially longer therapeutic time window than mainstay antivirals.</p><p>Formyl peptide receptor 2 (FPR2) located at the host cell surface was identified as an ERK stimulator (<xref rid="B110" ref-type="bibr">110</xref>). Antagonizing FPR2 promoted the survival of IAV-infected mice (<xref rid="B110" ref-type="bibr">110</xref>). Furthermore, FPR2 antagonists have been described to possess antiviral activity against not only IAV but also IBV infection (<xref rid="B111" ref-type="bibr">111</xref>), promoting the idea that antagonizing FPR2 to suppress Raf/MEK/ERK signaling cascade could potentially be a novel approach for the treatment of a broad spectrum of influenza viruses.</p></sec></sec><sec id="S2-4-2"><title>Apical Transport of Viral Components</title><p>After the nuclear export of the vRNP complexes, host cell’s intracellular transport mechanism is required to deliver vRNP complexes to the host plasma membrane for the assembly of viral RNAs and proteins at the final stage of viral replication. Among the various vesicular compartments found in a cell, the Rab11A<sup>+</sup> endosomes are known to recycle endocytosed membrane proteins and lipids to the plasma membrane for membrane homeostasis (<xref rid="B112" ref-type="bibr">112</xref>), a property utilized by many RNA viruses, including IAV (<xref rid="B87" ref-type="bibr">87</xref>, <xref rid="B113" ref-type="bibr">113</xref>–<xref rid="B115" ref-type="bibr">115</xref>). IAV progeny virus production was found to be significantly reduced in Rab11A<sup>+</sup> knockdown human cell lines (<xref rid="B116" ref-type="bibr">116</xref>). Furthermore, vRNP complex plasma membrane transport perturbation was observed in <italic>Rab11A</italic> knockdown cells (<xref rid="B114" ref-type="bibr">114</xref>, <xref rid="B115" ref-type="bibr">115</xref>); in cells expressing deletion mutant of Rab11 family interacting proteins (<xref rid="B87" ref-type="bibr">87</xref>); as well as cells treated with chemicals to interfere microtubule (<xref rid="B114" ref-type="bibr">114</xref>). Direct interaction of vRNP complex with Rab11A has also been verified (<xref rid="B114" ref-type="bibr">114</xref>, <xref rid="B115" ref-type="bibr">115</xref>), demonstrating the dependence of vRNA complex transport on Rab11A<sup>+</sup> vesicles and the microtubule network during viral replication. Since Rab11A proteins do not confer any mobile properties to the vesicle, molecular motors such as kinesins are required for the active transportation of vesicles through cytoskeletons.</p><p>KIF13A, a kinesin-3 family member, was recently identified as a molecular motor for plasma membrane transportation of vRNP-loaded Rab11A<sup>+</sup> vesicles (<xref rid="B117" ref-type="bibr">117</xref>). KIF13A knockdown was found to reduce progeny virus production. Overexpression of a mutant form of KIF13A lacking in motor capacity resulted in disruption of the plasma membrane distribution of vRNP complex during later stages of infection. This data suggest that the apical transport of viral components <italic>via</italic> Rab11A or KIF13A could potentially serve as therapeutic targets against IAV infection. Further examination is merited.</p><p>Tubulin acetylation and deacetylation affects microtubule stability (<xref rid="B118" ref-type="bibr">118</xref>). Histone deacetylase 6 (HDAC6) was found to deacetylate α-tubulin, one of the subunits of microtubule (<xref rid="B119" ref-type="bibr">119</xref>). A study has demonstrated that HDAC6 is involved in IAV replication (<xref rid="B120" ref-type="bibr">120</xref>). Inhibition of HDAC6 by tubacin or knockdown of HDAC6 gene resulted in an increase of progeny virus production with vRNP complex redistributed toward the periphery of infected cells. In addition, transportation of HA to the plasma membrane for viral budding was also found to be inhibited by HDAC6. This data suggests that activation of HDAC6 by its stimulant could be a potential approach to anti-IAV therapy, despite HDAC6 stimulants still being under development.</p></sec><sec id="S2-4-3"><title>Interference of Viral Budding</title><p>While several studies have suggested IAV transmission between cells through apical membranes (<xref rid="B121" ref-type="bibr">121</xref>) and intercellular connections (<xref rid="B122" ref-type="bibr">122</xref>), virus budding from cell membranes remains the major route for transmission of viruses to uninfected cells. NA is responsible for the cleavage of sialic acid to prevent the interaction between HA and the host cell during viral budding. Besides, viral NA, viral HA, M1 as well as M2, are also suggested to play an important role in the initiation of the budding process (<xref rid="B123" ref-type="bibr">123</xref>, <xref rid="B124" ref-type="bibr">124</xref>).</p><p>In Section “<xref ref-type="sec" rid="S2-1-3">Controlling Cholesterol Homeostasis</xref>,” we discussed the involvement of host cholesterol in viral membrane fusion and viral genome release to cytoplasm. Recent studies have demonstrated that host cholesterol may also play an important role in viral budding. It was demonstrated that overexpression of annexin A6 (AnxA6), a phospholipid binding protein, could lead to a decrease in cholesterol levels within the Golgi apparatus and plasma membrane (<xref rid="B55" ref-type="bibr">55</xref>), ultimately causing a reduction in egression of progeny virion from infected cells (<xref rid="B54" ref-type="bibr">54</xref>). This reduction could be reversed by the addition of exogenous cholesterol (<xref rid="B55" ref-type="bibr">55</xref>). Similar to AnxA6 overexpression, addition of a hydrophobic polyamine, U18666A, could reduce cholesterol level in plasma membrane, also inhibited viral replication (<xref rid="B55" ref-type="bibr">55</xref>). Since IAV is assumed to bud from lipid rafts (cholesterol-rich plasma membrane domains) (<xref rid="B123" ref-type="bibr">123</xref>), it was demonstrated that AnxA6 overexpression or U18666A treatment could hinder progeny virus production by lowering the cholesterol content in the plasma membrane. This hypothesis was strengthened through recent studies resolving the cholesterol-binding site of viral M2 protein, suggesting that IAV M2 clustering (which provides membrane curvature for scission) is mediated by cholesterol (<xref rid="B125" ref-type="bibr">125</xref>). A recent report utilizing two different FDA-approved cholesterol-lowering drugs, gemfibrozil and lovastatin, stated that there was reduction in stability and infectivity of progeny virus compared to that replicating within cholesterol-sufficient host cells (<xref rid="B126" ref-type="bibr">126</xref>). Taken together, this data suggests that controlling cellular cholesterol content would be an effective alternative with drugs available for repurposing IAV treatment. Further <italic>in vivo</italic> works are needed to confirm this hypothesis.</p><p>The Gi-type G-protein coupled receptor α2-adrenergic receptors (α2-ARs) have been recently identified as a key host factor involved in IAV replication (<xref rid="B127" ref-type="bibr">127</xref>). Apical transport of the viral protein HA is inhibited by low intracellular cAMP level after stimulating the α2-AR-mediated signaling. <italic>In vitro</italic> stimulation of α2-AR by its agonist clonidine inhibits IAV replication. Therapeutic administration of clonidine reduced pulmonary edema and improved survival rate of IAV-infected mice. Development of a new antiviral targeting the α2-AR-mediated signaling seems promising and deserves further investigation.</p></sec></sec><sec id="S2-5"><title>Interrupting the Virus Replication Cycle by Combinatory Use Targeting Both Virus and Host Factors</title><p>Although targeting host factors for viral interventions generally provides a better resistance barrier, emergence of resistance may still arise (<xref rid="B61" ref-type="bibr">61</xref>). Therefore, combined use of interventions targeting both virus and host factors have been recommended to reduce opportunities for viral development of resistance. One such example would be the combined administration of NA inhibitor (oseltamivir) alongside an anti-host factor [such as V-ATPase inhibitor diphyllin (<xref rid="B46" ref-type="bibr">46</xref>), HA maturation inhibitor nitazoxanide (<xref rid="B85" ref-type="bibr">85</xref>), FPR2 antagonists (<xref rid="B111" ref-type="bibr">111</xref>), and XPO1 inhibitor verdinexor (<xref rid="B96" ref-type="bibr">96</xref>)]. While further direct assessment for the ease of emergence of escape mutants between single and combinatory use of drugs is required, the synergistic effects of a combined, multi-drug approach observed thus far highly suggest an increased effectiveness over a single-drug approach.</p><p>Table <xref rid="T1" ref-type="table">1</xref> summarizes novel host targets regulating IAV replication. Compared to RNAi, small molecular chemicals remain the best choice as drug candidates due to their fast acting and easy-to-deliver properties. Although small molecular chemicals targeting certain host factors aforementioned have yet to be developed, their RNAi-identified involvement in the IAV replication cycle provide leads for the development of new IAV interventions.</p><table-wrap id="T1" position="float"><label>Table 1</label><caption><p>Advancements on targeting host factors for antivirals.</p></caption><table frame="hsides" rules="rows"><thead><tr><th valign="top" align="left" rowspan="1" colspan="1">Cellular target</th><th valign="top" align="left" rowspan="1" colspan="1">New potential therapeutic approach</th><th valign="top" align="left" rowspan="1" colspan="1">Suggested function</th><th valign="top" align="left" rowspan="1" colspan="1">Reference</th></tr></thead><tbody><tr><td align="left" valign="top" colspan="4" rowspan="1"><bold>Viral entry</bold></td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Serine proteases</td><td align="left" valign="top" rowspan="1" colspan="1">Camostat</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits HA0 cleavage</td><td align="left" valign="top" rowspan="1" colspan="1">Yamaya et al. (<xref rid="B35" ref-type="bibr">35</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">V-ATPase</td><td align="left" valign="top" rowspan="1" colspan="1">Diphyllin</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits endosomal acidification</td><td align="left" valign="top" rowspan="1" colspan="1">Chen et al. (<xref rid="B46" ref-type="bibr">46</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Acid phosphatase 2</td><td align="left" valign="top" rowspan="1" colspan="1">siRNA</td><td align="left" valign="top" rowspan="1" colspan="1">Indirectly disrupts cholesterol homeostasis</td><td align="left" valign="top" rowspan="1" colspan="1">Lee et al. (<xref rid="B52" ref-type="bibr">52</xref>)</td></tr><tr><td align="left" valign="top" colspan="4" rowspan="1"><bold>Nuclear import</bold></td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Importins</td><td align="left" valign="top" rowspan="1" colspan="1">Ivermectin</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits nuclear import of viral ribonucleoprotein (vRNP) complex</td><td align="left" valign="top" rowspan="1" colspan="1">Gotz et al. (<xref rid="B65" ref-type="bibr">65</xref>)</td></tr><tr><td align="left" valign="top" colspan="4" rowspan="1"><bold>Genomic replication and protein synthesis</bold></td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Cdc2-like kinase 1</td><td align="left" valign="top" rowspan="1" colspan="1">Clypearin</td><td align="left" valign="top" rowspan="1" colspan="1">Attenuates M2 splicing</td><td align="left" valign="top" rowspan="1" colspan="1">Zu et al. (<xref rid="B69" ref-type="bibr">69</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">RNA polymerase II</td><td align="left" valign="top" rowspan="1" colspan="1">Cyclosporine A</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits viral mRNA export</td><td align="left" valign="top" rowspan="1" colspan="1">Ma et al. (<xref rid="B73" ref-type="bibr">73</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Nuclear RNA export factor 1</td><td align="left" valign="top" rowspan="1" colspan="1">PD1</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits viral RNA export</td><td align="left" valign="top" rowspan="1" colspan="1">Morita et al. (<xref rid="B75" ref-type="bibr">75</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Eukaryotic initiation factor-4A</td><td align="left" valign="top" rowspan="1" colspan="1">a. Silvestrol<break></break>b. Pateamine A</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits mRNA translation</td><td align="left" valign="top" rowspan="1" colspan="1">Slaine et al. (<xref rid="B80" ref-type="bibr">80</xref>)</td></tr><tr><td align="left" valign="top" colspan="4" rowspan="1"><bold>vRNP complex nuclear export</bold></td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">XPO1</td><td align="left" valign="top" rowspan="1" colspan="1">a. Verdinexor<break></break>b. DP2392-E10</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibit vRNP complex nuclear export</td><td align="left" valign="top" rowspan="1" colspan="1">a. Perwitasari et al. (<xref rid="B95" ref-type="bibr">95</xref>, <xref rid="B96" ref-type="bibr">96</xref>)<break></break>b. Chutiwitoonchai et al. (<xref rid="B98" ref-type="bibr">98</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">CypA</td><td align="left" valign="top" rowspan="1" colspan="1">Cyclosporine A</td><td align="left" valign="top" rowspan="1" colspan="1">Promotes M1 degradation</td><td align="left" valign="top" rowspan="1" colspan="1">Liu et al. (<xref rid="B72" ref-type="bibr">72</xref>, <xref rid="B101" ref-type="bibr">101</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">CD151</td><td align="left" valign="top" rowspan="1" colspan="1">siRNA</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits vRNP complex nuclear export</td><td align="left" valign="top" rowspan="1" colspan="1">Qiao Y. et al. (<xref rid="B102" ref-type="bibr">102</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">MEK</td><td align="left" valign="top" rowspan="1" colspan="1">CI-1040</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits MEK to suppress phosphorylation of myosin light chain leading to nuclear retention of vRNP complex</td><td align="left" valign="top" rowspan="1" colspan="1">Haasbach et al. (<xref rid="B109" ref-type="bibr">109</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Formyl peptide receptor 2 (FPR2)</td><td align="left" valign="top" rowspan="1" colspan="1">WRW4</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits activation of Raf/MEK/ERK by the ligation of AnxA1 to FPR2</td><td align="left" valign="top" rowspan="1" colspan="1">Courtin et al. (<xref rid="B111" ref-type="bibr">111</xref>)</td></tr><tr><td align="left" valign="top" colspan="4" rowspan="1"><bold>Viral component apical transport</bold></td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">KIF13A</td><td align="left" valign="top" rowspan="1" colspan="1">To be determined</td><td align="left" valign="top" rowspan="1" colspan="1">Blocks vRNP apical transport</td><td align="left" valign="top" rowspan="1" colspan="1">Ramos-Nascimento et al. (<xref rid="B117" ref-type="bibr">117</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Histone deacetylase 6</td><td align="left" valign="top" rowspan="1" colspan="1">To be determined</td><td align="left" valign="top" rowspan="1" colspan="1">Regulates microtubule stability</td><td align="left" valign="top" rowspan="1" colspan="1">Husain et al. (<xref rid="B120" ref-type="bibr">120</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">AnxA6</td><td align="left" valign="top" rowspan="1" colspan="1">To be determined</td><td align="left" valign="top" rowspan="1" colspan="1">Reduces plasma membrane cholesterol level and decreases virion egress or stability</td><td align="left" valign="top" rowspan="1" colspan="1">Musiol et al. (<xref rid="B55" ref-type="bibr">55</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Cholesterol</td><td align="left" valign="top" rowspan="1" colspan="1">U18666A</td><td align="left" valign="top" rowspan="1" colspan="1">Reduces plasma membrane cholesterol level and decreases virion egress</td><td align="left" valign="top" rowspan="1" colspan="1">Musiol et al. (<xref rid="B55" ref-type="bibr">55</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">α2-adrenergic receptors</td><td align="left" valign="top" rowspan="1" colspan="1">Clonidine</td><td align="left" valign="top" rowspan="1" colspan="1">Reduces intracellular cAMP to impair Influenza A virus HA plasma membrane transport</td><td align="left" valign="top" rowspan="1" colspan="1">Matsui et al. (<xref rid="B127" ref-type="bibr">127</xref>)</td></tr><tr><td align="left" valign="top" colspan="4" rowspan="1"><bold>Other</bold></td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Cholesterol</td><td align="left" valign="top" rowspan="1" colspan="1">a. Gemfibrozil<break></break>b. Iovastatin</td><td align="left" valign="top" rowspan="1" colspan="1">Reduces progeny virus stability and infectivity</td><td align="left" valign="top" rowspan="1" colspan="1">Bajimaya et al. (<xref rid="B126" ref-type="bibr">126</xref>)</td></tr></tbody></table></table-wrap></sec></sec><sec id="S3"><title>Regulation of Aberrant Immune Responses in IAV Infection</title><p>The immune system aims to protect the host from infection and clear the pathogen once an infection occurs. In addition, the complex networks formed between the host physiology and the immune system co-operatively shape the disease outcome; modulations on the networks could alleviate disease severity in IAV infections.</p><p>The immunological responses elicited by IAV infection has been reviewed in detail (<xref rid="B128" ref-type="bibr">128</xref>–<xref rid="B130" ref-type="bibr">130</xref>). At the initial stage of IAV infection, the respiratory epithelial cells are the primary target for infection. Once the infection is initiated, the recognition of infection is accomplished <italic>via</italic> the detection of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs) (see <xref ref-type="sec" rid="S3-4-5">Toll-Like Receptors</xref>), and lead to the expression and secretion of different cytokines and chemokines, such as IL-6, IL-8, tumor necrosis factor (TNF)-α, and CCL2 as well as type I and III IFNs. As sentinel cells, alveolar macrophages could also be infected, inducing cytokines and is the main source of type I IFNs (<xref rid="B128" ref-type="bibr">128</xref>, <xref rid="B129" ref-type="bibr">129</xref>). Type I IFNs are known inducer for the upregulation of death receptor 5, which is the receptor for TNF-related apoptosis-inducing ligand (TRAIL), in lung pneumocytes (<xref rid="B128" ref-type="bibr">128</xref>). IL-8 and CCL2 produced by both epithelial cells and macrophages act as chemoattractants for neutrophils and monocytes, respectively. Neutrophils are one of the earliest immune cells being recruited to the site of infection (<xref rid="B131" ref-type="bibr">131</xref>) with transmigration of neutrophils carry out by adhesion molecules, such as CD11a, CD11b, and CD18 (<xref rid="B132" ref-type="bibr">132</xref>). In addition to the antiviral activity of neutrophil-released reactive oxygen species (ROS), defensin and pentraxin (<xref rid="B132" ref-type="bibr">132</xref>), uptaking IAV by neutrophils could also help in controlling viral propagation as these cells do not support replication of IAV (<xref rid="B133" ref-type="bibr">133</xref>). Besides controlling viral replication, neutrophils also play an important role in guiding the migration of IAV-specific CD8<sup>+</sup> T-cells in the infection site by secreting and leaving a trail of CXCL12 (<xref rid="B134" ref-type="bibr">134</xref>). Infiltrated monocytes will, however, differentiate into macrophages or dendritic cells (DCs). The monocytes-derived macrophages are reported to be a permissive host for IAV production (<xref rid="B135" ref-type="bibr">135</xref>), sustaining inflammation by producing cytokines in a magnitude larger than that of the resident alveolar macrophages. The monocyte-derived DC as well as the resident airway CD11c<sup>low</sup>B220<sup>+</sup> plasmacytoid DC (pDC) and two types of conventional DCs (CD103<sup>+</sup>CD11b<sup>low</sup> and CD103<sup>−</sup>CD11b<sup>hi</sup>) acquire the antigen of the invading pathogen through either direct infection or up-taking infected dead cells (<xref rid="B129" ref-type="bibr">129</xref>). In the presence of type I IFNs, DCs mature when encountering PAMPs from invading pathogen (<xref rid="B129" ref-type="bibr">129</xref>). Depending on the sub-cellular localization of the antigen, cytosolic and endosomal antigen will be loaded onto major histocompatibility complex (MHC) class I and II molecules respectively (<xref rid="B130" ref-type="bibr">130</xref>). Once mature, DCs migrate from the infection site to the draining lymph nodes <italic>via</italic> the interaction of CCR7 and CCL19/CCL21 (<xref rid="B130" ref-type="bibr">130</xref>, <xref rid="B136" ref-type="bibr">136</xref>) for antigen presentation <italic>via</italic> MHC class I and II to naïve CD8<sup>+</sup> and CD4<sup>+</sup> T-cells, respectively (<xref rid="B137" ref-type="bibr">137</xref>–<xref rid="B140" ref-type="bibr">140</xref>). Interestingly, monocytes-derived DCs that engulfed the infected dead cells are poor antigen presenters for CD8<sup>+</sup> T-cells and require the transfer of intact MHC class I/peptide complex to lymph node-resident CD8α<sup>+</sup> DCs which are the most efficient antigen-presenting cells to CD8<sup>+</sup> T-cells (<xref rid="B137" ref-type="bibr">137</xref>). In addition to antigen presentation, pDC are well known for their high ability in type I IFNs production to limit viral propagation (<xref rid="B141" ref-type="bibr">141</xref>).</p><p>Within the lymph node, naïve CD8<sup>+</sup> T-cells are activated by the DCs, differentiate and clonal expand into cytotoxic T-lymphocytes (CTLs) with the aid of various cytokines, including IFN-γ, IL-12, type I IFNs, and IL2 (<xref rid="B142" ref-type="bibr">142</xref>, <xref rid="B143" ref-type="bibr">143</xref>), and the help from activated CD4<sup>+</sup> T helper cells (<xref rid="B144" ref-type="bibr">144</xref>). Differentiated CTLs downregulate their lymph node homing receptor CCR7 and upregulate CCR4 and CXCR3 for the migration to the site of infection. Within the site of infection, CTLs control viral replication by targeting and inducing apoptosis of virus-infected cells <italic>via</italic> the secretion of perforin and granzymes as well as the ligation of death receptors on the infected cells by TNF, Fas ligand, and TRAIL. On the other hand, CD4<sup>+</sup> T-cells are activated by the presentation of MHC class II/antigen complex by DCs, with co-stimulatory receptors such as CD28 expressed on the T-cells and the ligand for CD28 (CD80 and CD86) expressed on DCs playing an important role (<xref rid="B144" ref-type="bibr">144</xref>). Activation of CD4<sup>+</sup> T-cells lead to differentiation into different effector cells subsets, including the classical Th1 and Th2, and the more recently identified regulatory T cells, follicular T helper cells, Th9, and Th17 subsets (<xref rid="B144" ref-type="bibr">144</xref>). Th1 cells regulate to the differentiation of CTLs as mentioned whereas Th2 cells contributes to the activation of B-cells through CD40L. Within the pregerminal center of the lymph node, the follicular T helper cells interact with antigen-primed B-cells and promote their proliferation. Antigen-primed B-cells differentiates into plasmablast and undergo antibody class-switching in the germinal center (<xref rid="B145" ref-type="bibr">145</xref>). Detailed functions of regulatory T cells, follicular T cells, Th9, and Th17 cells are discussed elsewhere (<xref rid="B144" ref-type="bibr">144</xref>, <xref rid="B145" ref-type="bibr">145</xref>). Plasmablasts enter the blood-stream, are recruited to the inflamed tissue, and terminally differentiate into plasma B cells which specialize in the production of antibody for pathogen neutralization, opsonization, and antibody-dependent cell-mediated cytotoxicity, etc. Memory T- and B-cells are also developed during the maturation process, and has been discussed and reviewed elsewhere (<xref rid="B146" ref-type="bibr">146</xref>–<xref rid="B149" ref-type="bibr">149</xref>). A schematic diagram showing a summary of the immune response after IAV infection has been illustrated in Figure <xref ref-type="fig" rid="F1">1</xref>.</p><fig id="F1" position="float"><label>Figure 1</label><caption><p>Immune responses of primary influenza A virus (IAV) infection. At the initial stage of infection (left), airway epithelial cells and pneumocytes are major targets for IAV. Various cytokines are secreted by these cells as well as alveolar macrophages to induce inflammation and recruits blood immune cells. Infiltrated neutrophils secrete different antimicrobial products to control viral replication. Besides, CXCL12 is secreted by neutrophils to guide the cytotoxic T-lymphocytes (CTLs) in the later stage of infection. Infiltrated monocytes will further differentiate into monocyte-derived macrophages and monocyte-derived dendritic cells (MoDC). Constant surveying of the airway and uptake of virus-infected dead cells by DCs lead to their maturation. Upregulation of CCR7 results in a CCL19/CCL21-dependent lymph node homing of DCs. Within the lymph node (middle), MoDCs cross-dress CD8α<sup>+</sup> DC. CD4<sup>+</sup> and CD8<sup>+</sup> T-cells are activated by DCs in the presence of cytokines and undergo clonal expansion. Antigen-primed B-cells mature with the aid from follicular T helper cells and further differentiate into plasmablasts in the germinal center. Differential expression of receptors upon maturation of T- and B-cells prompt them to leave the lymph node, enter the blood-stream and recruited to the lung. In the inflamed lung (right), neutrophils leave a trail of CXCL12 to guide CTLs migration. Measures utilized by CTLs for killing infected cells are depicted in inset. Plasmablasts further terminally differentiate into plasma cells and increase antibody production for IAV neutralization.</p></caption><graphic xlink:href="fimmu-09-01547-g001"></graphic></fig><p>The Yin and Yang theory is always used to describe the importance in balancing the host immune response. In the light of this theory, the treatment strategy aims to suppress the overwhelming activation of the host immune response and in reverse to compensate any unfavorable suppression.</p><p>Although adaptive immune responses are important in viral clearance, the immediate innate immunity play an important role in the early control of an infection, and conversely, is a major factor for disease severity due to immunopathology. Dysregulated immune responses caused by viral infections have been implicated in severe disease development (<xref rid="B150" ref-type="bibr">150</xref>, <xref rid="B151" ref-type="bibr">151</xref>), such as acute lung injury (ALI). ALI in its most severe form, known as acute respiratory distress syndrome (ARDS), is reported to be the most prevalent cause of mortality in IAV-infected patients (<xref rid="B152" ref-type="bibr">152</xref>).</p><p>Studies suggested that IAV strains could be associated with either over-activating (human infection by avian H5N1 and H7N9) (<xref rid="B153" ref-type="bibr">153</xref>, <xref rid="B154" ref-type="bibr">154</xref>) or suppressing (H1N1, H3N2) (<xref rid="B155" ref-type="bibr">155</xref>) immune response.</p><sec id="S3-1"><title>Regulation of Neutrophil Infiltration and Neutrophil Extracellular Trap</title><p>Recent history has seen the outbreak of IAV pandemics of varying severity takes place at the cost of millions of lives. One such example would be the deadly Spanish flu of 1918, which claimed the lives of 20–50 million of the 500 million people infected worldwide.</p><p>The pathological examination of lung sections from mice infected with reconstituted 1918 IAV virus revealed necrotizing bronchiolitis and severe alveolitis in tissue, with neutrophils observed as the predominant inflammatory cell type present (<xref rid="B156" ref-type="bibr">156</xref>), suggesting neutrophil involvement in the pathogenesis of IAV infection.</p><p>The majority of immune cells in blood circulation are neutrophils; of which they are among the first innate immune cells recruited to the site of infection (<xref rid="B131" ref-type="bibr">131</xref>). Neutrophils characteristically control microbial infections by generating bactericidal (<xref rid="B157" ref-type="bibr">157</xref>) neutrophil extracellular traps (NETs), consisting of granule proteins, histones, and decondensed chromatin (<xref rid="B131" ref-type="bibr">131</xref>). Both protective and destructive role of neutrophils in IAV infections have been described. The contrasting role of neutrophils could be explained by factors such as viral strain and viral dose used in different experimental setup, etc.</p><p>The protective role of neutrophils was observed when mice infected with a low, non-lethal dose of IAV H3N2 strain HKx31 displayed neutrophil-mediated viral clearance <italic>via</italic> phagocytosis (<xref rid="B132" ref-type="bibr">132</xref>, <xref rid="B158" ref-type="bibr">158</xref>). Depletion of neutrophils has found to enhance viral load in the IAV-infected animals (<xref rid="B158" ref-type="bibr">158</xref>).</p><p>On the contrary, this protective nature is disputed due to the association of neutrophil-generated NETs. Extensive NET formation was observed in mice infected with PR8, an IAV strain highly pathogenic to mice (<xref rid="B159" ref-type="bibr">159</xref>). Histones and myeloperoxidase within the NET induce cell death of lung epithelium and endothelium (<xref rid="B157" ref-type="bibr">157</xref>), leading to the loss of integrity of the alveolar-capillary barrier, a characteristic of ALI. Yet, while histones have been shown to suppress IAV replication <italic>in vitro</italic> (<xref rid="B160" ref-type="bibr">160</xref>), <italic>in vivo</italic> study demonstrated that there was increase in lung inflammation and damage in IAV-infected mice treated with histones (<xref rid="B161" ref-type="bibr">161</xref>). Interestingly, co-treatment of lethally infected mice with anti-histone antibody and oseltamivir resulted in an increase in animal survival when compared to infected mice groups treated solely with oseltamivir (<xref rid="B161" ref-type="bibr">161</xref>).</p><p>In agreement with the <italic>in vitro</italic> and <italic>in vivo</italic> data, it has been reported that NET produced by cultured neutrophils from patient with H7N9 and severe H1N1 infection increased alveolar epithelial cell permeability (<xref rid="B162" ref-type="bibr">162</xref>) leading to ALI. More importantly, plasma NET level positively correlated with the disease severity index (including higher acute physiology and chronic health evaluation II score) and multiple organ dysfunction syndrome (<xref rid="B162" ref-type="bibr">162</xref>), further demonstrating the detrimental role of NET in the pathogenesis of severe IAV infections.</p><p>Studies have demonstrated the involvement of superoxide dismutase and myeloperoxidase in NETosis, the formation of NET (<xref rid="B159" ref-type="bibr">159</xref>). The presence of anti-myeloperoxidase antibody as well as the superoxide dismutase inhibitor (DETC) significantly reduced NETosis. Finally, tetrahydroisoquinolines (<xref rid="B163" ref-type="bibr">163</xref>) and a pan-peptidylarginine deiminase (PAD) inhibitor, named Cl-amidine (<xref rid="B164" ref-type="bibr">164</xref>) have been suggested to inhibit NETosis. Despite it has been reported that during IAV H1N1 infection, PAD4 knockout mice displayed only slight improvement in weight loss and a slight prolonged but no end-point survival advantage was observed compared to WT mice (<xref rid="B165" ref-type="bibr">165</xref>), based on the extensive findings presented above, targeting NET to prevent ALI in the severe case of IAV infection, including the highly pathogenic avian IAV, remain promising and may warrant further investigation.</p></sec><sec id="S3-2"><title>Innate Lymphoid Cells (ILCs)</title><p>Innate lymphoid cells are cells of lymphoid lineages that do not express antigen-specific B- or T-cell receptors (<xref rid="B166" ref-type="bibr">166</xref>). Similar to T-helper cells, they are classified into subsets by their ability to produce type 1 (Th1), type 2 (Th2), and type 3 (Th17 and Th22) cytokines.</p><p>Previous studies confirmed the involvement of ILCs of group 2 linage (ILC2) in IAV infection and airway inflammation (<xref rid="B166" ref-type="bibr">166</xref>, <xref rid="B167" ref-type="bibr">167</xref>). On the positive side, during the recovery phase of IAV infection, ILC2 expresses amphiregulin which promote airway epithelium repair (<xref rid="B166" ref-type="bibr">166</xref>, <xref rid="B168" ref-type="bibr">168</xref>), thus facilitating the recovery of the infected lung.</p><p>On the other hand, in response to IL-33 produced by macrophages, DCs, and NKT cells, ILC2 secretes IL-5 and IL-13 and induce airway hyper-responsiveness. Recruitment of eosinophils by IL-5 to the lung also mediates airway inflammation (<xref rid="B166" ref-type="bibr">166</xref>). Since eosinophilia is a characteristic of allergic asthma and influenza is a major cause for morbidity and mortality in asthma patients (<xref rid="B166" ref-type="bibr">166</xref>), it will be of particular interest to investigate the role of ILC2 in IAV infection, particularly in asthma patients.</p><p>ILC1s have been initially described as immature NK cells residing in the liver and share many phenotypic similarities with NK cells (<xref rid="B169" ref-type="bibr">169</xref>). It was recently appreciated that tissue-resident ILC1s other than the previously recognized NK cells are the major early source of the antiviral IFN-γ at the primary site of various viral infection, including IAV (<xref rid="B170" ref-type="bibr">170</xref>). Interestingly, IFN-γ was found to suppress ILC2 activity and reduce IL5 production which exacerbates disease severity during influenza A(H1N1)pdm09 infection (<xref rid="B171" ref-type="bibr">171</xref>). This data may highlight a link between ILC1 and ILC2 and suggesting ILC1 can suppress ILC2 activity <italic>via</italic> IFN-γ production during IAV infection.</p><p>With ILCs finally identified, functions of these cells and their role in immune response to tumors and pathogen infections have been massively investigated in recent years. Type I IFNs, prostaglandin I<sub>2</sub>, corticosteroids, and testosterone have been reported to suppress ILC2 activity (<xref rid="B172" ref-type="bibr">172</xref>, <xref rid="B173" ref-type="bibr">173</xref>). In addition to IL-33, the epithelial cytokines IL-25, thymic stromal lymphopoietin, as well as the lipid mediator prostaglandin D<sub>2</sub> were found to activate ILC2 (<xref rid="B173" ref-type="bibr">173</xref>). The therapeutic potential of these ILC2 activators and suppressors is yet to be deduced. With more and more studies demonstrating the involvement of ILC in IAV infection, the interplay between different ILC subtypes in IAV infection would, therefore, be an interesting area to explore and modulate the ILC activity may be a future approach to combat IAV infection.</p></sec><sec id="S3-3"><title>Reactive Oxygen Species</title><p>Reactive oxygen species, generated by specialized enzymes such as NADPH oxidases, are released during IAV infection (<xref rid="B174" ref-type="bibr">174</xref>). The NADPH oxidase family consists of enzymes containing different catalytic subunit named Nox1–5 and dual oxidase (Duox) 1 and 2. ROS have been reported to display both beneficial (limiting viral replication) and detrimental (promoting ALI) effects in the course of IAV infection. Interestingly, the protective or destructive effect of ROS is dependent on the enzyme of which the ROS is generated (<xref rid="B174" ref-type="bibr">174</xref>).</p><p>Dual oxidase1 and 2 are found to be host-protective (<xref rid="B174" ref-type="bibr">174</xref>, <xref rid="B175" ref-type="bibr">175</xref>). <italic>In vitro</italic>, ROS generated by nuclear Duox indirectly regulates the splicing of IAV mRNAs <italic>via</italic> the nuclear speckle-associated splicing complex (<xref rid="B175" ref-type="bibr">175</xref>). In addition to altering viral mRNA splicing, ROS generated by Doux2 has been attributed to the production of IFN-λ, an important anti-IAV IFN. In response to IAV infection, increased viral mRNA replication was observed when <italic>Duox2</italic> was silenced <italic>in vitro</italic> (<xref rid="B176" ref-type="bibr">176</xref>). Increased viral replication was also observed in mice with <italic>Doux</italic> silenced (<xref rid="B175" ref-type="bibr">175</xref>), further depicting the protective role of Doux in IAV infection.</p><p>Unlike Doux, Nox2 activation could be harmful to host. IAV infection was reported to induce Nox2-dependent endosomal ROS production (<xref rid="B177" ref-type="bibr">177</xref>). ROS could target the conserved Cys98 on Toll-like receptor (TLR) 7, and inhibit TLR7-mediated type I IFN expression during a mild IAV H3N2 infection <italic>in vivo</italic> (<xref rid="B177" ref-type="bibr">177</xref>). IAV-infected mice treated with specific Nox2 inhibitor, cholestanol-conjugated gp91ds-TAT, were found to have reduction in endosomal ROS production, restored TLR7 activity, and displayed a decreased viral load (<xref rid="B177" ref-type="bibr">177</xref>). In addition to Nox2, Nox4-dependent ROS production has also been reported to activate MAPK/ERK signaling (<xref rid="B178" ref-type="bibr">178</xref>), enhancing the export of vRNP complex, thus increasing viral replication (see <xref ref-type="sec" rid="S2-4-1-2">Targeting the Raf/MEK/ERK Pathway</xref>). <italic>Nox4</italic> knockdown resulted in a reduction of viral replication <italic>in vitro</italic> (<xref rid="B178" ref-type="bibr">178</xref>).</p><p>Targeting the different NADPH oxidase isoforms, instead of scavenging ROS should be considered as the therapeutic approach for IAV infection, as Doux-mediated ROS production is beneficial (<xref rid="B175" ref-type="bibr">175</xref>, <xref rid="B176" ref-type="bibr">176</xref>), while Nox2 and Nox4 are harmful during IAV infections (<xref rid="B177" ref-type="bibr">177</xref>, <xref rid="B178" ref-type="bibr">178</xref>). Finally, NS1 (not to be confused with IAV NS1 protein) has been demonstrated to be a Nox inhibitor, which could inhibit the activity of Nox1, Nox2, and Nox4. A study demonstrated that NS1 suppresses IAV-induced Nox2 and significantly inhibits IAV virus replication (<xref rid="B179" ref-type="bibr">179</xref>). Besides cholestanol-conjugated gp91ds-TAT and NS1 aforementioned, apocynin, a phagocytic Nox2 inhibitor as well as ROS scavenger (<xref rid="B180" ref-type="bibr">180</xref>–<xref rid="B182" ref-type="bibr">182</xref>), has been demonstrated to ameliorate hyper upregulation of cytokines induced by IAV infection through SOCS1 and SOCS3 <italic>in vitro</italic> (<xref rid="B154" ref-type="bibr">154</xref>) and reduce peri-bronchial inflammation and viral titer <italic>in vivo</italic> (<xref rid="B183" ref-type="bibr">183</xref>). Interestingly, ebselen, another Nox2 inhibitor and glutathione peroxidase mimetic, could reduce inflammatory status measured in bronchoalveolar lavage fluid (BALF) of mice pre-exposed to cigarette smoke and subsequently infected with IAV (<xref rid="B184" ref-type="bibr">184</xref>). Taken together, these reports highlight the potential use of NADPH oxidases inhibitors and ROS scavengers to treat IAV infections.</p></sec><sec id="S3-4"><title>Soluble Mediators and Receptor-Based Immunomodulation</title><p>Dysregulated cytokine production has been associated with the elevated mortality rate observed in severe IAV infections (<xref rid="B185" ref-type="bibr">185</xref>, <xref rid="B186" ref-type="bibr">186</xref>). As such, the immunomodulation of cytokines are regarded as promising therapeutic tactics. Recent advancements developed with this approach will be highlighted in the following section.</p><sec id="S3-4-1"><title>Tumor Necrosis Factor</title><p>Tumor necrosis factor has two main functions during viral infection—it activates NF-κB, inducing the expression of cytokines responsible for the host immune response; and induces apoptosis through activation of a signaling cascade involving TRADD, FADD, and caspase 3, 7, 8, and 10 (<xref rid="B187" ref-type="bibr">187</xref>–<xref rid="B189" ref-type="bibr">189</xref>). TNF is known to be highly upregulated in IAV-infected hosts, especially in hosts infected with highly pathogenic IAV (<xref rid="B153" ref-type="bibr">153</xref>, <xref rid="B190" ref-type="bibr">190</xref>). However, it is both protective and counter-protective functions associated with TNF that makes it a target in the treatment of IAV.</p><p>The protective role of TNF is observed during infection by low pathogenic IAV, where extrinsically derived TNF is responsible for attenuating tissue-damaging CD8<sup>+</sup> T-cell response (<xref rid="B191" ref-type="bibr">191</xref>). In addition to recruiting monocytic cells to the infection site, CD8<sup>+</sup> T-cells response was observed to deteriorate lung pathology (<xref rid="B192" ref-type="bibr">192</xref>) and damage healthy, non-infected lung epithelial cells (<xref rid="B193" ref-type="bibr">193</xref>) upon IAV infection. Furthermore, TNF deficiency has been associated with an increased detection of IL-15 and IL-6 in BALF (<xref rid="B192" ref-type="bibr">192</xref>), which promote the survival of and proliferation of CD8<sup>+</sup> T-cells (<xref rid="B194" ref-type="bibr">194</xref>, <xref rid="B195" ref-type="bibr">195</xref>) and subsequent tissue damage. Exacerbated lung pathology caused by the upregulation of the monocyte chemoattractant protein-1 was observed in <italic>TNF</italic><sup>−/−</sup> mice infected with sub-lethal dose of IAV (<xref rid="B196" ref-type="bibr">196</xref>). In addition, decreased CD8<sup>+</sup> T-cell contraction due to enhanced expression of the anti-apoptotic protein Bcl-2 was observed in sub-lethally IAV-infected TNF-deficient mice when compared to WT mice (<xref rid="B192" ref-type="bibr">192</xref>). As a whole, there is substantial evidence supporting the protective role of TNF in IAV infection.</p><p>On the other hand, the correlation of TNF with pulmonary edema has been well-documented (<xref rid="B197" ref-type="bibr">197</xref>). TNF has been observed to stimulate the expression of CXCL2 in alveolar epithelial cells in a transgenic mice model resembling extensive IAV infection in lung tissue, causing alveolar damage, lung edema, and hemorrhage (<xref rid="B198" ref-type="bibr">198</xref>). In addition to lung edema, TNF has also been reported to correlate with IAV-associated encephalopathy (<xref rid="B199" ref-type="bibr">199</xref>, <xref rid="B200" ref-type="bibr">200</xref>). However, it is notable that despite IAV-associated encephalopathy, direct invasion of the central nervous system is rare (<xref rid="B201" ref-type="bibr">201</xref>), suggesting that IAV-associated encephalopathy could instead be a result of peripheral infection. Furthermore, TNF has been shown to increase the permeability of the blood–brain barrier (BBB) (<xref rid="B202" ref-type="bibr">202</xref>, <xref rid="B203" ref-type="bibr">203</xref>), contributing to neural damage (<xref rid="B204" ref-type="bibr">204</xref>). These studies further support an anti-TNF approach as a potential therapy for severe IAV infection.</p><p>At present, etanercept, an anti-TNF drug administered in the treatment of rheumatoid arthritis, is the only TNF inhibitor (or even TNF directed treatment) tested for IAV treatment. Etanercept has been shown to protect against the <italic>in vivo</italic> lethal infection of mice with a highly virulent, mouse-adapted IAV strain (<xref rid="B205" ref-type="bibr">205</xref>), with observations made of an increased survival rate with decreased morbidity, expression of the proinflammatory cytokine IL-6, lung injury, and edema (<xref rid="B205" ref-type="bibr">205</xref>).</p></sec><sec id="S3-4-2"><title>IL-6 and IL-27</title><p>The protective role of IL-6 was demonstrated in mice challenged with sub-lethal IAV infection. IL-6-deficient mice displayed exacerbated pulmonary damage (<xref rid="B206" ref-type="bibr">206</xref>, <xref rid="B207" ref-type="bibr">207</xref>) and lung injury due to an observed decline in the survival of alveolar type II cells and alveolar epithelial cells (<xref rid="B207" ref-type="bibr">207</xref>). IAV suppresses the anti-apoptotic Mcl-1 and Bcl-X<sub>L</sub> expression, causing cell death of neutrophils which are critical in viral clearance (<xref rid="B206" ref-type="bibr">206</xref>). Addition of IL-6 restored the expression of Mcl-1 and Bcl-X<sub>L</sub><italic>in vitro</italic> and is considered as the underlying mechanism for the observed survival advantage of WT mice over <italic>IL-6</italic> knockout mice during mild IAV infection.</p><p>IL-6 has also been shown to induce the proliferation of lung IL-10<sup>+</sup> regulatory T cells and IL-27, which act to limit excessive proliferation of CD8<sup>+</sup> T-cells and subsequent CD8<sup>+</sup>-inflicted damage. This would hence prevent the tissue damage observed in lung immunopathology (<xref rid="B208" ref-type="bibr">208</xref>).</p><p>Despite the apparent protective role of IL-6, high levels of IL-6 in serum or cerebrospinal fluid have been reported in severe neurologically complicated IAV cases, with IL-6 used as a marker for prognosis (<xref rid="B199" ref-type="bibr">199</xref>–<xref rid="B201" ref-type="bibr">201</xref>, <xref rid="B209" ref-type="bibr">209</xref>, <xref rid="B210" ref-type="bibr">210</xref>). The role of IL-6 in regulation of BBB permeability was reported (<xref rid="B211" ref-type="bibr">211</xref>), with potentially detrimental neurological complications. As such, the suppression of hyper-induced IL-6 as a form of therapy in severe IAV infection should be considered. One such option is the anti-IL6 antibody-based drug tocilizumab, which is currently administered clinically for the treatment of rheumatoid arthritis. However, study on the usage of this drug to treat hyper upregulation of IL-6 due to severe IAV infection has yet to be conducted. On the other hand, in a case of H1N1 virus-induced ARDS, the use of an extracorporeal cytokine hemoadsorption device to remove cytokines including TNF and IL-6 from the bloodstream (<xref rid="B212" ref-type="bibr">212</xref>) has showed beneficial to the patient (<xref rid="B213" ref-type="bibr">213</xref>). More research is required to confirm whether the removal or neutralization of IL-6 could be a potential therapy for severe IAV infections.</p><p>The activation of CD8<sup>+</sup> T-cell is crucial for viral clearance. It should, however, be tightly regulated to limit CD8<sup>+</sup> T-cell inflicted host cell damage. IL-6 mediates IL-27 induction (<xref rid="B208" ref-type="bibr">208</xref>). IL-27 acts to suppress CD8<sup>+</sup> T-cells and reduce morbidity through IL-10 and regulatory T-cells (<xref rid="B208" ref-type="bibr">208</xref>). Much like other immunomodulatory approaches, the timing for applying IL-27 should be carefully assessed. Compared to placebo-treated IAV-infected group, early administration of IL-27 to IAV-infected mice in fact led to poorer viral clearance, increased morbidity, and deteriorated lung histopathology, while IL-27 administration during the recovery phase (5–10 days post-infection) accelerated recovery and improve lung immunopathology (<xref rid="B214" ref-type="bibr">214</xref>). Notably, IL-27 could also suppress Th17 responses and increases susceptibility to secondary <italic>S. aureus</italic> infection (<xref rid="B215" ref-type="bibr">215</xref>). Therefore, co-administration of antibiotics should be considered when utilizing IL-27 as potential IAV treatment.</p></sec><sec id="S3-4-3"><title>Type I and III Interferons</title><p>Both type I and III IFNs have antiviral properties, with viruses counteract IFNs to gain an advantage for their propagation. The IAV viral protein NS1 inhibits the production of IFNs by antagonizing IRF-3, a key transcriptional factor for IFNs. This prevents the processing of cellular pre-mRNAs (including those for IFNs) and directly interacts with retinoic acid-inducible gene (RIG)-I receptors, which are critical in innate sensing, to suppress IFN production during infection (<xref rid="B216" ref-type="bibr">216</xref>, <xref rid="B217" ref-type="bibr">217</xref>). In addition to inhibiting IFN expression, the induction of SOCS3 inhibits IFNs signaling by suppressing cytokine signaling has been documented (<xref rid="B155" ref-type="bibr">155</xref>).</p><p>The recognition of 5′ triphosphate on viral RNA by RIG-I receptor is shown to induce the expression of SOCS3, which in turn represses type I IFNs expression (<xref rid="B155" ref-type="bibr">155</xref>). Due to IFNs being a key contributor to antiviral immune response, an impairment of type I or III IFN production may cause the escalation of otherwise mildly pathogenic IAV infection into a life-threatening one (<xref rid="B218" ref-type="bibr">218</xref>).</p><p>While type I IFN has been demonstrated to inhibit IAV replication <italic>in vitro</italic> (<xref rid="B219" ref-type="bibr">219</xref>); the <italic>in vivo</italic> administration of type I IFN in animal models only displayed effectiveness in a prophylactic capacity. A lowered viral titer was detected in the nasal wash of test animals. However, host susceptibility to IAV infection remained unchanged (<xref rid="B219" ref-type="bibr">219</xref>). Notably, this protective effect is only conferred by an optimal dose of type I IFN of low to moderate amounts (10–100 units per mice daily); with higher dosages (1,000–10,000 units per mice daily) shown to increase morbidity (<xref rid="B220" ref-type="bibr">220</xref>). In addition, clinical trials demonstrated that prophylactic administration of type I IFN reduced disease severity and lowered susceptibility to IAV in males and participants aged 50 or above (<xref rid="B221" ref-type="bibr">221</xref>).</p><p>Despite relatively successful results seen in the prophylactic use of IFNs, its therapeutic use is of greater clinical relevance. Mice treated with type I IFN post-IAV infection showed a successful reduction in lung IAV titer but displayed increased morbidity and mortality in comparison to vehicle-treated mice (<xref rid="B222" ref-type="bibr">222</xref>). A possible explanation for this phenomenon is the induction of excessive inflammatory response and TRAIL-DR5-mediated epithelial cell death by type I IFN (<xref rid="B223" ref-type="bibr">223</xref>), which accounts for the observed lung pathology in IAV-infected animals treated with type I IFN (<xref rid="B224" ref-type="bibr">224</xref>). In addition, downregulation of γδ T-cells by type I IFN has been correlated with increased susceptibility to secondary <italic>S. pneumoniae</italic> infection (<xref rid="B225" ref-type="bibr">225</xref>), further arguing against the potential use of type I IFNs for the treatment of IAV infection.</p><p>In comparison to type I IFNs, the administration of type III IFNs may provide advantages in the control of IAV replication (<xref rid="B176" ref-type="bibr">176</xref>, <xref rid="B222" ref-type="bibr">222</xref>, <xref rid="B224" ref-type="bibr">224</xref>) without the risk of previously reported type I IFNs-mediated immunopathologic side-effects (<xref rid="B222" ref-type="bibr">222</xref>, <xref rid="B224" ref-type="bibr">224</xref>, <xref rid="B226" ref-type="bibr">226</xref>). However, a recent study aiming to stimulate IFNs signaling through the systematic administration of RIG-I ligand post-IAV infection demonstrated that type I, but not type III IFNs signaling is important in conferring protection during fatal IAV infection <italic>in vivo</italic> (<xref rid="B227" ref-type="bibr">227</xref>). Though, this study did not measure the production of type I and III IFNs as well as any changes in viral load with respect to <italic>Ifnar</italic> or <italic>Ifnlr</italic> knockout. In addition, while human immune cells are not primary targets in IAV infection, they could be susceptible to IAV and become efficient host cells for virus replication. They are reported to possess a subpar response to type III IFNs (<xref rid="B222" ref-type="bibr">222</xref>); leading to the preliminary conclusion that solely using type III IFN as treatment may not be feasible. As such, reports suggesting the use of type III IFNs over type I IFNs as a front-line therapeutic agent to counter IAV infections may require further investigation.</p></sec><sec id="S3-4-4"><title>Prostaglandin E<sub>2</sub></title><p>The inhibition of COX-2 by selective inhibitors, nimesulide and celecoxib, was previously demonstrated to suppress the hyper upregulation of pro-inflammatory cytokines induced by highly pathogenic avian IAV (<xref rid="B228" ref-type="bibr">228</xref>–<xref rid="B230" ref-type="bibr">230</xref>). In addition, the use of zanamivir in tandem with a specific COX-2 inhibitor was shown to increase the survival rate of mice lethally infected with avian H7N9 IAV, when compared to mice treated solely with zanamivir (<xref rid="B229" ref-type="bibr">229</xref>).</p><p>Activated COX-2 regulates downstream prostaglandin production. One such example is PGE<sub>2</sub>, a major type of prostaglandin recently demonstrated to play an important role during IAV infection. PGE<sub>2</sub> was significantly upregulated in response to IAV infection, leading to the inhibition of antiviral type I IFN production in macrophages and the subsequent increase in virus replication (<xref rid="B231" ref-type="bibr">231</xref>). The use of chemicals AH6809 and GW627368X to antagonize PGE<sub>2</sub> downstream signaling molecules EP2 and EP4 respectively, was shown to induce antiviral type I IFN production. The <italic>in vivo</italic> treatment of mice lethally challenged IAV with both EP2 and EP4 antagonists significantly improved the survival rate.</p><p>A recent study demonstrated the ability of a modified TCM decoction to reduce PEG<sub>2</sub> production and subsequent morbidity in mice lethally challenged with IAV. Improved lung pathology was observed (<xref rid="B232" ref-type="bibr">232</xref>). The long history of clinical TCM use supports the clinical feasibility of PEG<sub>2</sub> inhibition as an option to treat severe IAV infections.</p></sec><sec id="S3-4-5"><title>Toll-Like Receptors (TLRs)</title><p>Pattern recognition receptors on host cells sense specific PAMPs present on the viral surface or generated during replication. PRRs can be broadly divided into two classes by their function or location. When defined by location, PRRs are classified into 3 groups—membrane-bound (TLRs and C-type lectin receptors), cytosolic (RIG-I-like and NOD-like receptors), and secreted (collectins and pentraxins) (<xref rid="B233" ref-type="bibr">233</xref>).</p><p>Significant research has been conducted on PRRs with regards to IAV infection. TLRs and RIG-I receptors have been extensively studied for their major roles in eliciting host immune responses (cytokine and IFN expression) during IAV infection (<xref rid="B234" ref-type="bibr">234</xref>–<xref rid="B236" ref-type="bibr">236</xref>). RIG-I receptors have been investigated for their functional relevance to IAV infection and targeting these receptors as a form of IAV treatment has been extensively reviewed (<xref rid="B237" ref-type="bibr">237</xref>–<xref rid="B239" ref-type="bibr">239</xref>). This section will cover recent research on TLRs and the targeting of different TLRs to treat IAV infection.</p><p>Humans have been identified to express TLR1–10, while mice have been identified to express functional TLR1–9 as well as TLR11–13 (<xref rid="B240" ref-type="bibr">240</xref>). Most TLRs—with the exception of TLR3—utilize MyD88 as an adaptor protein during signal transduction. TLR3 utilizes TRIF as an adaptor. TLR4 is known for its ability to utilize either MyD88 or TRIF, with the choice of adaptor dependent on its sub-cellular location (<xref rid="B241" ref-type="bibr">241</xref>). Different TLRs, such as TLR3, 7, and 8 (<xref rid="B240" ref-type="bibr">240</xref>) as well as TLR2, TLR4, and most recently TLR10 (<xref rid="B235" ref-type="bibr">235</xref>), have been revealed to play a role in the orchestration of host immune responses contributing to IAV pathogenesis.</p><p>With TLR10 being an exception (<xref rid="B242" ref-type="bibr">242</xref>–<xref rid="B244" ref-type="bibr">244</xref>), TLR activation largely causes the release of pro-inflammatory cytokines, with hypercytokinemia leading to ALI as a major cause of mortality in severe IAV infections. In addition to dysregulated cytokine release, excessive production of ROS has been associated with ALI development. In fact, lung injury during severe pulmonary infections, such as IAV and SARS, could be caused by oxidative stress (<xref rid="B245" ref-type="bibr">245</xref>). IAV infection activates NADPH oxidase that subsequently produces oxidized PAPC, an endogenous phospholipid. The oxidized PAPC serves as an agonist for TLR4, activating a TLR4-TRIF-TRAF6-NF-κB signaling cascade to eventually trigger the release of IL-6, ultimately inducing the onset of ALI. In addition to oxidized PAPC, the induction of endogenous protein S100A9 upon intracellular PRR DDX21 recognition of IAV subsequently induces the activation of TLR4, further contributing to IAV-induced mortality (<xref rid="B246" ref-type="bibr">246</xref>). Since TLR4 has been proven to be important in ALI induction (and hence IAV-related mortality), manipulating the stimulation and antagonism of TLR4 could potentially reduce the severity of IAV infections.</p><p>Eritoran (E5564) is a specific TLR4 antagonist initially purposed for the treatment of sepsis, but a failed a phase III clinical trial due to improved patient care in the placebo group prevented its eventual use in sepsis treatment (<xref rid="B247" ref-type="bibr">247</xref>). <italic>In vivo</italic> administration of eritoran in mice lethally infected with IAV resulted in improved clinical score, lung pathology results, and reduced viral titer. Delayed administration of eritoran, at day 6 after infection beyond the recommended therapeutic time window (within 48 h after the first display of clinical symptom) for use of oseltamivir (<xref rid="B248" ref-type="bibr">248</xref>), also demonstrated a significant benefit to infected mice compared to non-treated group, suggesting a prolonged therapeutic time window for IAV treatment when compared to mainstay antiviral drug treatment. A newer and structurally simpler specific TLR4 antagonist, FP7 (<xref rid="B249" ref-type="bibr">249</xref>), alongside a newly developed decoy peptide 2R9 that has been shown to disrupt TLR2, 4, 7, and 9 signaling <italic>via</italic> TIRAP, has been shown to protect mice from lethal IAV infection (<xref rid="B250" ref-type="bibr">250</xref>). These results support the potential use of TLR4 antagonism as a means to treat severe IAV infection.</p><p>The suppression of other TLR signaling pathways—such as blocking TLR2-mediated signaling through the use of an anti-TLR2 antibody, significantly protected against lethality when administered on day 2 and 4 post-IAV infection (<xref rid="B251" ref-type="bibr">251</xref>).</p><p>A study also demonstrated that H5N1-infected TLR3 knockout mice had better survival than H5N1-infected wild-type mice, which is evident through the significantly faster regaining of body weight post-infection, lower viral titer in the lung, and fewer pathological changes in the lung (<xref rid="B252" ref-type="bibr">252</xref>).</p><p>An increasing number of TLR antagonists are now under development (<xref rid="B253" ref-type="bibr">253</xref>, <xref rid="B254" ref-type="bibr">254</xref>), alongside several other agents also shown to have effects on TLRs. Polysaccharides isolated from <italic>R. isatidis</italic>, a traditional Chinese medicinal herb used to treat IAV infection, have recently been shown to inhibit pro-inflammatory cytokines such as IL-6 and CCL-5 <italic>in vitro</italic> by down-regulating upstream TLR3 expression (<xref rid="B255" ref-type="bibr">255</xref>). MENK, an endogenous protein expressed in the adrenal medulla, was shown to both prophylactically and therapeutically increase the survival rate while reducing viral-caused lung pathology and viral titer in mice lethally challenged with IAV (<xref rid="B256" ref-type="bibr">256</xref>). This was determined to be caused by the downregulation of TLR7. These results suggest the potential of down-regulating TLR expression in the treatment of IAV infection.</p><p>The above-mentioned data suggest modulation of TLR signaling or expression as a promising approach in treating severe influenza disease and deserves immediate investigation. Table <xref rid="T2" ref-type="table">2</xref> summarizes new immunomodulatory approaches to combat IAV infections.</p><table-wrap id="T2" position="float"><label>Table 2</label><caption><p>New immunomodulatory approaches to treat influenza A virus (IAV) infection.</p></caption><table frame="hsides" rules="rows"><thead><tr><th valign="top" align="left" rowspan="1" colspan="1">Potential target/approach</th><th valign="top" align="left" rowspan="1" colspan="1">Possible intervention</th><th valign="top" align="left" rowspan="1" colspan="1">Effect</th><th valign="top" align="left" rowspan="1" colspan="1">Reference</th></tr></thead><tbody><tr><td align="left" valign="top" rowspan="1" colspan="1">Histones</td><td align="left" valign="top" rowspan="1" colspan="1">Anti-histone antibodies</td><td align="left" valign="top" rowspan="1" colspan="1">Prevents lung inflammation and damage induced by histones</td><td align="left" valign="top" rowspan="1" colspan="1">Ashar et al. (<xref rid="B161" ref-type="bibr">161</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">NETosis</td><td align="left" valign="top" rowspan="1" colspan="1"><list list-type="alpha-lower"><list-item><p>Cl-amidine</p></list-item><list-item><p>Tetrahydroisoquinolines (both tested on NETosis, effect on IAV yet to be determined)</p></list-item></list></td><td align="left" valign="top" rowspan="1" colspan="1">Prevents lung injury mediated by NET</td><td align="left" valign="top" rowspan="1" colspan="1"><list list-type="alpha-lower"><list-item><p>Kusunoki et al. (<xref rid="B164" ref-type="bibr">164</xref>)</p></list-item><list-item><p>Martinez et al. (<xref rid="B163" ref-type="bibr">163</xref>)</p></list-item></list></td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">ILC2</td><td align="left" valign="top" rowspan="1" colspan="1">To be determined</td><td align="left" valign="top" rowspan="1" colspan="1">Promotes airway epithelium repair</td><td align="left" valign="top" rowspan="1" colspan="1">Califano et al. (<xref rid="B171" ref-type="bibr">171</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Nox2</td><td align="left" valign="top" rowspan="1" colspan="1"><list list-type="alpha-lower"><list-item><p>Cholestanol-conjugated gp91ds-TAT</p></list-item><list-item><p>Apocynin [also as reactive oxygen species (ROS) scavenger]</p></list-item><list-item><p>Ebselen (also as ROS scavenger and glutathione peroxidase mimetic)</p></list-item></list></td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits Nox2 activity</td><td align="left" valign="top" rowspan="1" colspan="1"><list list-type="alpha-lower"><list-item><p>To et al. (<xref rid="B177" ref-type="bibr">177</xref>)</p></list-item><list-item><p>Ye et al. (<xref rid="B154" ref-type="bibr">154</xref>)</p></list-item><list-item><p>Oostwoud et al. (<xref rid="B184" ref-type="bibr">184</xref>)</p></list-item></list></td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Tumor necrosis factor (TNF)</td><td align="left" valign="top" rowspan="1" colspan="1">Etanercept</td><td align="left" valign="top" rowspan="1" colspan="1">Prevents TNF-mediated lung injury and edema</td><td align="left" valign="top" rowspan="1" colspan="1">Shi et al. (<xref rid="B205" ref-type="bibr">205</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">IL-6</td><td align="left" valign="top" rowspan="1" colspan="1">Administration of IL-6</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits cell death of neutrophils; limits CD8<sup>+</sup> T-cell-induced lung injury</td><td align="left" valign="top" rowspan="1" colspan="1">Dienz et al. (<xref rid="B206" ref-type="bibr">206</xref>); Pyle et al. (<xref rid="B208" ref-type="bibr">208</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">IL-27</td><td align="left" valign="top" rowspan="1" colspan="1">Administration of IL-27 at recovery phase (5–10 days post-infection)</td><td align="left" valign="top" rowspan="1" colspan="1">Promotes recovery and improves lung immunopathology</td><td align="left" valign="top" rowspan="1" colspan="1">Liu et al. (<xref rid="B214" ref-type="bibr">214</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">Type III IFN</td><td align="left" valign="top" rowspan="1" colspan="1">Administration of type III IFN</td><td align="left" valign="top" rowspan="1" colspan="1">Controls IAV replication by type III IFN signaling pathways</td><td align="left" valign="top" rowspan="1" colspan="1">Davidson et al. (<xref rid="B222" ref-type="bibr">222</xref>); Kim et al. (<xref rid="B224" ref-type="bibr">224</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">PGE<sub>2</sub> signaling</td><td align="left" valign="top" rowspan="1" colspan="1"><list list-type="alpha-lower"><list-item><p>AH6809 (EP2 antagonist)</p></list-item><list-item><p>GW627368X (EP4 antagonist)</p></list-item></list></td><td align="left" valign="top" rowspan="1" colspan="1">Restores type I IFNs induction which are suppressed by PGE<sub>2</sub> in macrophages</td><td align="left" valign="top" rowspan="1" colspan="1">Coulombe et al. (<xref rid="B231" ref-type="bibr">231</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">TLR4 signaling</td><td align="left" valign="top" rowspan="1" colspan="1">TLR4 antagonists (a. Eritoran and b. FP7)</td><td align="left" valign="top" rowspan="1" colspan="1">Ameliorates TLR4-mediated lung injury</td><td align="left" valign="top" rowspan="1" colspan="1"><list list-type="alpha-lower"><list-item><p>Shirey et al. (<xref rid="B248" ref-type="bibr">248</xref>)</p></list-item><list-item><p>Perrin-Cocon et al. (<xref rid="B249" ref-type="bibr">249</xref>)</p></list-item></list></td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">TIRAP antagonism</td><td align="left" valign="top" rowspan="1" colspan="1">Peptide 2R9</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits multiple TLR signaling</td><td align="left" valign="top" rowspan="1" colspan="1">Piao et al. (<xref rid="B250" ref-type="bibr">250</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">TLR2 signaling</td><td align="left" valign="top" rowspan="1" colspan="1">Anti-TLR2 antibody</td><td align="left" valign="top" rowspan="1" colspan="1">Inhibits TLR2 signaling mediated lethality</td><td align="left" valign="top" rowspan="1" colspan="1">Shirey et al. (<xref rid="B251" ref-type="bibr">251</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">TLR3 signaling</td><td align="left" valign="top" rowspan="1" colspan="1">Polysaccharides isolated from <italic>R. isatidis</italic></td><td align="left" valign="top" rowspan="1" colspan="1">Down regulates TLR3 expression to inhibit hypercytokinemia</td><td align="left" valign="top" rowspan="1" colspan="1">Li et al. (<xref rid="B255" ref-type="bibr">255</xref>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">TLR7 signaling</td><td align="left" valign="top" rowspan="1" colspan="1">MENK</td><td align="left" valign="top" rowspan="1" colspan="1">Down regulates TLR7 expression and reduces lung pathology</td><td align="left" valign="top" rowspan="1" colspan="1">Tian et al. (<xref rid="B256" ref-type="bibr">256</xref>)</td></tr></tbody></table></table-wrap></sec></sec></sec><sec id="S4"><title>Modulation of Metabolism</title><p>It is well documented that patients with diabetes mellitus have a greater tendency to develop severe IAV infection than healthy patients (<xref rid="B257" ref-type="bibr">257</xref>). Hyperglycemia increases susceptibility of the host to IAV infection <italic>via</italic> viral uptake, through the promotion of V-ATPase assembly (<xref rid="B258" ref-type="bibr">258</xref>) and immunosuppression (<xref rid="B257" ref-type="bibr">257</xref>). In addition, viruses rely on host metabolism to perform essential functions during replication (<xref rid="B259" ref-type="bibr">259</xref>–<xref rid="B262" ref-type="bibr">262</xref>). These processes exert a large energy demand on the host within a very short period of time (<xref rid="B263" ref-type="bibr">263</xref>); energy of which is supplied by and is dependent on host metabolism. IAV viruses have been reported to modify the metabolic state of the host. For example, increased c-Myc-dependent glycolysis and glutaminolysis has been demonstrated in infected cells (<xref rid="B264" ref-type="bibr">264</xref>). The changes in glucose and glutamine metabolism were reversed upon the addition of BEZ235, which inhibited the IAV-mediated c-Myc induction. Administration of BEZ235 2 days prior to infection and up to 4 days post-infection was shown to decrease lung viral titer and improve the survival rate in IAV-infected mice. Small molecules such as clotrimazole and α-mangostin that target lipid metabolism have also been demonstrated to suppress IAV replication <italic>in vitro</italic> (<xref rid="B264" ref-type="bibr">264</xref>).</p><p>In addition to being important for generating energy and biosynthesis, recent research demonstrates that cellular metabolism affects immune cell function. Dysregulated immune responses observed in many diseases are associated with specific metabolic configurations. Viruses, influenza inclusive (<xref rid="B265" ref-type="bibr">265</xref>), were found to induce drastic alterations in metabolic levels and programs (<xref rid="B263" ref-type="bibr">263</xref>). Macrophages in infected hosts were observed to have marked differences in the Krebs cycle, a key metabolic pathway. This is of significance due to the role of macrophages, which are immune cells critical in the pathogenesis of many inflammatory diseases (<xref rid="B263" ref-type="bibr">263</xref>, <xref rid="B265" ref-type="bibr">265</xref>, <xref rid="B266" ref-type="bibr">266</xref>).</p><p>In activated macrophages, succinate, a Krebs cycle intermediate, was found to possess inflammatory signal. Accumulation of succinate generates ROS, leading to subsequent activation of hypoxia-inducible factor 1α and the induction of cytokines such as IL-1β (<xref rid="B267" ref-type="bibr">267</xref>). A recent study identified the ability of itaconate, another Krebs cycle-derived metabolite, to block the production of inflammatory factors. This prevented inflammation, protecting mice from lethal levels of inflammation that can occur during infection (<xref rid="B268" ref-type="bibr">268</xref>). This data suggest the critical roles of Krebs cycle intermediates in regulating cytokine profiles and inflammation. Metabolites generated by innate immune cells in distinct configurations could have different roles beyond that of bioenergetics, with functions in signaling regulation, transcription, and orchestrating innate immune responses.</p><p>Despite the lack of research conducted thus far on the application of immunometabolic approaches to influenza treatment, the prospect of manipulating immune responses by modulating immune cell metabolic state is promising. Further research should focus on the identification of metabolites for modulation of immune cell function with substantial improvement of therapeutic strategies to treat IAV disease.</p><p>Latest advancements in high-throughput technologies, e.g., metabolomics is a useful approach to systematically investigate the changes of metabolic mechanisms during IAV infections. Identification of important metabolites involved during IAV infection should be a new approach by modulating the host metabolism for interventions.</p></sec><sec id="S5"><title>Concluding Remarks</title><p>Multiple host-based intervention strategies against influenza have been developed or are under development. While approaches targeting host machinery required for virus replication seem to be promising thus far, additional research is needed to determine the effect of modulating host immune response on influenza treatment. This is increasingly important, since targeted host factors may play distinct roles in response to infection by different influenza viral strains (<xref rid="B252" ref-type="bibr">252</xref>), making the management of influenza through solely targeting a single specific host factor is difficult.</p><p>Host-based interventions offer obvious advantages over conventional antivirals, such as a higher barrier to drug resistance (<xref rid="B73" ref-type="bibr">73</xref>, <xref rid="B83" ref-type="bibr">83</xref>, <xref rid="B107" ref-type="bibr">107</xref>) due to greater genetic stability of host factors than the mutation-prone nature of viral components. In addition, administration feasibility is a key factor to consider the usage of drugs. The mainstays of antivirals for IAV infections, the NA inhibitors, and M2 blockers, are recommended to be administered within 48 h of symptom onset for optimal antiviral activity. This short treatment window may not be fully fulfilled in a clinical setting. Novel host-based interventions were reported to have therapeutic time windows longer than this conventional timeframe (<xref rid="B96" ref-type="bibr">96</xref>, <xref rid="B109" ref-type="bibr">109</xref>, <xref rid="B214" ref-type="bibr">214</xref>, <xref rid="B251" ref-type="bibr">251</xref>), even up to 6 days post-infection (<xref rid="B248" ref-type="bibr">248</xref>), providing a clear clinical advantage over NA inhibitors and M2 blockers. In addition, hypercytokinemia and ARDS could contribute to disease severity and mortality in instances of severe influenza infection, with virus-targeting antivirals providing little to no alleviation of such complications.</p><p>Since host immune response is indispensable in host defense against invading pathogens, the use of immune-modulators to suppress detrimental effects while retaining beneficial protection of the host remains challenging. The timing and dosage of medication administration would be critical in determining the drug effectiveness in influenza treatment.</p><p>Targeting virus-induced metabolic changes to restore host normal metabolism may be a new direction to combat influenza disease. Further research in the immunometabolism field, alongside studies on modulating immune response to infectious disease by altering host metabolic processes; would create a new direction for future research and is expected to yield significant discoveries that may provide new therapeutic options in the treatment of IAV infections.</p></sec><sec id="S6"><title>Author Contributions</title><p>SMYL conceptualized the work. IL and ASMS drafted some review sections and TFY and SMYL wrote the manuscript.</p></sec><sec id="S7"><title>Conflict of Interest Statement</title><p>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</p></sec></body><back><fn-group><fn fn-type="financial-disclosure"><p><bold>Funding.</bold> Funding was provided by Research Grants Council of Hong Kong, General Research Fund #17111714, and Theme-based Research Scheme #T11-705/14-N; Health and Medical Research Fund #12111822 and 14130662; and Procore France/Hong Kong Joint Research Scheme #F-HKU708/16T.</p></fn></fn-group><ref-list><title>References</title><ref id="B1"><label>1</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gurav</surname><given-names>YK</given-names></name><name><surname>Chadha</surname><given-names>MS</given-names></name><name><surname>Tandale</surname><given-names>BV</given-names></name><name><surname>Potdar</surname><given-names>VA</given-names></name><name><surname>Pawar</surname><given-names>SD</given-names></name><name><surname>Shil</surname><given-names>P</given-names></name><etal></etal></person-group><article-title>Influenza A(H1N1)pdm09 outbreak detected in inter-seasonal months during the surveillance of influenza-like illness in Pune, India, 2012-2015</article-title>. <source>Epidemiol Infect</source> (<year>2017</year>) <volume>145</volume>(<issue>9</issue>):<fpage>1898</fpage>–<lpage>909</lpage>.<pub-id pub-id-type="doi">10.1017/S0950268817000553</pub-id><pub-id pub-id-type="pmid">28367767</pub-id></mixed-citation></ref><ref id="B2"><label>2</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hui</surname><given-names>DSC</given-names></name><name><surname>Lee</surname><given-names>N</given-names></name><name><surname>Chan</surname><given-names>PKS</given-names></name></person-group><article-title>Avian influenza A (H7N9) virus infections in humans across five epidemics in mainland China, 2013-2017</article-title>. <source>J Thorac Dis</source> (<year>2017</year>) <volume>9</volume>(<issue>12</issue>):<fpage>4808</fpage>–<lpage>11</lpage>.<pub-id pub-id-type="doi">10.21037/jtd.2017.11.17</pub-id><pub-id pub-id-type="pmid">29312663</pub-id></mixed-citation></ref><ref id="B3"><label>3</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Olafsdottir</surname><given-names>TA</given-names></name><name><surname>Alexandersson</surname><given-names>KF</given-names></name><name><surname>Sveinbjornsson</surname><given-names>G</given-names></name><name><surname>Lapini</surname><given-names>G</given-names></name><name><surname>Palladino</surname><given-names>L</given-names></name><name><surname>Montomoli</surname><given-names>E</given-names></name><etal></etal></person-group><article-title>Age and influenza-specific pre-vaccination antibodies strongly affect influenza vaccine responses in the Icelandic population whereas disease and medication have small effects</article-title>. <source>Front Immunol</source> (<year>2017</year>) <volume>8</volume>:<fpage>1872</fpage><pub-id pub-id-type="doi">10.3389/fimmu.2017.01872</pub-id><pub-id pub-id-type="pmid">29358933</pub-id></mixed-citation></ref><ref id="B4"><label>4</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Moscona</surname><given-names>A</given-names></name></person-group><article-title>Global transmission of oseltamivir-resistant influenza</article-title>. <source>N Engl J Med</source> (<year>2009</year>) <volume>360</volume>(<issue>10</issue>):<fpage>953</fpage>–<lpage>6</lpage>.<pub-id pub-id-type="doi">10.1056/NEJMp0900648</pub-id><pub-id pub-id-type="pmid">19258250</pub-id></mixed-citation></ref><ref id="B5"><label>5</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Takashita</surname><given-names>E</given-names></name><name><surname>Fujisaki</surname><given-names>S</given-names></name><name><surname>Shirakura</surname><given-names>M</given-names></name><name><surname>Nakamura</surname><given-names>K</given-names></name><name><surname>Kishida</surname><given-names>N</given-names></name><name><surname>Kuwahara</surname><given-names>T</given-names></name><etal></etal></person-group><article-title>Influenza A(H1N1)pdm09 virus exhibiting enhanced cross-resistance to oseltamivir and peramivir due to a dual H275Y/G147R substitution, Japan, March 2016</article-title>. <source>Euro Surveill</source> (<year>2016</year>) <volume>21</volume>(<issue>24</issue>):<fpage>30258</fpage>.<pub-id pub-id-type="doi">10.2807/1560-7917.ES.2016.21.24.30258</pub-id><pub-id pub-id-type="pmid">27336226</pub-id></mixed-citation></ref><ref id="B6"><label>6</label><mixed-citation publication-type="journal"><collab>Centers for Disease Control and Prevention</collab>. <article-title>High levels of adamantane resistance among influenza A (H3N2) viruses and interim guidelines for use of antiviral agents – United States, 2005-06 influenza season</article-title>. <source>MMWR Morb Mortal Wkly Rep</source> (<year>2006</year>) <volume>55</volume>(<issue>2</issue>):<fpage>44</fpage>–<lpage>6</lpage>.<pub-id pub-id-type="pmid">16424859</pub-id></mixed-citation></ref><ref id="B7"><label>7</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Schaduangrat</surname><given-names>N</given-names></name><name><surname>Phanich</surname><given-names>J</given-names></name><name><surname>Rungrotmongkol</surname><given-names>T</given-names></name><name><surname>Lerdsamran</surname><given-names>H</given-names></name><name><surname>Puthavathana</surname><given-names>P</given-names></name><name><surname>Ubol</surname><given-names>S</given-names></name></person-group>. <article-title>The significance of naturally occurring neuraminidase quasispecies of H5N1 avian influenza virus on resistance to oseltamivir: a point of concern</article-title>. <source>J Gen Virol</source> (<year>2016</year>) <volume>97</volume>(<issue>6</issue>):<fpage>1311</fpage>–<lpage>23</lpage>.<pub-id pub-id-type="doi">10.1099/jgv.0.000444</pub-id><pub-id pub-id-type="pmid">26935590</pub-id></mixed-citation></ref><ref id="B8"><label>8</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lina</surname><given-names>B</given-names></name><name><surname>Boucher</surname><given-names>C</given-names></name><name><surname>Osterhaus</surname><given-names>A</given-names></name><name><surname>Monto</surname><given-names>AS</given-names></name><name><surname>Schutten</surname><given-names>M</given-names></name><name><surname>Whitley</surname><given-names>RJ</given-names></name><etal></etal></person-group><article-title>Five years of monitoring for the emergence of oseltamivir resistance in patients with influenza A infections in the Influenza Resistance Information Study</article-title>. <source>Influenza Other Respi Viruses</source> (<year>2018</year>) <volume>12</volume>(<issue>2</issue>):<fpage>267</fpage>–<lpage>78</lpage>.<pub-id pub-id-type="doi">10.1111/irv.12534</pub-id><pub-id pub-id-type="pmid">29265727</pub-id></mixed-citation></ref><ref id="B9"><label>9</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tandel</surname><given-names>K</given-names></name><name><surname>Sharma</surname><given-names>S</given-names></name><name><surname>Dash</surname><given-names>PK</given-names></name><name><surname>Parida</surname><given-names>M</given-names></name></person-group>. <article-title>Oseltamivir-resistant influenza A(H1N1)pdm09 virus associated with high case fatality, India 2015</article-title>. <source>J Med Virol</source> (<year>2018</year>) <volume>90</volume>(<issue>5</issue>):<fpage>836</fpage>–<lpage>43</lpage>.<pub-id pub-id-type="doi">10.1002/jmv.25013</pub-id><pub-id pub-id-type="pmid">29288584</pub-id></mixed-citation></ref><ref id="B10"><label>10</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Szretter</surname><given-names>KJ</given-names></name><name><surname>Gangappa</surname><given-names>S</given-names></name><name><surname>Lu</surname><given-names>X</given-names></name><name><surname>Smith</surname><given-names>C</given-names></name><name><surname>Shieh</surname><given-names>WJ</given-names></name><name><surname>Zaki</surname><given-names>SR</given-names></name><etal></etal></person-group><article-title>Role of host cytokine responses in the pathogenesis of avian H5N1 influenza viruses in mice</article-title>. <source>J Virol</source> (<year>2007</year>) <volume>81</volume>(<issue>6</issue>):<fpage>2736</fpage>–<lpage>44</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.02336-06</pub-id><pub-id pub-id-type="pmid">17182684</pub-id></mixed-citation></ref><ref id="B11"><label>11</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Short</surname><given-names>KR</given-names></name><name><surname>Veeris</surname><given-names>R</given-names></name><name><surname>Leijten</surname><given-names>LM</given-names></name><name><surname>van den Brand</surname><given-names>JM</given-names></name><name><surname>Jong</surname><given-names>VL</given-names></name><name><surname>Stittelaar</surname><given-names>K</given-names></name><etal></etal></person-group><article-title>Proinflammatory cytokine responses in extra-respiratory tissues during severe influenza</article-title>. <source>J Infect Dis</source> (<year>2017</year>) <volume>216</volume>(<issue>7</issue>):<fpage>829</fpage>–<lpage>33</lpage>.<pub-id pub-id-type="doi">10.1093/infdis/jix281</pub-id><pub-id pub-id-type="pmid">28973159</pub-id></mixed-citation></ref><ref id="B12"><label>12</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chi</surname><given-names>Y</given-names></name><name><surname>Zhu</surname><given-names>Y</given-names></name><name><surname>Wen</surname><given-names>T</given-names></name><name><surname>Cui</surname><given-names>L</given-names></name><name><surname>Ge</surname><given-names>Y</given-names></name><name><surname>Jiao</surname><given-names>Y</given-names></name><etal></etal></person-group><article-title>Cytokine and chemokine levels in patients infected with the novel avian influenza A (H7N9) virus in China</article-title>. <source>J Infect Dis</source> (<year>2013</year>) <volume>208</volume>(<issue>12</issue>):<fpage>1962</fpage>–<lpage>7</lpage>.<pub-id pub-id-type="doi">10.1093/infdis/jit440</pub-id><pub-id pub-id-type="pmid">23990573</pub-id></mixed-citation></ref><ref id="B13"><label>13</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lee</surname><given-names>SM</given-names></name><name><surname>Yen</surname><given-names>HL</given-names></name></person-group>. <article-title>Targeting the host or the virus: current and novel concepts for antiviral approaches against influenza virus infection</article-title>. <source>Antiviral Res</source> (<year>2012</year>) <volume>96</volume>(<issue>3</issue>):<fpage>391</fpage>–<lpage>404</lpage>.<pub-id pub-id-type="doi">10.1016/j.antiviral.2012.09.013</pub-id><pub-id pub-id-type="pmid">23022351</pub-id></mixed-citation></ref><ref id="B14"><label>14</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Konig</surname><given-names>R</given-names></name><name><surname>Stertz</surname><given-names>S</given-names></name><name><surname>Zhou</surname><given-names>Y</given-names></name><name><surname>Inoue</surname><given-names>A</given-names></name><name><surname>Hoffmann</surname><given-names>HH</given-names></name><name><surname>Bhattacharyya</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>Human host factors required for influenza virus replication</article-title>. <source>Nature</source> (<year>2010</year>) <volume>463</volume>(<issue>7282</issue>):<fpage>813</fpage>–<lpage>7</lpage>.<pub-id pub-id-type="doi">10.1038/nature08699</pub-id><pub-id pub-id-type="pmid">20027183</pub-id></mixed-citation></ref><ref id="B15"><label>15</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Karlas</surname><given-names>A</given-names></name><name><surname>Machuy</surname><given-names>N</given-names></name><name><surname>Shin</surname><given-names>Y</given-names></name><name><surname>Pleissner</surname><given-names>KP</given-names></name><name><surname>Artarini</surname><given-names>A</given-names></name><name><surname>Heuer</surname><given-names>D</given-names></name><etal></etal></person-group><article-title>Genome-wide RNAi screen identifies human host factors crucial for influenza virus replication</article-title>. <source>Nature</source> (<year>2010</year>) <volume>463</volume>(<issue>7282</issue>):<fpage>818</fpage>–<lpage>22</lpage>.<pub-id pub-id-type="doi">10.1038/nature08760</pub-id><pub-id pub-id-type="pmid">20081832</pub-id></mixed-citation></ref><ref id="B16"><label>16</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Edinger</surname><given-names>TO</given-names></name><name><surname>Pohl</surname><given-names>MO</given-names></name><name><surname>Stertz</surname><given-names>S</given-names></name></person-group>. <article-title>Entry of influenza A virus: host factors and antiviral targets</article-title>. <source>J Gen Virol</source> (<year>2014</year>) <volume>95</volume>(<issue>Pt 2</issue>):<fpage>263</fpage>–<lpage>77</lpage>.<pub-id pub-id-type="doi">10.1099/vir.0.059477-0</pub-id><pub-id pub-id-type="pmid">24225499</pub-id></mixed-citation></ref><ref id="B17"><label>17</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Luo</surname><given-names>M</given-names></name></person-group>. <article-title>Influenza virus entry</article-title>. <source>Adv Exp Med Biol</source> (<year>2012</year>) <volume>726</volume>:<fpage>201</fpage>–<lpage>21</lpage>.<pub-id pub-id-type="doi">10.1007/978-1-4614-0980-9_9</pub-id><pub-id pub-id-type="pmid">22297515</pub-id></mixed-citation></ref><ref id="B18"><label>18</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Rust</surname><given-names>MJ</given-names></name><name><surname>Lakadamyali</surname><given-names>M</given-names></name><name><surname>Zhang</surname><given-names>F</given-names></name><name><surname>Zhuang</surname><given-names>X</given-names></name></person-group>. <article-title>Assembly of endocytic machinery around individual influenza viruses during viral entry</article-title>. <source>Nat Struct Mol Biol</source> (<year>2004</year>) <volume>11</volume>(<issue>6</issue>):<fpage>567</fpage>–<lpage>73</lpage>.<pub-id pub-id-type="doi">10.1038/nsmb769</pub-id><pub-id pub-id-type="pmid">15122347</pub-id></mixed-citation></ref><ref id="B19"><label>19</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>de Vries</surname><given-names>E</given-names></name><name><surname>Tscherne</surname><given-names>DM</given-names></name><name><surname>Wienholts</surname><given-names>MJ</given-names></name><name><surname>Cobos-Jimenez</surname><given-names>V</given-names></name><name><surname>Scholte</surname><given-names>F</given-names></name><name><surname>Garcia-Sastre</surname><given-names>A</given-names></name><etal></etal></person-group><article-title>Dissection of the influenza A virus endocytic routes reveals macropinocytosis as an alternative entry pathway</article-title>. <source>PLoS Pathog</source> (<year>2011</year>) <volume>7</volume>(<issue>3</issue>):<fpage>e1001329</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.1001329</pub-id><pub-id pub-id-type="pmid">21483486</pub-id></mixed-citation></ref><ref id="B20"><label>20</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yasuda</surname><given-names>S</given-names></name><name><surname>Morishita</surname><given-names>S</given-names></name><name><surname>Fujita</surname><given-names>A</given-names></name><name><surname>Nanao</surname><given-names>T</given-names></name><name><surname>Wada</surname><given-names>N</given-names></name><name><surname>Waguri</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>Mon1-Ccz1 activates Rab7 only on late endosomes and dissociates from the lysosome in mammalian cells</article-title>. <source>J Cell Sci</source> (<year>2016</year>) <volume>129</volume>(<issue>2</issue>):<fpage>329</fpage>–<lpage>40</lpage>.<pub-id pub-id-type="doi">10.1242/jcs.178095</pub-id><pub-id pub-id-type="pmid">26627821</pub-id></mixed-citation></ref><ref id="B21"><label>21</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Rossman</surname><given-names>JS</given-names></name><name><surname>Leser</surname><given-names>GP</given-names></name><name><surname>Lamb</surname><given-names>RA</given-names></name></person-group>. <article-title>Filamentous influenza virus enters cells via macropinocytosis</article-title>. <source>J Virol</source> (<year>2012</year>) <volume>86</volume>(<issue>20</issue>):<fpage>10950</fpage>–<lpage>60</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.05992-11</pub-id><pub-id pub-id-type="pmid">22875971</pub-id></mixed-citation></ref><ref id="B22"><label>22</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Huotari</surname><given-names>J</given-names></name><name><surname>Helenius</surname><given-names>A</given-names></name></person-group>. <article-title>Endosome maturation</article-title>. <source>EMBO J</source> (<year>2011</year>) <volume>30</volume>(<issue>17</issue>):<fpage>3481</fpage>–<lpage>500</lpage>.<pub-id pub-id-type="doi">10.1038/emboj.2011.286</pub-id><pub-id pub-id-type="pmid">21878991</pub-id></mixed-citation></ref><ref id="B23"><label>23</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hu</surname><given-names>YB</given-names></name><name><surname>Dammer</surname><given-names>EB</given-names></name><name><surname>Ren</surname><given-names>RJ</given-names></name><name><surname>Wang</surname><given-names>G</given-names></name></person-group>. <article-title>The endosomal-lysosomal system: from acidification and cargo sorting to neurodegeneration</article-title>. <source>Transl Neurodegener</source> (<year>2015</year>) <volume>4</volume>:<fpage>18</fpage>.<pub-id pub-id-type="doi">10.1186/s40035-015-0041-1</pub-id><pub-id pub-id-type="pmid">26448863</pub-id></mixed-citation></ref><ref id="B24"><label>24</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>S</given-names></name><name><surname>Sieben</surname><given-names>C</given-names></name><name><surname>Ludwig</surname><given-names>K</given-names></name><name><surname>Hofer</surname><given-names>CT</given-names></name><name><surname>Chiantia</surname><given-names>S</given-names></name><name><surname>Herrmann</surname><given-names>A</given-names></name><etal></etal></person-group><article-title>pH-Controlled two-step uncoating of influenza virus</article-title>. <source>Biophys J</source> (<year>2014</year>) <volume>106</volume>(<issue>7</issue>):<fpage>1447</fpage>–<lpage>56</lpage>.<pub-id pub-id-type="doi">10.1016/j.bpj.2014.02.018</pub-id><pub-id pub-id-type="pmid">24703306</pub-id></mixed-citation></ref><ref id="B25"><label>25</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Steinhauer</surname><given-names>DA</given-names></name></person-group>. <article-title>Role of hemagglutinin cleavage for the pathogenicity of influenza virus</article-title>. <source>Virology</source> (<year>1999</year>) <volume>258</volume>(<issue>1</issue>):<fpage>1</fpage>–<lpage>20</lpage>.<pub-id pub-id-type="doi">10.1006/viro.1999.9716</pub-id><pub-id pub-id-type="pmid">10329563</pub-id></mixed-citation></ref><ref id="B26"><label>26</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhirnov</surname><given-names>OP</given-names></name><name><surname>Ikizler</surname><given-names>MR</given-names></name><name><surname>Wright</surname><given-names>PF</given-names></name></person-group>. <article-title>Cleavage of influenza a virus hemagglutinin in human respiratory epithelium is cell associated and sensitive to exogenous antiproteases</article-title>. <source>J Virol</source> (<year>2002</year>) <volume>76</volume>(<issue>17</issue>):<fpage>8682</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.76.17.8682-8689.2002</pub-id><pub-id pub-id-type="pmid">12163588</pub-id></mixed-citation></ref><ref id="B27"><label>27</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pielak</surname><given-names>RM</given-names></name><name><surname>Chou</surname><given-names>JJ</given-names></name></person-group><article-title>Influenza M2 proton channels</article-title>. <source>Biochim Biophys Acta</source> (<year>2011</year>) <volume>1808</volume>(<issue>2</issue>):<fpage>522</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.1016/j.bbamem.2010.04.015</pub-id><pub-id pub-id-type="pmid">20451491</pub-id></mixed-citation></ref><ref id="B28"><label>28</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ye</surname><given-names>Z</given-names></name><name><surname>Liu</surname><given-names>T</given-names></name><name><surname>Offringa</surname><given-names>DP</given-names></name><name><surname>McInnis</surname><given-names>J</given-names></name><name><surname>Levandowski</surname><given-names>RA</given-names></name></person-group>. <article-title>Association of influenza virus matrix protein with ribonucleoproteins</article-title>. <source>J Virol</source> (<year>1999</year>) <volume>73</volume>(<issue>9</issue>):<fpage>7467</fpage>–<lpage>73</lpage>.<pub-id pub-id-type="pmid">10438836</pub-id></mixed-citation></ref><ref id="B29"><label>29</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Byrd-Leotis</surname><given-names>L</given-names></name><name><surname>Galloway</surname><given-names>SE</given-names></name><name><surname>Agbogu</surname><given-names>E</given-names></name><name><surname>Steinhauer</surname><given-names>DA</given-names></name></person-group>. <article-title>Influenza hemagglutinin (HA) stem region mutations that stabilize or destabilize the structure of multiple HA subtypes</article-title>. <source>J Virol</source> (<year>2015</year>) <volume>89</volume>(<issue>8</issue>):<fpage>4504</fpage>–<lpage>16</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.00057-15</pub-id><pub-id pub-id-type="pmid">25653452</pub-id></mixed-citation></ref><ref id="B30"><label>30</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lu</surname><given-names>X</given-names></name><name><surname>Shi</surname><given-names>Y</given-names></name><name><surname>Gao</surname><given-names>F</given-names></name><name><surname>Xiao</surname><given-names>H</given-names></name><name><surname>Wang</surname><given-names>M</given-names></name><name><surname>Qi</surname><given-names>J</given-names></name><etal></etal></person-group><article-title>Insights into avian influenza virus pathogenicity: the hemagglutinin precursor HA0 of subtype H16 has an alpha-helix structure in its cleavage site with inefficient HA1/HA2 cleavage</article-title>. <source>J Virol</source> (<year>2012</year>) <volume>86</volume>(<issue>23</issue>):<fpage>12861</fpage>–<lpage>70</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.01606-12</pub-id><pub-id pub-id-type="pmid">22993148</pub-id></mixed-citation></ref><ref id="B31"><label>31</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bottcher</surname><given-names>E</given-names></name><name><surname>Matrosovich</surname><given-names>T</given-names></name><name><surname>Beyerle</surname><given-names>M</given-names></name><name><surname>Klenk</surname><given-names>HD</given-names></name><name><surname>Garten</surname><given-names>W</given-names></name><name><surname>Matrosovich</surname><given-names>M</given-names></name></person-group>. <article-title>Proteolytic activation of influenza viruses by serine proteases TMPRSS2 and HAT from human airway epithelium</article-title>. <source>J Virol</source> (<year>2006</year>) <volume>80</volume>(<issue>19</issue>):<fpage>9896</fpage>–<lpage>8</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.01118-06</pub-id><pub-id pub-id-type="pmid">16973594</pub-id></mixed-citation></ref><ref id="B32"><label>32</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xin</surname><given-names>Y</given-names></name><name><surname>Liu</surname><given-names>L</given-names></name><name><surname>Chen</surname><given-names>B</given-names></name><name><surname>Zhang</surname><given-names>L</given-names></name><name><surname>Tong</surname><given-names>Y</given-names></name></person-group>. <article-title>Affinity purification of aprotinin from bovine lung</article-title>. <source>J Sep Sci</source> (<year>2015</year>) <volume>38</volume>(<issue>9</issue>):<fpage>1441</fpage>–<lpage>8</lpage>.<pub-id pub-id-type="doi">10.1002/jssc.201401188</pub-id><pub-id pub-id-type="pmid">25677462</pub-id></mixed-citation></ref><ref id="B33"><label>33</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Swaminathan</surname><given-names>M</given-names></name><name><surname>Stuart</surname><given-names>M</given-names></name><name><surname>Hughes</surname><given-names>GC</given-names></name><name><surname>Jaggers</surname><given-names>J</given-names></name><name><surname>Hill</surname><given-names>SE</given-names></name><name><surname>Milano</surname><given-names>CA</given-names></name><etal></etal></person-group><article-title>Institutional response to FDA warning on aprotinin and impact on outcomes</article-title>. <source>HSR Proc Intensive Care Cardiovasc Anesth</source> (<year>2009</year>) <volume>1</volume>(<issue>1</issue>):<fpage>30</fpage>–<lpage>6</lpage>.<pub-id pub-id-type="pmid">23439283</pub-id></mixed-citation></ref><ref id="B34"><label>34</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ovcharenko</surname><given-names>AV</given-names></name><name><surname>Zhirnov</surname><given-names>OP</given-names></name></person-group>. <article-title>Aprotinin aerosol treatment of influenza and paramyxovirus bronchopneumonia of mice</article-title>. <source>Antiviral Res</source> (<year>1994</year>) <volume>23</volume>(<issue>2</issue>):<fpage>107</fpage>–<lpage>18</lpage>.<pub-id pub-id-type="doi">10.1016/0166-3542(94)90038-8</pub-id><pub-id pub-id-type="pmid">7511880</pub-id></mixed-citation></ref><ref id="B35"><label>35</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yamaya</surname><given-names>M</given-names></name><name><surname>Shimotai</surname><given-names>Y</given-names></name><name><surname>Hatachi</surname><given-names>Y</given-names></name><name><surname>Lusamba Kalonji</surname><given-names>N</given-names></name><name><surname>Tando</surname><given-names>Y</given-names></name><name><surname>Kitajima</surname><given-names>Y</given-names></name><etal></etal></person-group><article-title>The serine protease inhibitor camostat inhibits influenza virus replication and cytokine production in primary cultures of human tracheal epithelial cells</article-title>. <source>Pulm Pharmacol Ther</source> (<year>2015</year>) <volume>33</volume>:<fpage>66</fpage>–<lpage>74</lpage>.<pub-id pub-id-type="doi">10.1016/j.pupt.2015.07.001</pub-id><pub-id pub-id-type="pmid">26166259</pub-id></mixed-citation></ref><ref id="B36"><label>36</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhirnov</surname><given-names>OP</given-names></name><name><surname>Klenk</surname><given-names>HD</given-names></name><name><surname>Wright</surname><given-names>PF</given-names></name></person-group>. <article-title>Aprotinin and similar protease inhibitors as drugs against influenza</article-title>. <source>Antiviral Res</source> (<year>2011</year>) <volume>92</volume>(<issue>1</issue>):<fpage>27</fpage>–<lpage>36</lpage>.<pub-id pub-id-type="doi">10.1016/j.antiviral.2011.07.014</pub-id><pub-id pub-id-type="pmid">21802447</pub-id></mixed-citation></ref><ref id="B37"><label>37</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lee</surname><given-names>MG</given-names></name><name><surname>Kim</surname><given-names>KH</given-names></name><name><surname>Park</surname><given-names>KY</given-names></name><name><surname>Kim</surname><given-names>JS</given-names></name></person-group>. <article-title>Evaluation of anti-influenza effects of camostat in mice infected with non-adapted human influenza viruses</article-title>. <source>Arch Virol</source> (<year>1996</year>) <volume>141</volume>(<issue>10</issue>):<fpage>1979</fpage>–<lpage>89</lpage>.<pub-id pub-id-type="doi">10.1007/BF01718208</pub-id><pub-id pub-id-type="pmid">8920829</pub-id></mixed-citation></ref><ref id="B38"><label>38</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ota</surname><given-names>S</given-names></name><name><surname>Hara</surname><given-names>Y</given-names></name><name><surname>Kanoh</surname><given-names>S</given-names></name><name><surname>Shinoda</surname><given-names>M</given-names></name><name><surname>Kawano</surname><given-names>S</given-names></name><name><surname>Fujikura</surname><given-names>Y</given-names></name><etal></etal></person-group><article-title>Acute eosinophilic pneumonia caused by camostat mesilate: the first case report</article-title>. <source>Respir Med Case Rep</source> (<year>2016</year>) <volume>19</volume>:<fpage>21</fpage>–<lpage>3</lpage>.<pub-id pub-id-type="doi">10.1016/j.rmcr.2016.06.005</pub-id><pub-id pub-id-type="pmid">27408783</pub-id></mixed-citation></ref><ref id="B39"><label>39</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shen</surname><given-names>LW</given-names></name><name><surname>Mao</surname><given-names>HJ</given-names></name><name><surname>Wu</surname><given-names>YL</given-names></name><name><surname>Tanaka</surname><given-names>Y</given-names></name><name><surname>Zhang</surname><given-names>W</given-names></name></person-group>. <article-title>TMPRSS2: a potential target for treatment of influenza virus and coronavirus infections</article-title>. <source>Biochimie</source> (<year>2017</year>) <volume>142</volume>:<fpage>1</fpage>–<lpage>10</lpage>.<pub-id pub-id-type="doi">10.1016/j.biochi.2017.07.016</pub-id><pub-id pub-id-type="pmid">28778717</pub-id></mixed-citation></ref><ref id="B40"><label>40</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Stieneke-Grober</surname><given-names>A</given-names></name><name><surname>Vey</surname><given-names>M</given-names></name><name><surname>Angliker</surname><given-names>H</given-names></name><name><surname>Shaw</surname><given-names>E</given-names></name><name><surname>Thomas</surname><given-names>G</given-names></name><name><surname>Roberts</surname><given-names>C</given-names></name><etal></etal></person-group><article-title>Influenza virus hemagglutinin with multibasic cleavage site is activated by furin, a subtilisin-like endoprotease</article-title>. <source>EMBO J</source> (<year>1992</year>) <volume>11</volume>(<issue>7</issue>):<fpage>2407</fpage>–<lpage>14</lpage>.<pub-id pub-id-type="pmid">1628614</pub-id></mixed-citation></ref><ref id="B41"><label>41</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bahgat</surname><given-names>MM</given-names></name><name><surname>Blazejewska</surname><given-names>P</given-names></name><name><surname>Schughart</surname><given-names>K</given-names></name></person-group>. <article-title>Inhibition of lung serine proteases in mice: a potentially new approach to control influenza infection</article-title>. <source>Virol J</source> (<year>2011</year>) <volume>8</volume>:<fpage>27</fpage>.<pub-id pub-id-type="doi">10.1186/1743-422X-8-27</pub-id><pub-id pub-id-type="pmid">21251300</pub-id></mixed-citation></ref><ref id="B42"><label>42</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Matlin</surname><given-names>KS</given-names></name><name><surname>Reggio</surname><given-names>H</given-names></name><name><surname>Helenius</surname><given-names>A</given-names></name><name><surname>Simons</surname><given-names>K</given-names></name></person-group>. <article-title>Infectious entry pathway of influenza virus in a canine kidney cell line</article-title>. <source>J Cell Biol</source> (<year>1981</year>) <volume>91</volume>(<issue>3 Pt 1</issue>):<fpage>601</fpage>–<lpage>13</lpage>.<pub-id pub-id-type="doi">10.1083/jcb.91.3.601</pub-id><pub-id pub-id-type="pmid">7328111</pub-id></mixed-citation></ref><ref id="B43"><label>43</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ochiai</surname><given-names>H</given-names></name><name><surname>Sakai</surname><given-names>S</given-names></name><name><surname>Hirabayashi</surname><given-names>T</given-names></name><name><surname>Shimizu</surname><given-names>Y</given-names></name><name><surname>Terasawa</surname><given-names>K</given-names></name></person-group>. <article-title>Inhibitory effect of bafilomycin A1, a specific inhibitor of vacuolar-type proton pump, on the growth of influenza A and B viruses in MDCK cells</article-title>. <source>Antiviral Res</source> (<year>1995</year>) <volume>27</volume>(<issue>4</issue>):<fpage>425</fpage>–<lpage>30</lpage>.<pub-id pub-id-type="doi">10.1016/0166-3542(95)00040-S</pub-id><pub-id pub-id-type="pmid">8540761</pub-id></mixed-citation></ref><ref id="B44"><label>44</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yeganeh</surname><given-names>B</given-names></name><name><surname>Ghavami</surname><given-names>S</given-names></name><name><surname>Kroeker</surname><given-names>AL</given-names></name><name><surname>Mahood</surname><given-names>TH</given-names></name><name><surname>Stelmack</surname><given-names>GL</given-names></name><name><surname>Klonisch</surname><given-names>T</given-names></name><etal></etal></person-group><article-title>Suppression of influenza A virus replication in human lung epithelial cells by noncytotoxic concentrations bafilomycin A1</article-title>. <source>Am J Physiol Lung Cell Mol Physiol</source> (<year>2015</year>) <volume>308</volume>(<issue>3</issue>):<fpage>L270</fpage>–<lpage>86</lpage>.<pub-id pub-id-type="doi">10.1152/ajplung.00011.2014</pub-id><pub-id pub-id-type="pmid">25361566</pub-id></mixed-citation></ref><ref id="B45"><label>45</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sorensen</surname><given-names>MG</given-names></name><name><surname>Henriksen</surname><given-names>K</given-names></name><name><surname>Neutzsky-Wulff</surname><given-names>AV</given-names></name><name><surname>Dziegiel</surname><given-names>MH</given-names></name><name><surname>Karsdal</surname><given-names>MA</given-names></name></person-group>. <article-title>Diphyllin, a novel and naturally potent V-ATPase inhibitor, abrogates acidification of the osteoclastic resorption lacunae and bone resorption</article-title>. <source>J Bone Miner Res</source> (<year>2007</year>) <volume>22</volume>(<issue>10</issue>):<fpage>1640</fpage>–<lpage>8</lpage>.<pub-id pub-id-type="doi">10.1359/jbmr.070613</pub-id><pub-id pub-id-type="pmid">17576165</pub-id></mixed-citation></ref><ref id="B46"><label>46</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chen</surname><given-names>HW</given-names></name><name><surname>Cheng</surname><given-names>JX</given-names></name><name><surname>Liu</surname><given-names>MT</given-names></name><name><surname>King</surname><given-names>K</given-names></name><name><surname>Peng</surname><given-names>JY</given-names></name><name><surname>Zhang</surname><given-names>XQ</given-names></name><etal></etal></person-group><article-title>Inhibitory and combinatorial effect of diphyllin, a v-ATPase blocker, on influenza viruses</article-title>. <source>Antiviral Res</source> (<year>2013</year>) <volume>99</volume>(<issue>3</issue>):<fpage>371</fpage>–<lpage>82</lpage>.<pub-id pub-id-type="doi">10.1016/j.antiviral.2013.06.014</pub-id><pub-id pub-id-type="pmid">23820269</pub-id></mixed-citation></ref><ref id="B47"><label>47</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Diamond</surname><given-names>MS</given-names></name><name><surname>Farzan</surname><given-names>M</given-names></name></person-group>. <article-title>The broad-spectrum antiviral functions of IFIT and IFITM proteins</article-title>. <source>Nat Rev Immunol</source> (<year>2013</year>) <volume>13</volume>(<issue>1</issue>):<fpage>46</fpage>–<lpage>57</lpage>.<pub-id pub-id-type="doi">10.1038/nri3344</pub-id><pub-id pub-id-type="pmid">23237964</pub-id></mixed-citation></ref><ref id="B48"><label>48</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shi</surname><given-names>G</given-names></name><name><surname>Schwartz</surname><given-names>O</given-names></name><name><surname>Compton</surname><given-names>AA</given-names></name></person-group>. <article-title>More than meets the I: the diverse antiviral and cellular functions of interferon-induced transmembrane proteins</article-title>. <source>Retrovirology</source> (<year>2017</year>) <volume>14</volume>(<issue>1</issue>):<fpage>53</fpage>.<pub-id pub-id-type="doi">10.1186/s12977-017-0377-y</pub-id><pub-id pub-id-type="pmid">29162141</pub-id></mixed-citation></ref><ref id="B49"><label>49</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Perreira</surname><given-names>JM</given-names></name><name><surname>Chin</surname><given-names>CR</given-names></name><name><surname>Feeley</surname><given-names>EM</given-names></name><name><surname>Brass</surname><given-names>AL</given-names></name></person-group>. <article-title>IFITMs restrict the replication of multiple pathogenic viruses</article-title>. <source>J Mol Biol</source> (<year>2013</year>) <volume>425</volume>(<issue>24</issue>):<fpage>4937</fpage>–<lpage>55</lpage>.<pub-id pub-id-type="doi">10.1016/j.jmb.2013.09.024</pub-id><pub-id pub-id-type="pmid">24076421</pub-id></mixed-citation></ref><ref id="B50"><label>50</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>K</given-names></name><name><surname>Markosyan</surname><given-names>RM</given-names></name><name><surname>Zheng</surname><given-names>YM</given-names></name><name><surname>Golfetto</surname><given-names>O</given-names></name><name><surname>Bungart</surname><given-names>B</given-names></name><name><surname>Li</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>IFITM proteins restrict viral membrane hemifusion</article-title>. <source>PLoS Pathog</source> (<year>2013</year>) <volume>9</volume>(<issue>1</issue>):<fpage>e1003124</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.1003124</pub-id><pub-id pub-id-type="pmid">23358889</pub-id></mixed-citation></ref><ref id="B51"><label>51</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Amini-Bavil-Olyaee</surname><given-names>S</given-names></name><name><surname>Choi</surname><given-names>YJ</given-names></name><name><surname>Lee</surname><given-names>JH</given-names></name><name><surname>Shi</surname><given-names>M</given-names></name><name><surname>Huang</surname><given-names>IC</given-names></name><name><surname>Farzan</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>The antiviral effector IFITM3 disrupts intracellular cholesterol homeostasis to block viral entry</article-title>. <source>Cell Host Microbe</source> (<year>2013</year>) <volume>13</volume>(<issue>4</issue>):<fpage>452</fpage>–<lpage>64</lpage>.<pub-id pub-id-type="doi">10.1016/j.chom.2013.03.006</pub-id><pub-id pub-id-type="pmid">23601107</pub-id></mixed-citation></ref><ref id="B52"><label>52</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lee</surname><given-names>J</given-names></name><name><surname>Kim</surname><given-names>J</given-names></name><name><surname>Son</surname><given-names>K</given-names></name><name><surname>d’Alexandry d’Orengiani</surname><given-names>AP</given-names></name><name><surname>Min</surname><given-names>JY</given-names></name></person-group>. <article-title>Acid phosphatase 2 (ACP2) is required for membrane fusion during influenza virus entry</article-title>. <source>Sci Rep</source> (<year>2017</year>) <volume>7</volume>:<fpage>43893</fpage>.<pub-id pub-id-type="doi">10.1038/srep43893</pub-id><pub-id pub-id-type="pmid">28272419</pub-id></mixed-citation></ref><ref id="B53"><label>53</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Desai</surname><given-names>TM</given-names></name><name><surname>Marin</surname><given-names>M</given-names></name><name><surname>Chin</surname><given-names>CR</given-names></name><name><surname>Savidis</surname><given-names>G</given-names></name><name><surname>Brass</surname><given-names>AL</given-names></name><name><surname>Melikyan</surname><given-names>GB</given-names></name></person-group>. <article-title>IFITM3 restricts influenza A virus entry by blocking the formation of fusion pores following virus-endosome hemifusion</article-title>. <source>PLoS Pathog</source> (<year>2014</year>) <volume>10</volume>(<issue>4</issue>):<fpage>e1004048</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.1004048</pub-id><pub-id pub-id-type="pmid">24699674</pub-id></mixed-citation></ref><ref id="B54"><label>54</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ma</surname><given-names>H</given-names></name><name><surname>Kien</surname><given-names>F</given-names></name><name><surname>Maniere</surname><given-names>M</given-names></name><name><surname>Zhang</surname><given-names>Y</given-names></name><name><surname>Lagarde</surname><given-names>N</given-names></name><name><surname>Tse</surname><given-names>KS</given-names></name><etal></etal></person-group><article-title>Human annexin A6 interacts with influenza a virus protein M2 and negatively modulates infection</article-title>. <source>J Virol</source> (<year>2012</year>) <volume>86</volume>(<issue>3</issue>):<fpage>1789</fpage>–<lpage>801</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.06003-11</pub-id><pub-id pub-id-type="pmid">22114333</pub-id></mixed-citation></ref><ref id="B55"><label>55</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Musiol</surname><given-names>A</given-names></name><name><surname>Gran</surname><given-names>S</given-names></name><name><surname>Ehrhardt</surname><given-names>C</given-names></name><name><surname>Ludwig</surname><given-names>S</given-names></name><name><surname>Grewal</surname><given-names>T</given-names></name><name><surname>Gerke</surname><given-names>V</given-names></name><etal></etal></person-group><article-title>Annexin A6-balanced late endosomal cholesterol controls influenza A replication and propagation</article-title>. <source>MBio</source> (<year>2013</year>) <volume>4</volume>(<issue>6</issue>):<fpage>e608</fpage>–<lpage>13</lpage>.<pub-id pub-id-type="doi">10.1128/mBio.00608-13</pub-id><pub-id pub-id-type="pmid">24194536</pub-id></mixed-citation></ref><ref id="B56"><label>56</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hu</surname><given-names>Y</given-names></name><name><surname>Jiang</surname><given-names>L</given-names></name><name><surname>Lai</surname><given-names>W</given-names></name><name><surname>Qin</surname><given-names>Y</given-names></name><name><surname>Zhang</surname><given-names>T</given-names></name><name><surname>Wang</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>MicroRNA-33a disturbs influenza A virus replication by targeting ARCN1 and inhibiting viral ribonucleoprotein activity</article-title>. <source>J Gen Virol</source> (<year>2016</year>) <volume>97</volume>(<issue>1</issue>):<fpage>27</fpage>–<lpage>38</lpage>.<pub-id pub-id-type="doi">10.1099/jgv.0.000311</pub-id><pub-id pub-id-type="pmid">26498766</pub-id></mixed-citation></ref><ref id="B57"><label>57</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xu</surname><given-names>X</given-names></name><name><surname>Kedlaya</surname><given-names>R</given-names></name><name><surname>Higuchi</surname><given-names>H</given-names></name><name><surname>Ikeda</surname><given-names>S</given-names></name><name><surname>Justice</surname><given-names>MJ</given-names></name><name><surname>Setaluri</surname><given-names>V</given-names></name><etal></etal></person-group><article-title>Mutation in archain 1, a subunit of COPI coatomer complex, causes diluted coat color and Purkinje cell degeneration</article-title>. <source>PLoS Genet</source> (<year>2010</year>) <volume>6</volume>(<issue>5</issue>):<fpage>e1000956</fpage>.<pub-id pub-id-type="doi">10.1371/journal.pgen.1000956</pub-id><pub-id pub-id-type="pmid">20502676</pub-id></mixed-citation></ref><ref id="B58"><label>58</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sun</surname><given-names>E</given-names></name><name><surname>He</surname><given-names>J</given-names></name><name><surname>Zhuang</surname><given-names>X</given-names></name></person-group>. <article-title>Dissecting the role of COPI complexes in influenza virus infection</article-title>. <source>J Virol</source> (<year>2013</year>) <volume>87</volume>(<issue>5</issue>):<fpage>2673</fpage>–<lpage>85</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.02277-12</pub-id><pub-id pub-id-type="pmid">23255804</pub-id></mixed-citation></ref><ref id="B59"><label>59</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Eisfeld</surname><given-names>AJ</given-names></name><name><surname>Neumann</surname><given-names>G</given-names></name><name><surname>Kawaoka</surname><given-names>Y</given-names></name></person-group>. <article-title>At the centre: influenza A virus ribonucleoproteins</article-title>. <source>Nat Rev Microbiol</source> (<year>2015</year>) <volume>13</volume>(<issue>1</issue>):<fpage>28</fpage>–<lpage>41</lpage>.<pub-id pub-id-type="doi">10.1038/nrmicro3367</pub-id><pub-id pub-id-type="pmid">25417656</pub-id></mixed-citation></ref><ref id="B60"><label>60</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Babcock</surname><given-names>HP</given-names></name><name><surname>Chen</surname><given-names>C</given-names></name><name><surname>Zhuang</surname><given-names>X</given-names></name></person-group>. <article-title>Using single-particle tracking to study nuclear trafficking of viral genes</article-title>. <source>Biophys J</source> (<year>2004</year>) <volume>87</volume>(<issue>4</issue>):<fpage>2749</fpage>–<lpage>58</lpage>.<pub-id pub-id-type="doi">10.1529/biophysj.104.042234</pub-id><pub-id pub-id-type="pmid">15454466</pub-id></mixed-citation></ref><ref id="B61"><label>61</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Resa-Infante</surname><given-names>P</given-names></name><name><surname>Paterson</surname><given-names>D</given-names></name><name><surname>Bonet</surname><given-names>J</given-names></name><name><surname>Otte</surname><given-names>A</given-names></name><name><surname>Oliva</surname><given-names>B</given-names></name><name><surname>Fodor</surname><given-names>E</given-names></name><etal></etal></person-group><article-title>Targeting importin-alpha7 as a therapeutic approach against pandemic influenza viruses</article-title>. <source>J Virol</source> (<year>2015</year>) <volume>89</volume>(<issue>17</issue>):<fpage>9010</fpage>–<lpage>20</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.00583-15</pub-id><pub-id pub-id-type="pmid">26085167</pub-id></mixed-citation></ref><ref id="B62"><label>62</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gabriel</surname><given-names>G</given-names></name><name><surname>Klingel</surname><given-names>K</given-names></name><name><surname>Otte</surname><given-names>A</given-names></name><name><surname>Thiele</surname><given-names>S</given-names></name><name><surname>Hudjetz</surname><given-names>B</given-names></name><name><surname>Arman-Kalcek</surname><given-names>G</given-names></name><etal></etal></person-group><article-title>Differential use of importin-alpha isoforms governs cell tropism and host adaptation of influenza virus</article-title>. <source>Nat Commun</source> (<year>2011</year>) <volume>2</volume>:<fpage>156</fpage><pub-id pub-id-type="doi">10.1038/ncomms1158</pub-id><pub-id pub-id-type="pmid">21245837</pub-id></mixed-citation></ref><ref id="B63"><label>63</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Rosenblatt</surname><given-names>JE</given-names></name></person-group>. <article-title>Antiparasitic agents</article-title>. <source>Mayo Clin Proc</source> (<year>1992</year>) <volume>67</volume>(<issue>3</issue>):<fpage>276</fpage>–<lpage>87</lpage>.<pub-id pub-id-type="doi">10.1016/S0025-6196(12)60105-0</pub-id><pub-id pub-id-type="pmid">1545596</pub-id></mixed-citation></ref><ref id="B64"><label>64</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wagstaff</surname><given-names>KM</given-names></name><name><surname>Sivakumaran</surname><given-names>H</given-names></name><name><surname>Heaton</surname><given-names>SM</given-names></name><name><surname>Harrich</surname><given-names>D</given-names></name><name><surname>Jans</surname><given-names>DA</given-names></name></person-group><article-title>Ivermectin is a specific inhibitor of importin alpha/beta-mediated nuclear import able to inhibit replication of HIV-1 and dengue virus</article-title>. <source>Biochem J</source> (<year>2012</year>) <volume>443</volume>(<issue>3</issue>):<fpage>851</fpage>–<lpage>6</lpage>.<pub-id pub-id-type="doi">10.1042/BJ20120150</pub-id><pub-id pub-id-type="pmid">22417684</pub-id></mixed-citation></ref><ref id="B65"><label>65</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gotz</surname><given-names>V</given-names></name><name><surname>Magar</surname><given-names>L</given-names></name><name><surname>Dornfeld</surname><given-names>D</given-names></name><name><surname>Giese</surname><given-names>S</given-names></name><name><surname>Pohlmann</surname><given-names>A</given-names></name><name><surname>Hoper</surname><given-names>D</given-names></name><etal></etal></person-group><article-title>Influenza A viruses escape from MxA restriction at the expense of efficient nuclear vRNP import</article-title>. <source>Sci Rep</source> (<year>2016</year>) <volume>6</volume>:<fpage>23138</fpage>.<pub-id pub-id-type="doi">10.1038/srep23138</pub-id><pub-id pub-id-type="pmid">26988202</pub-id></mixed-citation></ref><ref id="B66"><label>66</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mor</surname><given-names>A</given-names></name><name><surname>White</surname><given-names>A</given-names></name><name><surname>Zhang</surname><given-names>K</given-names></name><name><surname>Thompson</surname><given-names>M</given-names></name><name><surname>Esparza</surname><given-names>M</given-names></name><name><surname>Munoz-Moreno</surname><given-names>R</given-names></name><etal></etal></person-group><article-title>Influenza virus mRNA trafficking through host nuclear speckles</article-title>. <source>Nat Microbiol</source> (<year>2016</year>) <volume>1</volume>(<issue>7</issue>):<fpage>16069</fpage><pub-id pub-id-type="doi">10.1038/nmicrobiol.2016.69</pub-id><pub-id pub-id-type="pmid">27572970</pub-id></mixed-citation></ref><ref id="B67"><label>67</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dubois</surname><given-names>J</given-names></name><name><surname>Terrier</surname><given-names>O</given-names></name><name><surname>Rosa-Calatrava</surname><given-names>M</given-names></name></person-group>. <article-title>Influenza viruses and mRNA splicing: doing more with less</article-title>. <source>MBio</source> (<year>2014</year>) <volume>5</volume>(<issue>3</issue>):<fpage>e70</fpage>–<lpage>14</lpage>.<pub-id pub-id-type="doi">10.1128/mBio.00070-14</pub-id><pub-id pub-id-type="pmid">24825008</pub-id></mixed-citation></ref><ref id="B68"><label>68</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bullock</surname><given-names>AN</given-names></name><name><surname>Das</surname><given-names>S</given-names></name><name><surname>Debreczeni</surname><given-names>JE</given-names></name><name><surname>Rellos</surname><given-names>P</given-names></name><name><surname>Fedorov</surname><given-names>O</given-names></name><name><surname>Niesen</surname><given-names>FH</given-names></name><etal></etal></person-group><article-title>Kinase domain insertions define distinct roles of CLK kinases in SR protein phosphorylation</article-title>. <source>Structure</source> (<year>2009</year>) <volume>17</volume>(<issue>3</issue>):<fpage>352</fpage>–<lpage>62</lpage>.<pub-id pub-id-type="doi">10.1016/j.str.2008.12.023</pub-id><pub-id pub-id-type="pmid">19278650</pub-id></mixed-citation></ref><ref id="B69"><label>69</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zu</surname><given-names>M</given-names></name><name><surname>Li</surname><given-names>C</given-names></name><name><surname>Fang</surname><given-names>JS</given-names></name><name><surname>Lian</surname><given-names>WW</given-names></name><name><surname>Liu</surname><given-names>AL</given-names></name><name><surname>Zheng</surname><given-names>LS</given-names></name><etal></etal></person-group><article-title>Drug discovery of host CLK1 inhibitors for influenza treatment</article-title>. <source>Molecules</source> (<year>2015</year>) <volume>20</volume>(<issue>11</issue>):<fpage>19735</fpage>–<lpage>47</lpage>.<pub-id pub-id-type="doi">10.3390/molecules201119653</pub-id><pub-id pub-id-type="pmid">26540031</pub-id></mixed-citation></ref><ref id="B70"><label>70</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Amorim</surname><given-names>MJ</given-names></name><name><surname>Read</surname><given-names>EK</given-names></name><name><surname>Dalton</surname><given-names>RM</given-names></name><name><surname>Medcalf</surname><given-names>L</given-names></name><name><surname>Digard</surname><given-names>P</given-names></name></person-group>. <article-title>Nuclear export of influenza A virus mRNAs requires ongoing RNA polymerase II activity</article-title>. <source>Traffic</source> (<year>2007</year>) <volume>8</volume>(<issue>1</issue>):<fpage>1</fpage>–<lpage>11</lpage>.<pub-id pub-id-type="doi">10.1111/j.1600-0854.2006.00507.x</pub-id><pub-id pub-id-type="pmid">17132145</pub-id></mixed-citation></ref><ref id="B71"><label>71</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Utine</surname><given-names>CA</given-names></name><name><surname>Stern</surname><given-names>M</given-names></name><name><surname>Akpek</surname><given-names>EK</given-names></name></person-group>. <article-title>Clinical review: topical ophthalmic use of cyclosporin A</article-title>. <source>Ocul Immunol Inflamm</source> (<year>2010</year>) <volume>18</volume>(<issue>5</issue>):<fpage>352</fpage>–<lpage>61</lpage>.<pub-id pub-id-type="doi">10.3109/09273948.2010.498657</pub-id><pub-id pub-id-type="pmid">20735287</pub-id></mixed-citation></ref><ref id="B72"><label>72</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>X</given-names></name><name><surname>Zhao</surname><given-names>Z</given-names></name><name><surname>Li</surname><given-names>Z</given-names></name><name><surname>Xu</surname><given-names>C</given-names></name><name><surname>Sun</surname><given-names>L</given-names></name><name><surname>Chen</surname><given-names>J</given-names></name><etal></etal></person-group><article-title>Cyclosporin A inhibits the influenza virus replication through cyclophilin A-dependent and -independent pathways</article-title>. <source>PLoS One</source> (<year>2012</year>) <volume>7</volume>(<issue>5</issue>):<fpage>e37277</fpage>.<pub-id pub-id-type="doi">10.1371/journal.pone.0037277</pub-id><pub-id pub-id-type="pmid">22615963</pub-id></mixed-citation></ref><ref id="B73"><label>73</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ma</surname><given-names>C</given-names></name><name><surname>Li</surname><given-names>F</given-names></name><name><surname>Musharrafieh</surname><given-names>RG</given-names></name><name><surname>Wang</surname><given-names>J</given-names></name></person-group><article-title>Discovery of cyclosporine A and its analogs as broad-spectrum anti-influenza drugs with a high in vitro genetic barrier of drug resistance</article-title>. <source>Antiviral Res</source> (<year>2016</year>) <volume>133</volume>:<fpage>62</fpage>–<lpage>72</lpage>.<pub-id pub-id-type="doi">10.1016/j.antiviral.2016.07.019</pub-id><pub-id pub-id-type="pmid">27478032</pub-id></mixed-citation></ref><ref id="B74"><label>74</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Read</surname><given-names>EK</given-names></name><name><surname>Digard</surname><given-names>P</given-names></name></person-group>. <article-title>Individual influenza A virus mRNAs show differential dependence on cellular NXF1/TAP for their nuclear export</article-title>. <source>J Gen Virol</source> (<year>2010</year>) <volume>91</volume>(<issue>Pt 5</issue>):<fpage>1290</fpage>–<lpage>301</lpage>.<pub-id pub-id-type="doi">10.1099/vir.0.018564-0</pub-id><pub-id pub-id-type="pmid">20071484</pub-id></mixed-citation></ref><ref id="B75"><label>75</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Morita</surname><given-names>M</given-names></name><name><surname>Kuba</surname><given-names>K</given-names></name><name><surname>Ichikawa</surname><given-names>A</given-names></name><name><surname>Nakayama</surname><given-names>M</given-names></name><name><surname>Katahira</surname><given-names>J</given-names></name><name><surname>Iwamoto</surname><given-names>R</given-names></name><etal></etal></person-group><article-title>The lipid mediator protectin D1 inhibits influenza virus replication and improves severe influenza</article-title>. <source>Cell</source> (<year>2013</year>) <volume>153</volume>(<issue>1</issue>):<fpage>112</fpage>–<lpage>25</lpage>.<pub-id pub-id-type="doi">10.1016/j.cell.2013.02.027</pub-id><pub-id pub-id-type="pmid">23477864</pub-id></mixed-citation></ref><ref id="B76"><label>76</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cencic</surname><given-names>R</given-names></name><name><surname>Pelletier</surname><given-names>J</given-names></name></person-group>. <article-title>Hippuristanol – a potent steroid inhibitor of eukaryotic initiation factor 4A</article-title>. <source>Translation (Austin)</source> (<year>2016</year>) <volume>4</volume>(<issue>1</issue>):<fpage>e1137381</fpage>.<pub-id pub-id-type="doi">10.1080/21690731.2015.1137381</pub-id><pub-id pub-id-type="pmid">27335721</pub-id></mixed-citation></ref><ref id="B77"><label>77</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sokabe</surname><given-names>M</given-names></name><name><surname>Fraser</surname><given-names>CS</given-names></name></person-group>. <article-title>A helicase-independent activity of eIF4A in promoting mRNA recruitment to the human ribosome</article-title>. <source>Proc Natl Acad Sci U S A</source> (<year>2017</year>) <volume>114</volume>(<issue>24</issue>):<fpage>6304</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.1073/pnas.1620426114</pub-id><pub-id pub-id-type="pmid">28559306</pub-id></mixed-citation></ref><ref id="B78"><label>78</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Muller</surname><given-names>C</given-names></name><name><surname>Schulte</surname><given-names>FW</given-names></name><name><surname>Lange-Grunweller</surname><given-names>K</given-names></name><name><surname>Obermann</surname><given-names>W</given-names></name><name><surname>Madhugiri</surname><given-names>R</given-names></name><name><surname>Pleschka</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>Broad-spectrum antiviral activity of the eIF4A inhibitor silvestrol against corona- and picornaviruses</article-title>. <source>Antiviral Res</source> (<year>2017</year>) <volume>150</volume>:<fpage>123</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.1016/j.antiviral.2017.12.010</pub-id><pub-id pub-id-type="pmid">29258862</pub-id></mixed-citation></ref><ref id="B79"><label>79</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yanguez</surname><given-names>E</given-names></name><name><surname>Castello</surname><given-names>A</given-names></name><name><surname>Welnowska</surname><given-names>E</given-names></name><name><surname>Carrasco</surname><given-names>L</given-names></name><name><surname>Goodfellow</surname><given-names>I</given-names></name><name><surname>Nieto</surname><given-names>A</given-names></name></person-group>. <article-title>Functional impairment of eIF4A and eIF4G factors correlates with inhibition of influenza virus mRNA translation</article-title>. <source>Virology</source> (<year>2011</year>) <volume>413</volume>(<issue>1</issue>):<fpage>93</fpage>–<lpage>102</lpage>.<pub-id pub-id-type="doi">10.1016/j.virol.2011.02.012</pub-id><pub-id pub-id-type="pmid">21377182</pub-id></mixed-citation></ref><ref id="B80"><label>80</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Slaine</surname><given-names>PD</given-names></name><name><surname>Kleer</surname><given-names>M</given-names></name><name><surname>Smith</surname><given-names>NK</given-names></name><name><surname>Khaperskyy</surname><given-names>DA</given-names></name><name><surname>McCormick</surname><given-names>C</given-names></name></person-group>. <article-title>Stress granule-inducing eukaryotic translation initiation factor 4A inhibitors block influenza A virus replication</article-title>. <source>Viruses</source> (<year>2017</year>) <volume>9</volume>(<issue>12</issue>):<fpage>E388</fpage>.<pub-id pub-id-type="doi">10.3390/v9120388</pub-id><pub-id pub-id-type="pmid">29258238</pub-id></mixed-citation></ref><ref id="B81"><label>81</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Malina</surname><given-names>A</given-names></name><name><surname>Mills</surname><given-names>JR</given-names></name><name><surname>Pelletier</surname><given-names>J</given-names></name></person-group>. <article-title>Emerging therapeutics targeting mRNA translation</article-title>. <source>Cold Spring Harb Perspect Biol</source> (<year>2012</year>) <volume>4</volume>(<issue>4</issue>):<fpage>a012377</fpage>.<pub-id pub-id-type="doi">10.1101/cshperspect.a012377</pub-id><pub-id pub-id-type="pmid">22474009</pub-id></mixed-citation></ref><ref id="B82"><label>82</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Rossignol</surname><given-names>JF</given-names></name><name><surname>La Frazia</surname><given-names>S</given-names></name><name><surname>Chiappa</surname><given-names>L</given-names></name><name><surname>Ciucci</surname><given-names>A</given-names></name><name><surname>Santoro</surname><given-names>MG</given-names></name></person-group>. <article-title>Thiazolides, a new class of anti-influenza molecules targeting viral hemagglutinin at the post-translational level</article-title>. <source>J Biol Chem</source> (<year>2009</year>) <volume>284</volume>(<issue>43</issue>):<fpage>29798</fpage>–<lpage>808</lpage>.<pub-id pub-id-type="doi">10.1074/jbc.M109.029470</pub-id><pub-id pub-id-type="pmid">19638339</pub-id></mixed-citation></ref><ref id="B83"><label>83</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Rossignol</surname><given-names>JF</given-names></name></person-group>. <article-title>Nitazoxanide: a first-in-class broad-spectrum antiviral agent</article-title>. <source>Antiviral Res</source> (<year>2014</year>) <volume>110</volume>:<fpage>94</fpage>–<lpage>103</lpage>.<pub-id pub-id-type="doi">10.1016/j.antiviral.2014.07.014</pub-id><pub-id pub-id-type="pmid">25108173</pub-id></mixed-citation></ref><ref id="B84"><label>84</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tilmanis</surname><given-names>D</given-names></name><name><surname>van Baalen</surname><given-names>C</given-names></name><name><surname>Oh</surname><given-names>DY</given-names></name><name><surname>Rossignol</surname><given-names>JF</given-names></name><name><surname>Hurt</surname><given-names>AC</given-names></name></person-group>. <article-title>The susceptibility of circulating human influenza viruses to tizoxanide, the active metabolite of nitazoxanide</article-title>. <source>Antiviral Res</source> (<year>2017</year>) <volume>147</volume>:<fpage>142</fpage>–<lpage>8</lpage>.<pub-id pub-id-type="doi">10.1016/j.antiviral.2017.10.002</pub-id><pub-id pub-id-type="pmid">28986103</pub-id></mixed-citation></ref><ref id="B85"><label>85</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Belardo</surname><given-names>G</given-names></name><name><surname>Cenciarelli</surname><given-names>O</given-names></name><name><surname>La Frazia</surname><given-names>S</given-names></name><name><surname>Rossignol</surname><given-names>JF</given-names></name><name><surname>Santoro</surname><given-names>MG</given-names></name></person-group>. <article-title>Synergistic effect of nitazoxanide with neuraminidase inhibitors against influenza A viruses in vitro</article-title>. <source>Antimicrob Agents Chemother</source> (<year>2015</year>) <volume>59</volume>(<issue>2</issue>):<fpage>1061</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.1128/AAC.03947-14</pub-id><pub-id pub-id-type="pmid">25451059</pub-id></mixed-citation></ref><ref id="B86"><label>86</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lakdawala</surname><given-names>SS</given-names></name><name><surname>Wu</surname><given-names>Y</given-names></name><name><surname>Wawrzusin</surname><given-names>P</given-names></name><name><surname>Kabat</surname><given-names>J</given-names></name><name><surname>Broadbent</surname><given-names>AJ</given-names></name><name><surname>Lamirande</surname><given-names>EW</given-names></name><etal></etal></person-group><article-title>Influenza a virus assembly intermediates fuse in the cytoplasm</article-title>. <source>PLoS Pathog</source> (<year>2014</year>) <volume>10</volume>(<issue>3</issue>):<fpage>e1003971</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.1003971</pub-id><pub-id pub-id-type="pmid">24603687</pub-id></mixed-citation></ref><ref id="B87"><label>87</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Momose</surname><given-names>F</given-names></name><name><surname>Sekimoto</surname><given-names>T</given-names></name><name><surname>Ohkura</surname><given-names>T</given-names></name><name><surname>Jo</surname><given-names>S</given-names></name><name><surname>Kawaguchi</surname><given-names>A</given-names></name><name><surname>Nagata</surname><given-names>K</given-names></name><etal></etal></person-group><article-title>Apical transport of influenza A virus ribonucleoprotein requires Rab11-positive recycling endosome</article-title>. <source>PLoS One</source> (<year>2011</year>) <volume>6</volume>(<issue>6</issue>):<fpage>e21123</fpage>.<pub-id pub-id-type="doi">10.1371/journal.pone.0021123</pub-id><pub-id pub-id-type="pmid">21731653</pub-id></mixed-citation></ref><ref id="B88"><label>88</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kudo</surname><given-names>N</given-names></name><name><surname>Khochbin</surname><given-names>S</given-names></name><name><surname>Nishi</surname><given-names>K</given-names></name><name><surname>Kitano</surname><given-names>K</given-names></name><name><surname>Yanagida</surname><given-names>M</given-names></name><name><surname>Yoshida</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>Molecular cloning and cell cycle-dependent expression of mammalian CRM1, a protein involved in nuclear export of proteins</article-title>. <source>J Biol Chem</source> (<year>1997</year>) <volume>272</volume>(<issue>47</issue>):<fpage>29742</fpage>–<lpage>51</lpage>.<pub-id pub-id-type="doi">10.1074/jbc.272.47.29742</pub-id><pub-id pub-id-type="pmid">9368044</pub-id></mixed-citation></ref><ref id="B89"><label>89</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kohler</surname><given-names>A</given-names></name><name><surname>Hurt</surname><given-names>E</given-names></name></person-group>. <article-title>Exporting RNA from the nucleus to the cytoplasm</article-title>. <source>Nat Rev Mol Cell Biol</source> (<year>2007</year>) <volume>8</volume>(<issue>10</issue>):<fpage>761</fpage>–<lpage>73</lpage>.<pub-id pub-id-type="doi">10.1038/nrm2255</pub-id><pub-id pub-id-type="pmid">17786152</pub-id></mixed-citation></ref><ref id="B90"><label>90</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Fischer</surname><given-names>U</given-names></name><name><surname>Huber</surname><given-names>J</given-names></name><name><surname>Boelens</surname><given-names>WC</given-names></name><name><surname>Mattaj</surname><given-names>IW</given-names></name><name><surname>Luhrmann</surname><given-names>R</given-names></name></person-group>. <article-title>The HIV-1 Rev activation domain is a nuclear export signal that accesses an export pathway used by specific cellular RNAs</article-title>. <source>Cell</source> (<year>1995</year>) <volume>82</volume>(<issue>3</issue>):<fpage>475</fpage>–<lpage>83</lpage>.<pub-id pub-id-type="doi">10.1016/0092-8674(95)90436-0</pub-id><pub-id pub-id-type="pmid">7543368</pub-id></mixed-citation></ref><ref id="B91"><label>91</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Brunotte</surname><given-names>L</given-names></name><name><surname>Flies</surname><given-names>J</given-names></name><name><surname>Bolte</surname><given-names>H</given-names></name><name><surname>Reuther</surname><given-names>P</given-names></name><name><surname>Vreede</surname><given-names>F</given-names></name><name><surname>Schwemmle</surname><given-names>M</given-names></name></person-group>. <article-title>The nuclear export protein of H5N1 influenza A viruses recruits Matrix 1 (M1) protein to the viral ribonucleoprotein to mediate nuclear export</article-title>. <source>J Biol Chem</source> (<year>2014</year>) <volume>289</volume>(<issue>29</issue>):<fpage>20067</fpage>–<lpage>77</lpage>.<pub-id pub-id-type="doi">10.1074/jbc.M114.569178</pub-id><pub-id pub-id-type="pmid">24891509</pub-id></mixed-citation></ref><ref id="B92"><label>92</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Elton</surname><given-names>D</given-names></name><name><surname>Simpson-Holley</surname><given-names>M</given-names></name><name><surname>Archer</surname><given-names>K</given-names></name><name><surname>Medcalf</surname><given-names>L</given-names></name><name><surname>Hallam</surname><given-names>R</given-names></name><name><surname>McCauley</surname><given-names>J</given-names></name><etal></etal></person-group><article-title>Interaction of the influenza virus nucleoprotein with the cellular CRM1-mediated nuclear export pathway</article-title>. <source>J Virol</source> (<year>2001</year>) <volume>75</volume>(<issue>1</issue>):<fpage>408</fpage>–<lpage>19</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.75.1.408-419.2001</pub-id><pub-id pub-id-type="pmid">11119609</pub-id></mixed-citation></ref><ref id="B93"><label>93</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Watanabe</surname><given-names>K</given-names></name><name><surname>Takizawa</surname><given-names>N</given-names></name><name><surname>Katoh</surname><given-names>M</given-names></name><name><surname>Hoshida</surname><given-names>K</given-names></name><name><surname>Kobayashi</surname><given-names>N</given-names></name><name><surname>Nagata</surname><given-names>K</given-names></name></person-group>. <article-title>Inhibition of nuclear export of ribonucleoprotein complexes of influenza virus by leptomycin B</article-title>. <source>Virus Res</source> (<year>2001</year>) <volume>77</volume>(<issue>1</issue>):<fpage>31</fpage>–<lpage>42</lpage>.<pub-id pub-id-type="doi">10.1016/S0168-1702(01)00263-5</pub-id><pub-id pub-id-type="pmid">11451485</pub-id></mixed-citation></ref><ref id="B94"><label>94</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Newlands</surname><given-names>ES</given-names></name><name><surname>Rustin</surname><given-names>GJ</given-names></name><name><surname>Brampton</surname><given-names>MH</given-names></name></person-group>. <article-title>Phase I trial of elactocin</article-title>. <source>Br J Cancer</source> (<year>1996</year>) <volume>74</volume>(<issue>4</issue>):<fpage>648</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.1038/bjc.1996.415</pub-id><pub-id pub-id-type="pmid">8761384</pub-id></mixed-citation></ref><ref id="B95"><label>95</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Perwitasari</surname><given-names>O</given-names></name><name><surname>Johnson</surname><given-names>S</given-names></name><name><surname>Yan</surname><given-names>X</given-names></name><name><surname>Howerth</surname><given-names>E</given-names></name><name><surname>Shacham</surname><given-names>S</given-names></name><name><surname>Landesman</surname><given-names>Y</given-names></name><etal></etal></person-group><article-title>Verdinexor, a novel selective inhibitor of nuclear export, reduces influenza a virus replication in vitro and in vivo</article-title>. <source>J Virol</source> (<year>2014</year>) <volume>88</volume>(<issue>17</issue>):<fpage>10228</fpage>–<lpage>43</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.01774-14</pub-id><pub-id pub-id-type="pmid">24965445</pub-id></mixed-citation></ref><ref id="B96"><label>96</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Perwitasari</surname><given-names>O</given-names></name><name><surname>Johnson</surname><given-names>S</given-names></name><name><surname>Yan</surname><given-names>X</given-names></name><name><surname>Register</surname><given-names>E</given-names></name><name><surname>Crabtree</surname><given-names>J</given-names></name><name><surname>Gabbard</surname><given-names>J</given-names></name><etal></etal></person-group><article-title>Antiviral efficacy of verdinexor in vivo in two animal models of influenza A virus infection</article-title>. <source>PLoS One</source> (<year>2016</year>) <volume>11</volume>(<issue>11</issue>):<fpage>e0167221</fpage>.<pub-id pub-id-type="doi">10.1371/journal.pone.0167221</pub-id><pub-id pub-id-type="pmid">27893810</pub-id></mixed-citation></ref><ref id="B97"><label>97</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Muthuri</surname><given-names>SG</given-names></name><name><surname>Venkatesan</surname><given-names>S</given-names></name><name><surname>Myles</surname><given-names>PR</given-names></name><name><surname>Leonardi-Bee</surname><given-names>J</given-names></name><name><surname>Al Khuwaitir</surname><given-names>TS</given-names></name><name><surname>Al Mamun</surname><given-names>A</given-names></name><etal></etal></person-group><article-title>Effectiveness of neuraminidase inhibitors in reducing mortality in patients admitted to hospital with influenza A H1N1pdm09 virus infection: a meta-analysis of individual participant data</article-title>. <source>Lancet Respir Med</source> (<year>2014</year>) <volume>2</volume>(<issue>5</issue>):<fpage>395</fpage>–<lpage>404</lpage>.<pub-id pub-id-type="doi">10.1016/S2213-2600(14)70041-4</pub-id><pub-id pub-id-type="pmid">24815805</pub-id></mixed-citation></ref><ref id="B98"><label>98</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chutiwitoonchai</surname><given-names>N</given-names></name><name><surname>Mano</surname><given-names>T</given-names></name><name><surname>Kakisaka</surname><given-names>M</given-names></name><name><surname>Sato</surname><given-names>H</given-names></name><name><surname>Kondoh</surname><given-names>Y</given-names></name><name><surname>Osada</surname><given-names>H</given-names></name><etal></etal></person-group><article-title>Inhibition of CRM1-mediated nuclear export of influenza A nucleoprotein and nuclear export protein as a novel target for antiviral drug development</article-title>. <source>Virology</source> (<year>2017</year>) <volume>507</volume>:<fpage>32</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.1016/j.virol.2017.04.001</pub-id><pub-id pub-id-type="pmid">28399435</pub-id></mixed-citation></ref><ref id="B99"><label>99</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>J</given-names></name><name><surname>Chen</surname><given-names>C</given-names></name><name><surname>Wong</surname><given-names>G</given-names></name><name><surname>Dong</surname><given-names>W</given-names></name><name><surname>Zheng</surname><given-names>W</given-names></name><name><surname>Li</surname><given-names>Y</given-names></name><etal></etal></person-group><article-title>Cyclophilin A protects mice against infection by influenza A virus</article-title>. <source>Sci Rep</source> (<year>2016</year>) <volume>6</volume>:<fpage>28978</fpage>.<pub-id pub-id-type="doi">10.1038/srep28978</pub-id><pub-id pub-id-type="pmid">27354005</pub-id></mixed-citation></ref><ref id="B100"><label>100</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>X</given-names></name><name><surname>Sun</surname><given-names>L</given-names></name><name><surname>Yu</surname><given-names>M</given-names></name><name><surname>Wang</surname><given-names>Z</given-names></name><name><surname>Xu</surname><given-names>C</given-names></name><name><surname>Xue</surname><given-names>Q</given-names></name><etal></etal></person-group><article-title>Cyclophilin A interacts with influenza A virus M1 protein and impairs the early stage of the viral replication</article-title>. <source>Cell Microbiol</source> (<year>2009</year>) <volume>11</volume>(<issue>5</issue>):<fpage>730</fpage>–<lpage>41</lpage>.<pub-id pub-id-type="doi">10.1111/j.1462-5822.2009.01286.x</pub-id><pub-id pub-id-type="pmid">19207730</pub-id></mixed-citation></ref><ref id="B101"><label>101</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>X</given-names></name><name><surname>Zhao</surname><given-names>Z</given-names></name><name><surname>Xu</surname><given-names>C</given-names></name><name><surname>Sun</surname><given-names>L</given-names></name><name><surname>Chen</surname><given-names>J</given-names></name><name><surname>Zhang</surname><given-names>L</given-names></name><etal></etal></person-group><article-title>Cyclophilin A restricts influenza A virus replication through degradation of the M1 protein</article-title>. <source>PLoS One</source> (<year>2012</year>) <volume>7</volume>(<issue>2</issue>):<fpage>e31063</fpage>.<pub-id pub-id-type="doi">10.1371/journal.pone.0031063</pub-id><pub-id pub-id-type="pmid">22347431</pub-id></mixed-citation></ref><ref id="B102"><label>102</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Qiao</surname><given-names>Y</given-names></name><name><surname>Yan</surname><given-names>Y</given-names></name><name><surname>Tan</surname><given-names>KS</given-names></name><name><surname>Tan</surname><given-names>SS</given-names></name><name><surname>Seet</surname><given-names>JE</given-names></name><name><surname>Arumugam</surname><given-names>TV</given-names></name><etal></etal></person-group><article-title>CD151, a novel host factor of nuclear export signaling in influenza virus infection</article-title>. <source>J Allergy Clin Immunol</source> (<year>2018</year>) <volume>141</volume>(<issue>5</issue>):<fpage>1799</fpage>–<lpage>817</lpage>.<pub-id pub-id-type="doi">10.1016/j.jaci.2017.11.032</pub-id><pub-id pub-id-type="pmid">29274410</pub-id></mixed-citation></ref><ref id="B103"><label>103</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gavara</surname><given-names>MM</given-names></name><name><surname>Zaveri</surname><given-names>K</given-names></name><name><surname>Badana</surname><given-names>AK</given-names></name><name><surname>Gugalavath</surname><given-names>S</given-names></name><name><surname>Amajala</surname><given-names>KC</given-names></name><name><surname>Patnala</surname><given-names>K</given-names></name><etal></etal></person-group><article-title>A novel small molecule inhibitor of CD151 inhibits proliferation of metastatic triple negative breast cancer cell lines</article-title>. <source>Proc Biochem</source> (<year>2018</year>) <volume>66</volume>:<fpage>254</fpage>–<lpage>62</lpage>.<pub-id pub-id-type="doi">10.1016/j.procbio.2017.12.004</pub-id></mixed-citation></ref><ref id="B104"><label>104</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Haidari</surname><given-names>M</given-names></name><name><surname>Zhang</surname><given-names>W</given-names></name><name><surname>Ganjehei</surname><given-names>L</given-names></name><name><surname>Ali</surname><given-names>M</given-names></name><name><surname>Chen</surname><given-names>Z</given-names></name></person-group><article-title>Inhibition of MLC phosphorylation restricts replication of influenza virus – a mechanism of action for anti-influenza agents</article-title>. <source>PLoS One</source> (<year>2011</year>) <volume>6</volume>(<issue>6</issue>):<fpage>e21444</fpage><pub-id pub-id-type="doi">10.1371/journal.pone.0021444</pub-id><pub-id pub-id-type="pmid">21731751</pub-id></mixed-citation></ref><ref id="B105"><label>105</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pleschka</surname><given-names>S</given-names></name><name><surname>Wolff</surname><given-names>T</given-names></name><name><surname>Ehrhardt</surname><given-names>C</given-names></name><name><surname>Hobom</surname><given-names>G</given-names></name><name><surname>Planz</surname><given-names>O</given-names></name><name><surname>Rapp</surname><given-names>UR</given-names></name><etal></etal></person-group><article-title>Influenza virus propagation is impaired by inhibition of the Raf/MEK/ERK signalling cascade</article-title>. <source>Nat Cell Biol</source> (<year>2001</year>) <volume>3</volume>(<issue>3</issue>):<fpage>301</fpage>–<lpage>5</lpage>.<pub-id pub-id-type="doi">10.1038/35060098</pub-id><pub-id pub-id-type="pmid">11231581</pub-id></mixed-citation></ref><ref id="B106"><label>106</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Droebner</surname><given-names>K</given-names></name><name><surname>Pleschka</surname><given-names>S</given-names></name><name><surname>Ludwig</surname><given-names>S</given-names></name><name><surname>Planz</surname><given-names>O</given-names></name></person-group>. <article-title>Antiviral activity of the MEK-inhibitor U0126 against pandemic H1N1v and highly pathogenic avian influenza virus in vitro and in vivo</article-title>. <source>Antiviral Res</source> (<year>2011</year>) <volume>92</volume>(<issue>2</issue>):<fpage>195</fpage>–<lpage>203</lpage>.<pub-id pub-id-type="doi">10.1016/j.antiviral.2011.08.002</pub-id><pub-id pub-id-type="pmid">21854809</pub-id></mixed-citation></ref><ref id="B107"><label>107</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ludwig</surname><given-names>S</given-names></name><name><surname>Wolff</surname><given-names>T</given-names></name><name><surname>Ehrhardt</surname><given-names>C</given-names></name><name><surname>Wurzer</surname><given-names>WJ</given-names></name><name><surname>Reinhardt</surname><given-names>J</given-names></name><name><surname>Planz</surname><given-names>O</given-names></name><etal></etal></person-group><article-title>MEK inhibition impairs influenza B virus propagation without emergence of resistant variants</article-title>. <source>FEBS Lett</source> (<year>2004</year>) <volume>561</volume>(<issue>1–3</issue>):<fpage>37</fpage>–<lpage>43</lpage>.<pub-id pub-id-type="doi">10.1016/S0014-5793(04)00108-5</pub-id><pub-id pub-id-type="pmid">15013748</pub-id></mixed-citation></ref><ref id="B108"><label>108</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Planz</surname><given-names>O</given-names></name><name><surname>Pleschka</surname><given-names>S</given-names></name><name><surname>Ludwig</surname><given-names>S</given-names></name></person-group>. <article-title>MEK-specific inhibitor U0126 blocks spread of Borna disease virus in cultured cells</article-title>. <source>J Virol</source> (<year>2001</year>) <volume>75</volume>(<issue>10</issue>):<fpage>4871</fpage>–<lpage>7</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.75.10.4871-4877.2001</pub-id><pub-id pub-id-type="pmid">11312358</pub-id></mixed-citation></ref><ref id="B109"><label>109</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Haasbach</surname><given-names>E</given-names></name><name><surname>Muller</surname><given-names>C</given-names></name><name><surname>Ehrhardt</surname><given-names>C</given-names></name><name><surname>Schreiber</surname><given-names>A</given-names></name><name><surname>Pleschka</surname><given-names>S</given-names></name><name><surname>Ludwig</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>The MEK-inhibitor CI-1040 displays a broad anti-influenza virus activity in vitro and provides a prolonged treatment window compared to standard of care in vivo</article-title>. <source>Antiviral Res</source> (<year>2017</year>) <volume>142</volume>:<fpage>178</fpage>–<lpage>84</lpage>.<pub-id pub-id-type="doi">10.1016/j.antiviral.2017.03.024</pub-id><pub-id pub-id-type="pmid">28377100</pub-id></mixed-citation></ref><ref id="B110"><label>110</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tcherniuk</surname><given-names>S</given-names></name><name><surname>Cenac</surname><given-names>N</given-names></name><name><surname>Comte</surname><given-names>M</given-names></name><name><surname>Frouard</surname><given-names>J</given-names></name><name><surname>Errazuriz-Cerda</surname><given-names>E</given-names></name><name><surname>Galabov</surname><given-names>A</given-names></name><etal></etal></person-group><article-title>Formyl peptide receptor 2 plays a deleterious role during influenza A virus infections</article-title>. <source>J Infect Dis</source> (<year>2016</year>) <volume>214</volume>(<issue>2</issue>):<fpage>237</fpage>–<lpage>47</lpage>.<pub-id pub-id-type="doi">10.1093/infdis/jiw127</pub-id><pub-id pub-id-type="pmid">27034344</pub-id></mixed-citation></ref><ref id="B111"><label>111</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Courtin</surname><given-names>N</given-names></name><name><surname>Fotso</surname><given-names>AF</given-names></name><name><surname>Fautrad</surname><given-names>P</given-names></name><name><surname>Mas</surname><given-names>F</given-names></name><name><surname>Alessi</surname><given-names>MC</given-names></name><name><surname>Riteau</surname><given-names>B</given-names></name></person-group>. <article-title>Antiviral activity of formyl peptide receptor 2 antagonists against influenza viruses</article-title>. <source>Antiviral Res</source> (<year>2017</year>) <volume>143</volume>:<fpage>252</fpage>–<lpage>61</lpage>.<pub-id pub-id-type="doi">10.1016/j.antiviral.2017.05.001</pub-id><pub-id pub-id-type="pmid">28483551</pub-id></mixed-citation></ref><ref id="B112"><label>112</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Grant</surname><given-names>BD</given-names></name><name><surname>Donaldson</surname><given-names>JG</given-names></name></person-group>. <article-title>Pathways and mechanisms of endocytic recycling</article-title>. <source>Nat Rev Mol Cell Biol</source> (<year>2009</year>) <volume>10</volume>(<issue>9</issue>):<fpage>597</fpage>–<lpage>608</lpage>.<pub-id pub-id-type="doi">10.1038/nrm2755</pub-id><pub-id pub-id-type="pmid">19696797</pub-id></mixed-citation></ref><ref id="B113"><label>113</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bruce</surname><given-names>EA</given-names></name><name><surname>Stuart</surname><given-names>A</given-names></name><name><surname>McCaffrey</surname><given-names>MW</given-names></name><name><surname>Digard</surname><given-names>P</given-names></name></person-group>. <article-title>Role of the Rab11 pathway in negative-strand virus assembly</article-title>. <source>Biochem Soc Trans</source> (<year>2012</year>) <volume>40</volume>(<issue>6</issue>):<fpage>1409</fpage>–<lpage>15</lpage>.<pub-id pub-id-type="doi">10.1042/BST20120166</pub-id><pub-id pub-id-type="pmid">23176490</pub-id></mixed-citation></ref><ref id="B114"><label>114</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Amorim</surname><given-names>MJ</given-names></name><name><surname>Bruce</surname><given-names>EA</given-names></name><name><surname>Read</surname><given-names>EK</given-names></name><name><surname>Foeglein</surname><given-names>A</given-names></name><name><surname>Mahen</surname><given-names>R</given-names></name><name><surname>Stuart</surname><given-names>AD</given-names></name><etal></etal></person-group><article-title>A Rab11- and microtubule-dependent mechanism for cytoplasmic transport of influenza A virus viral RNA</article-title>. <source>J Virol</source> (<year>2011</year>) <volume>85</volume>(<issue>9</issue>):<fpage>4143</fpage>–<lpage>56</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.02606-10</pub-id><pub-id pub-id-type="pmid">21307188</pub-id></mixed-citation></ref><ref id="B115"><label>115</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Eisfeld</surname><given-names>AJ</given-names></name><name><surname>Kawakami</surname><given-names>E</given-names></name><name><surname>Watanabe</surname><given-names>T</given-names></name><name><surname>Neumann</surname><given-names>G</given-names></name><name><surname>Kawaoka</surname><given-names>Y</given-names></name></person-group>. <article-title>RAB11A is essential for transport of the influenza virus genome to the plasma membrane</article-title>. <source>J Virol</source> (<year>2011</year>) <volume>85</volume>(<issue>13</issue>):<fpage>6117</fpage>–<lpage>26</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.00378-11</pub-id><pub-id pub-id-type="pmid">21525351</pub-id></mixed-citation></ref><ref id="B116"><label>116</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bruce</surname><given-names>EA</given-names></name><name><surname>Digard</surname><given-names>P</given-names></name><name><surname>Stuart</surname><given-names>AD</given-names></name></person-group>. <article-title>The Rab11 pathway is required for influenza A virus budding and filament formation</article-title>. <source>J Virol</source> (<year>2010</year>) <volume>84</volume>(<issue>12</issue>):<fpage>5848</fpage>–<lpage>59</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.00307-10</pub-id><pub-id pub-id-type="pmid">20357086</pub-id></mixed-citation></ref><ref id="B117"><label>117</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ramos-Nascimento</surname><given-names>A</given-names></name><name><surname>Kellen</surname><given-names>B</given-names></name><name><surname>Ferreira</surname><given-names>F</given-names></name><name><surname>Alenquer</surname><given-names>M</given-names></name><name><surname>Vale-Costa</surname><given-names>S</given-names></name><name><surname>Raposo</surname><given-names>G</given-names></name><etal></etal></person-group><article-title>KIF13A mediates trafficking of influenza A virus ribonucleoproteins</article-title>. <source>J Cell Sci</source> (<year>2017</year>) <volume>130</volume>(<issue>23</issue>):<fpage>4038</fpage>–<lpage>50</lpage>.<pub-id pub-id-type="doi">10.1242/jcs.210807</pub-id><pub-id pub-id-type="pmid">29061883</pub-id></mixed-citation></ref><ref id="B118"><label>118</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Portran</surname><given-names>D</given-names></name><name><surname>Schaedel</surname><given-names>L</given-names></name><name><surname>Xu</surname><given-names>Z</given-names></name><name><surname>Thery</surname><given-names>M</given-names></name><name><surname>Nachury</surname><given-names>MV</given-names></name></person-group>. <article-title>Tubulin acetylation protects long-lived microtubules against mechanical ageing</article-title>. <source>Nat Cell Biol</source> (<year>2017</year>) <volume>19</volume>(<issue>4</issue>):<fpage>391</fpage>–<lpage>8</lpage>.<pub-id pub-id-type="doi">10.1038/ncb3481</pub-id><pub-id pub-id-type="pmid">28250419</pub-id></mixed-citation></ref><ref id="B119"><label>119</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hubbert</surname><given-names>C</given-names></name><name><surname>Guardiola</surname><given-names>A</given-names></name><name><surname>Shao</surname><given-names>R</given-names></name><name><surname>Kawaguchi</surname><given-names>Y</given-names></name><name><surname>Ito</surname><given-names>A</given-names></name><name><surname>Nixon</surname><given-names>A</given-names></name><etal></etal></person-group><article-title>HDAC6 is a microtubule-associated deacetylase</article-title>. <source>Nature</source> (<year>2002</year>) <volume>417</volume>(<issue>6887</issue>):<fpage>455</fpage>–<lpage>8</lpage>.<pub-id pub-id-type="doi">10.1038/417455a</pub-id><pub-id pub-id-type="pmid">12024216</pub-id></mixed-citation></ref><ref id="B120"><label>120</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Husain</surname><given-names>M</given-names></name><name><surname>Cheung</surname><given-names>CY</given-names></name></person-group>. <article-title>Histone deacetylase 6 inhibits influenza A virus release by downregulating the trafficking of viral components to the plasma membrane via its substrate, acetylated microtubules</article-title>. <source>J Virol</source> (<year>2014</year>) <volume>88</volume>(<issue>19</issue>):<fpage>11229</fpage>–<lpage>39</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.00727-14</pub-id><pub-id pub-id-type="pmid">25031336</pub-id></mixed-citation></ref><ref id="B121"><label>121</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mori</surname><given-names>K</given-names></name><name><surname>Haruyama</surname><given-names>T</given-names></name><name><surname>Nagata</surname><given-names>K</given-names></name></person-group>. <article-title>Tamiflu-resistant but HA-mediated cell-to-cell transmission through apical membranes of cell-associated influenza viruses</article-title>. <source>PLoS One</source> (<year>2011</year>) <volume>6</volume>(<issue>11</issue>):<fpage>e28178</fpage>.<pub-id pub-id-type="doi">10.1371/journal.pone.0028178</pub-id><pub-id pub-id-type="pmid">22140536</pub-id></mixed-citation></ref><ref id="B122"><label>122</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Roberts</surname><given-names>KL</given-names></name><name><surname>Manicassamy</surname><given-names>B</given-names></name><name><surname>Lamb</surname><given-names>RA</given-names></name></person-group>. <article-title>Influenza A virus uses intercellular connections to spread to neighboring cells</article-title>. <source>J Virol</source> (<year>2015</year>) <volume>89</volume>(<issue>3</issue>):<fpage>1537</fpage>–<lpage>49</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.03306-14</pub-id><pub-id pub-id-type="pmid">25428869</pub-id></mixed-citation></ref><ref id="B123"><label>123</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Rossman</surname><given-names>JS</given-names></name><name><surname>Lamb</surname><given-names>RA</given-names></name></person-group>. <article-title>Influenza virus assembly and budding</article-title>. <source>Virology</source> (<year>2011</year>) <volume>411</volume>(<issue>2</issue>):<fpage>229</fpage>–<lpage>36</lpage>.<pub-id pub-id-type="doi">10.1016/j.virol.2010.12.003</pub-id><pub-id pub-id-type="pmid">21237476</pub-id></mixed-citation></ref><ref id="B124"><label>124</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Martyna</surname><given-names>A</given-names></name><name><surname>Rossman</surname><given-names>J</given-names></name></person-group>. <article-title>Alterations of membrane curvature during influenza virus budding</article-title>. <source>Biochem Soc Trans</source> (<year>2014</year>) <volume>42</volume>(<issue>5</issue>):<fpage>1425</fpage>–<lpage>8</lpage>.<pub-id pub-id-type="doi">10.1042/BST20140136</pub-id><pub-id pub-id-type="pmid">25233426</pub-id></mixed-citation></ref><ref id="B125"><label>125</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Elkins</surname><given-names>MR</given-names></name><name><surname>Williams</surname><given-names>JK</given-names></name><name><surname>Gelenter</surname><given-names>MD</given-names></name><name><surname>Dai</surname><given-names>P</given-names></name><name><surname>Kwon</surname><given-names>B</given-names></name><name><surname>Sergeyev</surname><given-names>IV</given-names></name><etal></etal></person-group><article-title>Cholesterol-binding site of the influenza M2 protein in lipid bilayers from solid-state NMR</article-title>. <source>Proc Natl Acad Sci U S A</source> (<year>2017</year>) <volume>114</volume>(<issue>49</issue>):<fpage>12946</fpage>–<lpage>51</lpage>.<pub-id pub-id-type="doi">10.1073/pnas.1715127114</pub-id><pub-id pub-id-type="pmid">29158386</pub-id></mixed-citation></ref><ref id="B126"><label>126</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bajimaya</surname><given-names>S</given-names></name><name><surname>Frankl</surname><given-names>T</given-names></name><name><surname>Hayashi</surname><given-names>T</given-names></name><name><surname>Takimoto</surname><given-names>T</given-names></name></person-group>. <article-title>Cholesterol is required for stability and infectivity of influenza A and respiratory syncytial viruses</article-title>. <source>Virology</source> (<year>2017</year>) <volume>510</volume>:<fpage>234</fpage>–<lpage>41</lpage>.<pub-id pub-id-type="doi">10.1016/j.virol.2017.07.024</pub-id><pub-id pub-id-type="pmid">28750327</pub-id></mixed-citation></ref><ref id="B127"><label>127</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Matsui</surname><given-names>K</given-names></name><name><surname>Ozawa</surname><given-names>M</given-names></name><name><surname>Kiso</surname><given-names>M</given-names></name><name><surname>Yamashita</surname><given-names>M</given-names></name><name><surname>Maekawa</surname><given-names>T</given-names></name><name><surname>Kubota</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>Stimulation of alpha2-adrenergic receptors impairs influenza virus infection</article-title>. <source>Sci Rep</source> (<year>2018</year>) <volume>8</volume>(<issue>1</issue>):<fpage>4631</fpage>.<pub-id pub-id-type="doi">10.1038/s41598-018-22927-0</pub-id><pub-id pub-id-type="pmid">29545586</pub-id></mixed-citation></ref><ref id="B128"><label>128</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Herold</surname><given-names>S</given-names></name><name><surname>Becker</surname><given-names>C</given-names></name><name><surname>Ridge</surname><given-names>KM</given-names></name><name><surname>Budinger</surname><given-names>GR</given-names></name></person-group>. <article-title>Influenza virus-induced lung injury: pathogenesis and implications for treatment</article-title>. <source>Eur Respir J</source> (<year>2015</year>) <volume>45</volume>(<issue>5</issue>):<fpage>1463</fpage>–<lpage>78</lpage>.<pub-id pub-id-type="doi">10.1183/09031936.00186214</pub-id><pub-id pub-id-type="pmid">25792631</pub-id></mixed-citation></ref><ref id="B129"><label>129</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pulendran</surname><given-names>B</given-names></name><name><surname>Maddur</surname><given-names>MS</given-names></name></person-group>. <article-title>Innate immune sensing and response to influenza</article-title>. <source>Curr Top Microbiol Immunol</source> (<year>2015</year>) <volume>386</volume>:<fpage>23</fpage>–<lpage>71</lpage>.<pub-id pub-id-type="doi">10.1007/82_2014_405</pub-id><pub-id pub-id-type="pmid">25078919</pub-id></mixed-citation></ref><ref id="B130"><label>130</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chen</surname><given-names>X</given-names></name><name><surname>Liu</surname><given-names>S</given-names></name><name><surname>Goraya</surname><given-names>MU</given-names></name><name><surname>Maarouf</surname><given-names>M</given-names></name><name><surname>Huang</surname><given-names>S</given-names></name><name><surname>Chen</surname><given-names>JL</given-names></name></person-group>. <article-title>Host immune response to influenza A virus infection</article-title>. <source>Front Immunol</source> (<year>2018</year>) <volume>9</volume>:<fpage>320</fpage>.<pub-id pub-id-type="doi">10.3389/fimmu.2018.00320</pub-id><pub-id pub-id-type="pmid">29556226</pub-id></mixed-citation></ref><ref id="B131"><label>131</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kruger</surname><given-names>P</given-names></name><name><surname>Saffarzadeh</surname><given-names>M</given-names></name><name><surname>Weber</surname><given-names>AN</given-names></name><name><surname>Rieber</surname><given-names>N</given-names></name><name><surname>Radsak</surname><given-names>M</given-names></name><name><surname>von Bernuth</surname><given-names>H</given-names></name><etal></etal></person-group><article-title>Neutrophils: between host defence, immune modulation, and tissue injury</article-title>. <source>PLoS Pathog</source> (<year>2015</year>) <volume>11</volume>(<issue>3</issue>):<fpage>e1004651</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.1004651</pub-id><pub-id pub-id-type="pmid">25764063</pub-id></mixed-citation></ref><ref id="B132"><label>132</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tate</surname><given-names>MD</given-names></name><name><surname>Brooks</surname><given-names>AG</given-names></name><name><surname>Reading</surname><given-names>PC</given-names></name></person-group>. <article-title>The role of neutrophils in the upper and lower respiratory tract during influenza virus infection of mice</article-title>. <source>Respir Res</source> (<year>2008</year>) <volume>9</volume>:<fpage>57</fpage>.<pub-id pub-id-type="doi">10.1186/1465-9921-9-57</pub-id><pub-id pub-id-type="pmid">18671884</pub-id></mixed-citation></ref><ref id="B133"><label>133</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tate</surname><given-names>MD</given-names></name><name><surname>Ioannidis</surname><given-names>LJ</given-names></name><name><surname>Croker</surname><given-names>B</given-names></name><name><surname>Brown</surname><given-names>LE</given-names></name><name><surname>Brooks</surname><given-names>AG</given-names></name><name><surname>Reading</surname><given-names>PC</given-names></name></person-group>. <article-title>The role of neutrophils during mild and severe influenza virus infections of mice</article-title>. <source>PLoS One</source> (<year>2011</year>) <volume>6</volume>(<issue>3</issue>):<fpage>e17618</fpage>.<pub-id pub-id-type="doi">10.1371/journal.pone.0017618</pub-id><pub-id pub-id-type="pmid">21423798</pub-id></mixed-citation></ref><ref id="B134"><label>134</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lim</surname><given-names>K</given-names></name><name><surname>Hyun</surname><given-names>YM</given-names></name><name><surname>Lambert-Emo</surname><given-names>K</given-names></name><name><surname>Capece</surname><given-names>T</given-names></name><name><surname>Bae</surname><given-names>S</given-names></name><name><surname>Miller</surname><given-names>R</given-names></name><etal></etal></person-group><article-title>Neutrophil trails guide influenza-specific CD8(+) T cells in the airways</article-title>. <source>Science</source> (<year>2015</year>) <volume>349</volume>(<issue>6252</issue>):<fpage>aaa4352</fpage><pub-id pub-id-type="doi">10.1126/science.aaa4352</pub-id><pub-id pub-id-type="pmid">26339033</pub-id></mixed-citation></ref><ref id="B135"><label>135</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>van Riel</surname><given-names>D</given-names></name><name><surname>Leijten</surname><given-names>LM</given-names></name><name><surname>van der Eerden</surname><given-names>M</given-names></name><name><surname>Hoogsteden</surname><given-names>HC</given-names></name><name><surname>Boven</surname><given-names>LA</given-names></name><name><surname>Lambrecht</surname><given-names>BN</given-names></name><etal></etal></person-group><article-title>Highly pathogenic avian influenza virus H5N1 infects alveolar macrophages without virus production or excessive TNF-alpha induction</article-title>. <source>PLoS Pathog</source> (<year>2011</year>) <volume>7</volume>(<issue>6</issue>):<fpage>e1002099</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.1002099</pub-id><pub-id pub-id-type="pmid">21731493</pub-id></mixed-citation></ref><ref id="B136"><label>136</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Seth</surname><given-names>S</given-names></name><name><surname>Oberdorfer</surname><given-names>L</given-names></name><name><surname>Hyde</surname><given-names>R</given-names></name><name><surname>Hoff</surname><given-names>K</given-names></name><name><surname>Thies</surname><given-names>V</given-names></name><name><surname>Worbs</surname><given-names>T</given-names></name><etal></etal></person-group><article-title>CCR7 essentially contributes to the homing of plasmacytoid dendritic cells to lymph nodes under steady-state as well as inflammatory conditions</article-title>. <source>J Immunol</source> (<year>2011</year>) <volume>186</volume>(<issue>6</issue>):<fpage>3364</fpage>–<lpage>72</lpage>.<pub-id pub-id-type="doi">10.4049/jimmunol.1002598</pub-id><pub-id pub-id-type="pmid">21296980</pub-id></mixed-citation></ref><ref id="B137"><label>137</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Qu</surname><given-names>C</given-names></name><name><surname>Nguyen</surname><given-names>VA</given-names></name><name><surname>Merad</surname><given-names>M</given-names></name><name><surname>Randolph</surname><given-names>GJ</given-names></name></person-group>. <article-title>MHC class I/peptide transfer between dendritic cells overcomes poor cross-presentation by monocyte-derived APCs that engulf dying cells</article-title>. <source>J Immunol</source> (<year>2009</year>) <volume>182</volume>(<issue>6</issue>):<fpage>3650</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.4049/jimmunol.0801532</pub-id><pub-id pub-id-type="pmid">19265143</pub-id></mixed-citation></ref><ref id="B138"><label>138</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Allan</surname><given-names>RS</given-names></name><name><surname>Waithman</surname><given-names>J</given-names></name><name><surname>Bedoui</surname><given-names>S</given-names></name><name><surname>Jones</surname><given-names>CM</given-names></name><name><surname>Villadangos</surname><given-names>JA</given-names></name><name><surname>Zhan</surname><given-names>Y</given-names></name><etal></etal></person-group><article-title>Migratory dendritic cells transfer antigen to a lymph node-resident dendritic cell population for efficient CTL priming</article-title>. <source>Immunity</source> (<year>2006</year>) <volume>25</volume>(<issue>1</issue>):<fpage>153</fpage>–<lpage>62</lpage>.<pub-id pub-id-type="doi">10.1016/j.immuni.2006.04.017</pub-id><pub-id pub-id-type="pmid">16860764</pub-id></mixed-citation></ref><ref id="B139"><label>139</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Leon</surname><given-names>B</given-names></name><name><surname>Ardavin</surname><given-names>C</given-names></name></person-group>. <article-title>Monocyte-derived dendritic cells in innate and adaptive immunity</article-title>. <source>Immunol Cell Biol</source> (<year>2008</year>) <volume>86</volume>(<issue>4</issue>):<fpage>320</fpage>–<lpage>4</lpage>.<pub-id pub-id-type="doi">10.1038/icb.2008.14</pub-id><pub-id pub-id-type="pmid">18362945</pub-id></mixed-citation></ref><ref id="B140"><label>140</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Qu</surname><given-names>C</given-names></name><name><surname>Brinck-Jensen</surname><given-names>NS</given-names></name><name><surname>Zang</surname><given-names>M</given-names></name><name><surname>Chen</surname><given-names>K</given-names></name></person-group>. <article-title>Monocyte-derived dendritic cells: targets as potent antigen-presenting cells for the design of vaccines against infectious diseases</article-title>. <source>Int J Infect Dis</source> (<year>2014</year>) <volume>19</volume>:<fpage>1</fpage>–<lpage>5</lpage>.<pub-id pub-id-type="doi">10.1016/j.ijid.2013.09.023</pub-id><pub-id pub-id-type="pmid">24216295</pub-id></mixed-citation></ref><ref id="B141"><label>141</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Swiecki</surname><given-names>M</given-names></name><name><surname>Gilfillan</surname><given-names>S</given-names></name><name><surname>Vermi</surname><given-names>W</given-names></name><name><surname>Wang</surname><given-names>Y</given-names></name><name><surname>Colonna</surname><given-names>M</given-names></name></person-group>. <article-title>Plasmacytoid dendritic cell ablation impacts early interferon responses and antiviral NK and CD8(+) T cell accrual</article-title>. <source>Immunity</source> (<year>2010</year>) <volume>33</volume>(<issue>6</issue>):<fpage>955</fpage>–<lpage>66</lpage>.<pub-id pub-id-type="doi">10.1016/j.immuni.2010.11.020</pub-id><pub-id pub-id-type="pmid">21130004</pub-id></mixed-citation></ref><ref id="B142"><label>142</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hochrein</surname><given-names>H</given-names></name><name><surname>Shortman</surname><given-names>K</given-names></name><name><surname>Vremec</surname><given-names>D</given-names></name><name><surname>Scott</surname><given-names>B</given-names></name><name><surname>Hertzog</surname><given-names>P</given-names></name><name><surname>O’Keeffe</surname><given-names>M</given-names></name></person-group>. <article-title>Differential production of IL-12, IFN-alpha, and IFN-gamma by mouse dendritic cell subsets</article-title>. <source>J Immunol</source> (<year>2001</year>) <volume>166</volume>(<issue>9</issue>):<fpage>5448</fpage>–<lpage>55</lpage>.<pub-id pub-id-type="doi">10.4049/jimmunol.166.9.5448</pub-id><pub-id pub-id-type="pmid">11313382</pub-id></mixed-citation></ref><ref id="B143"><label>143</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pipkin</surname><given-names>ME</given-names></name><name><surname>Sacks</surname><given-names>JA</given-names></name><name><surname>Cruz-Guilloty</surname><given-names>F</given-names></name><name><surname>Lichtenheld</surname><given-names>MG</given-names></name><name><surname>Bevan</surname><given-names>MJ</given-names></name><name><surname>Rao</surname><given-names>A</given-names></name></person-group>. <article-title>Interleukin-2 and inflammation induce distinct transcriptional programs that promote the differentiation of effector cytolytic T cells</article-title>. <source>Immunity</source> (<year>2010</year>) <volume>32</volume>(<issue>1</issue>):<fpage>79</fpage>–<lpage>90</lpage>.<pub-id pub-id-type="doi">10.1016/j.immuni.2009.11.012</pub-id><pub-id pub-id-type="pmid">20096607</pub-id></mixed-citation></ref><ref id="B144"><label>144</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Luckheeram</surname><given-names>RV</given-names></name><name><surname>Zhou</surname><given-names>R</given-names></name><name><surname>Verma</surname><given-names>AD</given-names></name><name><surname>Xia</surname><given-names>B</given-names></name></person-group><article-title>CD4(+)T cells: differentiation and functions</article-title>. <source>Clin Dev Immunol</source> (<year>2012</year>) <volume>2012</volume>:<fpage>925135</fpage><pub-id pub-id-type="doi">10.1155/2012/925135</pub-id><pub-id pub-id-type="pmid">22474485</pub-id></mixed-citation></ref><ref id="B145"><label>145</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Crotty</surname><given-names>S</given-names></name></person-group>. <article-title>T follicular helper cell differentiation, function, and roles in disease</article-title>. <source>Immunity</source> (<year>2014</year>) <volume>41</volume>(<issue>4</issue>):<fpage>529</fpage>–<lpage>42</lpage>.<pub-id pub-id-type="doi">10.1016/j.immuni.2014.10.004</pub-id><pub-id pub-id-type="pmid">25367570</pub-id></mixed-citation></ref><ref id="B146"><label>146</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kurosaki</surname><given-names>T</given-names></name><name><surname>Kometani</surname><given-names>K</given-names></name><name><surname>Ise</surname><given-names>W</given-names></name></person-group>. <article-title>Memory B cells</article-title>. <source>Nat Rev Immunol</source> (<year>2015</year>) <volume>15</volume>(<issue>3</issue>):<fpage>149</fpage>–<lpage>59</lpage>.<pub-id pub-id-type="doi">10.1038/nri3802</pub-id><pub-id pub-id-type="pmid">25677494</pub-id></mixed-citation></ref><ref id="B147"><label>147</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jameson</surname><given-names>SC</given-names></name><name><surname>Masopust</surname><given-names>D</given-names></name></person-group>. <article-title>Understanding subset diversity in T cell memory</article-title>. <source>Immunity</source> (<year>2018</year>) <volume>48</volume>(<issue>2</issue>):<fpage>214</fpage>–<lpage>26</lpage>.<pub-id pub-id-type="doi">10.1016/j.immuni.2018.02.010</pub-id><pub-id pub-id-type="pmid">29466754</pub-id></mixed-citation></ref><ref id="B148"><label>148</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Obar</surname><given-names>JJ</given-names></name><name><surname>Lefrancois</surname><given-names>L</given-names></name></person-group>. <article-title>Memory CD8+ T cell differentiation</article-title>. <source>Ann N Y Acad Sci</source> (<year>2010</year>) <volume>1183</volume>:<fpage>251</fpage>–<lpage>66</lpage>.<pub-id pub-id-type="doi">10.1111/j.1749-6632.2009.05126.x</pub-id><pub-id pub-id-type="pmid">20146720</pub-id></mixed-citation></ref><ref id="B149"><label>149</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>MacLeod</surname><given-names>MK</given-names></name><name><surname>Kappler</surname><given-names>JW</given-names></name><name><surname>Marrack</surname><given-names>P</given-names></name></person-group>. <article-title>Memory CD4 T cells: generation, reactivation and re-assignment</article-title>. <source>Immunology</source> (<year>2010</year>) <volume>130</volume>(<issue>1</issue>):<fpage>10</fpage>–<lpage>5</lpage>.<pub-id pub-id-type="doi">10.1111/j.1365-2567.2010.03260.x</pub-id><pub-id pub-id-type="pmid">20331469</pub-id></mixed-citation></ref><ref id="B150"><label>150</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kong</surname><given-names>KF</given-names></name><name><surname>Delroux</surname><given-names>K</given-names></name><name><surname>Wang</surname><given-names>X</given-names></name><name><surname>Qian</surname><given-names>F</given-names></name><name><surname>Arjona</surname><given-names>A</given-names></name><name><surname>Malawista</surname><given-names>SE</given-names></name><etal></etal></person-group><article-title>Dysregulation of TLR3 impairs the innate immune response to West Nile virus in the elderly</article-title>. <source>J Virol</source> (<year>2008</year>) <volume>82</volume>(<issue>15</issue>):<fpage>7613</fpage>–<lpage>23</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.00618-08</pub-id><pub-id pub-id-type="pmid">18508883</pub-id></mixed-citation></ref><ref id="B151"><label>151</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Openshaw</surname><given-names>PJ</given-names></name><name><surname>Chiu</surname><given-names>C</given-names></name></person-group>. <article-title>Protective and dysregulated T cell immunity in RSV infection</article-title>. <source>Curr Opin Virol</source> (<year>2013</year>) <volume>3</volume>(<issue>4</issue>):<fpage>468</fpage>–<lpage>74</lpage>.<pub-id pub-id-type="doi">10.1016/j.coviro.2013.05.005</pub-id><pub-id pub-id-type="pmid">23806514</pub-id></mixed-citation></ref><ref id="B152"><label>152</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hendrickson</surname><given-names>CM</given-names></name><name><surname>Matthay</surname><given-names>MA</given-names></name></person-group>. <article-title>Viral pathogens and acute lung injury: investigations inspired by the SARS epidemic and the 2009 H1N1 influenza pandemic</article-title>. <source>Semin Respir Crit Care Med</source> (<year>2013</year>) <volume>34</volume>(<issue>4</issue>):<fpage>475</fpage>–<lpage>86</lpage>.<pub-id pub-id-type="doi">10.1055/s-0033-1351122</pub-id><pub-id pub-id-type="pmid">23934716</pub-id></mixed-citation></ref><ref id="B153"><label>153</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cheung</surname><given-names>CY</given-names></name><name><surname>Poon</surname><given-names>LL</given-names></name><name><surname>Lau</surname><given-names>AS</given-names></name><name><surname>Luk</surname><given-names>W</given-names></name><name><surname>Lau</surname><given-names>YL</given-names></name><name><surname>Shortridge</surname><given-names>KF</given-names></name><etal></etal></person-group><article-title>Induction of proinflammatory cytokines in human macrophages by influenza A (H5N1) viruses: a mechanism for the unusual severity of human disease?</article-title><source>Lancet</source> (<year>2002</year>) <volume>360</volume>(<issue>9348</issue>):<fpage>1831</fpage>–<lpage>7</lpage>.<pub-id pub-id-type="doi">10.1016/S0140-6736(02)11772-7</pub-id><pub-id pub-id-type="pmid">12480361</pub-id></mixed-citation></ref><ref id="B154"><label>154</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ye</surname><given-names>S</given-names></name><name><surname>Lowther</surname><given-names>S</given-names></name><name><surname>Stambas</surname><given-names>J</given-names></name></person-group>. <article-title>Inhibition of reactive oxygen species production ameliorates inflammation induced by influenza A viruses via upregulation of SOCS1 and SOCS3</article-title>. <source>J Virol</source> (<year>2015</year>) <volume>89</volume>(<issue>5</issue>):<fpage>2672</fpage>–<lpage>83</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.03529-14</pub-id><pub-id pub-id-type="pmid">25520513</pub-id></mixed-citation></ref><ref id="B155"><label>155</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pauli</surname><given-names>EK</given-names></name><name><surname>Schmolke</surname><given-names>M</given-names></name><name><surname>Wolff</surname><given-names>T</given-names></name><name><surname>Viemann</surname><given-names>D</given-names></name><name><surname>Roth</surname><given-names>J</given-names></name><name><surname>Bode</surname><given-names>JG</given-names></name><etal></etal></person-group><article-title>Influenza A virus inhibits type I IFN signaling via NF-kappaB-dependent induction of SOCS-3 expression</article-title>. <source>PLoS Pathog</source> (<year>2008</year>) <volume>4</volume>(<issue>11</issue>):<fpage>e1000196</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.1000196</pub-id><pub-id pub-id-type="pmid">18989459</pub-id></mixed-citation></ref><ref id="B156"><label>156</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tumpey</surname><given-names>TM</given-names></name><name><surname>Basler</surname><given-names>CF</given-names></name><name><surname>Aguilar</surname><given-names>PV</given-names></name><name><surname>Zeng</surname><given-names>H</given-names></name><name><surname>Solorzano</surname><given-names>A</given-names></name><name><surname>Swayne</surname><given-names>DE</given-names></name><etal></etal></person-group><article-title>Characterization of the reconstructed 1918 Spanish influenza pandemic virus</article-title>. <source>Science</source> (<year>2005</year>) <volume>310</volume>(<issue>5745</issue>):<fpage>77</fpage>–<lpage>80</lpage>.<pub-id pub-id-type="doi">10.1126/science.1119392</pub-id><pub-id pub-id-type="pmid">16210530</pub-id></mixed-citation></ref><ref id="B157"><label>157</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Saffarzadeh</surname><given-names>M</given-names></name><name><surname>Juenemann</surname><given-names>C</given-names></name><name><surname>Queisser</surname><given-names>MA</given-names></name><name><surname>Lochnit</surname><given-names>G</given-names></name><name><surname>Barreto</surname><given-names>G</given-names></name><name><surname>Galuska</surname><given-names>SP</given-names></name><etal></etal></person-group><article-title>Neutrophil extracellular traps directly induce epithelial and endothelial cell death: a predominant role of histones</article-title>. <source>PLoS One</source> (<year>2012</year>) <volume>7</volume>(<issue>2</issue>):<fpage>e32366</fpage>.<pub-id pub-id-type="doi">10.1371/journal.pone.0032366</pub-id><pub-id pub-id-type="pmid">22389696</pub-id></mixed-citation></ref><ref id="B158"><label>158</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tate</surname><given-names>MD</given-names></name><name><surname>Deng</surname><given-names>YM</given-names></name><name><surname>Jones</surname><given-names>JE</given-names></name><name><surname>Anderson</surname><given-names>GP</given-names></name><name><surname>Brooks</surname><given-names>AG</given-names></name><name><surname>Reading</surname><given-names>PC</given-names></name></person-group>. <article-title>Neutrophils ameliorate lung injury and the development of severe disease during influenza infection</article-title>. <source>J Immunol</source> (<year>2009</year>) <volume>183</volume>(<issue>11</issue>):<fpage>7441</fpage>–<lpage>50</lpage>.<pub-id pub-id-type="doi">10.4049/jimmunol.0902497</pub-id><pub-id pub-id-type="pmid">19917678</pub-id></mixed-citation></ref><ref id="B159"><label>159</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Narasaraju</surname><given-names>T</given-names></name><name><surname>Yang</surname><given-names>E</given-names></name><name><surname>Samy</surname><given-names>RP</given-names></name><name><surname>Ng</surname><given-names>HH</given-names></name><name><surname>Poh</surname><given-names>WP</given-names></name><name><surname>Liew</surname><given-names>AA</given-names></name><etal></etal></person-group><article-title>Excessive neutrophils and neutrophil extracellular traps contribute to acute lung injury of influenza pneumonitis</article-title>. <source>Am J Pathol</source> (<year>2011</year>) <volume>179</volume>(<issue>1</issue>):<fpage>199</fpage>–<lpage>210</lpage>.<pub-id pub-id-type="doi">10.1016/j.ajpath.2011.03.013</pub-id><pub-id pub-id-type="pmid">21703402</pub-id></mixed-citation></ref><ref id="B160"><label>160</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hoeksema</surname><given-names>M</given-names></name><name><surname>Tripathi</surname><given-names>S</given-names></name><name><surname>White</surname><given-names>M</given-names></name><name><surname>Qi</surname><given-names>L</given-names></name><name><surname>Taubenberger</surname><given-names>J</given-names></name><name><surname>van Eijk</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>Arginine-rich histones have strong antiviral activity for influenza A viruses</article-title>. <source>Innate Immun</source> (<year>2015</year>) <volume>21</volume>(<issue>7</issue>):<fpage>736</fpage>–<lpage>45</lpage>.<pub-id pub-id-type="doi">10.1177/1753425915593794</pub-id><pub-id pub-id-type="pmid">26138524</pub-id></mixed-citation></ref><ref id="B161"><label>161</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ashar</surname><given-names>HK</given-names></name><name><surname>Mueller</surname><given-names>NC</given-names></name><name><surname>Rudd</surname><given-names>JM</given-names></name><name><surname>Snider</surname><given-names>TA</given-names></name><name><surname>Achanta</surname><given-names>M</given-names></name><name><surname>Prasanthi</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>The role of extracellular histones in influenza virus pathogenesis</article-title>. <source>Am J Pathol</source> (<year>2018</year>) <volume>188</volume>(<issue>1</issue>):<fpage>135</fpage>–<lpage>48</lpage>.<pub-id pub-id-type="doi">10.1016/j.ajpath.2017.09.014</pub-id><pub-id pub-id-type="pmid">29107075</pub-id></mixed-citation></ref><ref id="B162"><label>162</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhu</surname><given-names>L</given-names></name><name><surname>Liu</surname><given-names>L</given-names></name><name><surname>Zhang</surname><given-names>Y</given-names></name><name><surname>Pu</surname><given-names>L</given-names></name><name><surname>Liu</surname><given-names>J</given-names></name><name><surname>Li</surname><given-names>X</given-names></name><etal></etal></person-group><article-title>High level of neutrophil extracellular traps correlates with poor prognosis of severe influenza A infection</article-title>. <source>J Infect Dis</source> (<year>2018</year>) <volume>217</volume>(<issue>3</issue>):<fpage>428</fpage>–<lpage>37</lpage>.<pub-id pub-id-type="doi">10.1093/infdis/jix475</pub-id><pub-id pub-id-type="pmid">29325098</pub-id></mixed-citation></ref><ref id="B163"><label>163</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Martinez</surname><given-names>NE</given-names></name><name><surname>Zimmermann</surname><given-names>TJ</given-names></name><name><surname>Goosmann</surname><given-names>C</given-names></name><name><surname>Alexander</surname><given-names>T</given-names></name><name><surname>Hedberg</surname><given-names>C</given-names></name><name><surname>Ziegler</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>Tetrahydroisoquinolines: new inhibitors of Neutrophil Extracellular Trap (NET) formation</article-title>. <source>Chembiochem</source> (<year>2017</year>) <volume>18</volume>(<issue>10</issue>):<fpage>888</fpage>–<lpage>93</lpage>.<pub-id pub-id-type="doi">10.1002/cbic.201600650</pub-id><pub-id pub-id-type="pmid">28240414</pub-id></mixed-citation></ref><ref id="B164"><label>164</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kusunoki</surname><given-names>Y</given-names></name><name><surname>Nakazawa</surname><given-names>D</given-names></name><name><surname>Shida</surname><given-names>H</given-names></name><name><surname>Hattanda</surname><given-names>F</given-names></name><name><surname>Miyoshi</surname><given-names>A</given-names></name><name><surname>Masuda</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>Peptidylarginine deiminase inhibitor suppresses neutrophil extracellular trap formation and MPO-ANCA production</article-title>. <source>Front Immunol</source> (<year>2016</year>) <volume>7</volume>:<fpage>227</fpage>.<pub-id pub-id-type="doi">10.3389/fimmu.2016.00227</pub-id><pub-id pub-id-type="pmid">27375623</pub-id></mixed-citation></ref><ref id="B165"><label>165</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hemmers</surname><given-names>S</given-names></name><name><surname>Teijaro</surname><given-names>JR</given-names></name><name><surname>Arandjelovic</surname><given-names>S</given-names></name><name><surname>Mowen</surname><given-names>KA</given-names></name></person-group>. <article-title>PAD4-mediated neutrophil extracellular trap formation is not required for immunity against influenza infection</article-title>. <source>PLoS One</source> (<year>2011</year>) <volume>6</volume>(<issue>7</issue>):<fpage>e22043</fpage>.<pub-id pub-id-type="doi">10.1371/journal.pone.0022043</pub-id><pub-id pub-id-type="pmid">21779371</pub-id></mixed-citation></ref><ref id="B166"><label>166</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kim</surname><given-names>HY</given-names></name><name><surname>Umetsu</surname><given-names>DT</given-names></name><name><surname>Dekruyff</surname><given-names>RH</given-names></name></person-group>. <article-title>Innate lymphoid cells in asthma: will they take your breath away?</article-title><source>Eur J Immunol</source> (<year>2016</year>) <volume>46</volume>(<issue>4</issue>):<fpage>795</fpage>–<lpage>806</lpage>.<pub-id pub-id-type="doi">10.1002/eji.201444557</pub-id><pub-id pub-id-type="pmid">26891006</pub-id></mixed-citation></ref><ref id="B167"><label>167</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Monticelli</surname><given-names>LA</given-names></name><name><surname>Sonnenberg</surname><given-names>GF</given-names></name><name><surname>Artis</surname><given-names>D</given-names></name></person-group>. <article-title>Innate lymphoid cells: critical regulators of allergic inflammation and tissue repair in the lung</article-title>. <source>Curr Opin Immunol</source> (<year>2012</year>) <volume>24</volume>(<issue>3</issue>):<fpage>284</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.1016/j.coi.2012.03.012</pub-id><pub-id pub-id-type="pmid">22521139</pub-id></mixed-citation></ref><ref id="B168"><label>168</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Monticelli</surname><given-names>LA</given-names></name><name><surname>Sonnenberg</surname><given-names>GF</given-names></name><name><surname>Abt</surname><given-names>MC</given-names></name><name><surname>Alenghat</surname><given-names>T</given-names></name><name><surname>Ziegler</surname><given-names>CG</given-names></name><name><surname>Doering</surname><given-names>TA</given-names></name><etal></etal></person-group><article-title>Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus</article-title>. <source>Nat Immunol</source> (<year>2011</year>) <volume>12</volume>(<issue>11</issue>):<fpage>1045</fpage>–<lpage>54</lpage>.<pub-id pub-id-type="doi">10.1031/ni.2131</pub-id><pub-id pub-id-type="pmid">21946417</pub-id></mixed-citation></ref><ref id="B169"><label>169</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jiao</surname><given-names>Y</given-names></name><name><surname>Huntington</surname><given-names>ND</given-names></name><name><surname>Belz</surname><given-names>GT</given-names></name><name><surname>Seillet</surname><given-names>C</given-names></name></person-group><article-title>Type 1 innate lymphoid cell biology: lessons learnt from natural killer cells</article-title>. <source>Front Immunol</source> (<year>2016</year>) <volume>7</volume>:<fpage>426</fpage><pub-id pub-id-type="doi">10.3389/fimmu.2016.00426</pub-id><pub-id pub-id-type="pmid">27785129</pub-id></mixed-citation></ref><ref id="B170"><label>170</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Weizman</surname><given-names>OE</given-names></name><name><surname>Adams</surname><given-names>NM</given-names></name><name><surname>Schuster</surname><given-names>IS</given-names></name><name><surname>Krishna</surname><given-names>C</given-names></name><name><surname>Pritykin</surname><given-names>Y</given-names></name><name><surname>Lau</surname><given-names>C</given-names></name><etal></etal></person-group><article-title>ILC1 confer early host protection at initial sites of viral infection</article-title>. <source>Cell</source> (<year>2017</year>) <volume>171</volume>(<issue>4</issue>):<fpage>795</fpage>–<lpage>808.e12</lpage>.<pub-id pub-id-type="doi">10.1016/j.cell.2017.09.052</pub-id><pub-id pub-id-type="pmid">29056343</pub-id></mixed-citation></ref><ref id="B171"><label>171</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Califano</surname><given-names>D</given-names></name><name><surname>Furuya</surname><given-names>Y</given-names></name><name><surname>Roberts</surname><given-names>S</given-names></name><name><surname>Avram</surname><given-names>D</given-names></name><name><surname>McKenzie</surname><given-names>ANJ</given-names></name><name><surname>Metzger</surname><given-names>DW</given-names></name></person-group><article-title>IFN-γ increases susceptibility to influenza A infection through suppression of group II innate lymphoid cells</article-title>. <source>Mucosal Immunol</source> (<year>2017</year>) <volume>11</volume>(<issue>1</issue>):<fpage>209</fpage>–<lpage>19</lpage>.<pub-id pub-id-type="doi">10.1038/mi.2017.41</pub-id><pub-id pub-id-type="pmid">28513592</pub-id></mixed-citation></ref><ref id="B172"><label>172</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cephus</surname><given-names>JY</given-names></name><name><surname>Stier</surname><given-names>MT</given-names></name><name><surname>Fuseini</surname><given-names>H</given-names></name><name><surname>Yung</surname><given-names>JA</given-names></name><name><surname>Toki</surname><given-names>S</given-names></name><name><surname>Bloodworth</surname><given-names>MH</given-names></name><etal></etal></person-group><article-title>Testosterone attenuates Group 2 innate lymphoid cell-mediated airway inflammation</article-title>. <source>Cell Rep</source> (<year>2017</year>) <volume>21</volume>(<issue>9</issue>):<fpage>2487</fpage>–<lpage>99</lpage>.<pub-id pub-id-type="doi">10.1016/j.celrep.2017.10.110</pub-id><pub-id pub-id-type="pmid">29186686</pub-id></mixed-citation></ref><ref id="B173"><label>173</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Doherty</surname><given-names>TA</given-names></name><name><surname>Broide</surname><given-names>DH</given-names></name></person-group><article-title>Pathways to limit group 2 innate lymphoid cell activation</article-title>. <source>J Allergy Clin Immunol</source> (<year>2017</year>) <volume>139</volume>(<issue>5</issue>):<fpage>1465</fpage>–<lpage>7</lpage>.<pub-id pub-id-type="doi">10.1016/j.jaci.2016.12.003</pub-id><pub-id pub-id-type="pmid">28087226</pub-id></mixed-citation></ref><ref id="B174"><label>174</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Vlahos</surname><given-names>R</given-names></name><name><surname>Selemidis</surname><given-names>S</given-names></name></person-group>. <article-title>NADPH oxidases as novel pharmacologic targets against influenza A virus infection</article-title>. <source>Mol Pharmacol</source> (<year>2014</year>) <volume>86</volume>(<issue>6</issue>):<fpage>747</fpage>–<lpage>59</lpage>.<pub-id pub-id-type="doi">10.1124/mol.114.095216</pub-id><pub-id pub-id-type="pmid">25301784</pub-id></mixed-citation></ref><ref id="B175"><label>175</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Strengert</surname><given-names>M</given-names></name><name><surname>Jennings</surname><given-names>R</given-names></name><name><surname>Davanture</surname><given-names>S</given-names></name><name><surname>Hayes</surname><given-names>P</given-names></name><name><surname>Gabriel</surname><given-names>G</given-names></name><name><surname>Knaus</surname><given-names>UG</given-names></name></person-group>. <article-title>Mucosal reactive oxygen species are required for antiviral response: role of Duox in influenza a virus infection</article-title>. <source>Antioxid Redox Signal</source> (<year>2014</year>) <volume>20</volume>(<issue>17</issue>):<fpage>2695</fpage>–<lpage>709</lpage>.<pub-id pub-id-type="doi">10.1089/ars.2013.5353</pub-id><pub-id pub-id-type="pmid">24128054</pub-id></mixed-citation></ref><ref id="B176"><label>176</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kim</surname><given-names>HJ</given-names></name><name><surname>Kim</surname><given-names>CH</given-names></name><name><surname>Ryu</surname><given-names>JH</given-names></name><name><surname>Kim</surname><given-names>MJ</given-names></name><name><surname>Park</surname><given-names>CY</given-names></name><name><surname>Lee</surname><given-names>JM</given-names></name><etal></etal></person-group><article-title>Reactive oxygen species induce antiviral innate immune response through IFN-lambda regulation in human nasal epithelial cells</article-title>. <source>Am J Respir Cell Mol Biol</source> (<year>2013</year>) <volume>49</volume>(<issue>5</issue>):<fpage>855</fpage>–<lpage>65</lpage>.<pub-id pub-id-type="doi">10.1165/rcmb.2013-0003OC</pub-id><pub-id pub-id-type="pmid">23786562</pub-id></mixed-citation></ref><ref id="B177"><label>177</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>To</surname><given-names>EE</given-names></name><name><surname>Vlahos</surname><given-names>R</given-names></name><name><surname>Luong</surname><given-names>R</given-names></name><name><surname>Halls</surname><given-names>ML</given-names></name><name><surname>Reading</surname><given-names>PC</given-names></name><name><surname>King</surname><given-names>PT</given-names></name><etal></etal></person-group><article-title>Endosomal NOX2 oxidase exacerbates virus pathogenicity and is a target for antiviral therapy</article-title>. <source>Nat Commun</source> (<year>2017</year>) <volume>8</volume>(<issue>1</issue>):<fpage>69</fpage>.<pub-id pub-id-type="doi">10.1038/s41467-017-00057-x</pub-id><pub-id pub-id-type="pmid">28701733</pub-id></mixed-citation></ref><ref id="B178"><label>178</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Amatore</surname><given-names>D</given-names></name><name><surname>Sgarbanti</surname><given-names>R</given-names></name><name><surname>Aquilano</surname><given-names>K</given-names></name><name><surname>Baldelli</surname><given-names>S</given-names></name><name><surname>Limongi</surname><given-names>D</given-names></name><name><surname>Civitelli</surname><given-names>L</given-names></name><etal></etal></person-group><article-title>Influenza virus replication in lung epithelial cells depends on redox-sensitive pathways activated by NOX4-derived ROS</article-title>. <source>Cell Microbiol</source> (<year>2015</year>) <volume>17</volume>(<issue>1</issue>):<fpage>131</fpage>–<lpage>45</lpage>.<pub-id pub-id-type="doi">10.1111/cmi.12343</pub-id><pub-id pub-id-type="pmid">25154738</pub-id></mixed-citation></ref><ref id="B179"><label>179</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lejal</surname><given-names>N</given-names></name><name><surname>Truchet</surname><given-names>S</given-names></name><name><surname>Bechor</surname><given-names>E</given-names></name><name><surname>Bouguyon</surname><given-names>E</given-names></name><name><surname>Khedkar</surname><given-names>V</given-names></name><name><surname>Bertho</surname><given-names>N</given-names></name><etal></etal></person-group><article-title>Turning off NADPH oxidase-2 by impeding p67(phox) activation in infected mouse macrophages reduced viral entry and inflammation</article-title>. <source>Biochim Biophys Acta</source> (<year>2018</year>) <volume>1862</volume>(<issue>6</issue>):<fpage>1263</fpage>–<lpage>75</lpage>.<pub-id pub-id-type="doi">10.1016/j.bbagen.2018.03.004</pub-id><pub-id pub-id-type="pmid">29524539</pub-id></mixed-citation></ref><ref id="B180"><label>180</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wind</surname><given-names>S</given-names></name><name><surname>Beuerlein</surname><given-names>K</given-names></name><name><surname>Eucker</surname><given-names>T</given-names></name><name><surname>Muller</surname><given-names>H</given-names></name><name><surname>Scheurer</surname><given-names>P</given-names></name><name><surname>Armitage</surname><given-names>ME</given-names></name><etal></etal></person-group><article-title>Comparative pharmacology of chemically distinct NADPH oxidase inhibitors</article-title>. <source>Br J Pharmacol</source> (<year>2010</year>) <volume>161</volume>(<issue>4</issue>):<fpage>885</fpage>–<lpage>98</lpage>.<pub-id pub-id-type="doi">10.1111/j.1476-5381.2010.00920.x</pub-id><pub-id pub-id-type="pmid">20860666</pub-id></mixed-citation></ref><ref id="B181"><label>181</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Altenhofer</surname><given-names>S</given-names></name><name><surname>Kleikers</surname><given-names>PW</given-names></name><name><surname>Radermacher</surname><given-names>KA</given-names></name><name><surname>Scheurer</surname><given-names>P</given-names></name><name><surname>Rob Hermans</surname><given-names>JJ</given-names></name><name><surname>Schiffers</surname><given-names>P</given-names></name><etal></etal></person-group><article-title>The NOX toolbox: validating the role of NADPH oxidases in physiology and disease</article-title>. <source>Cell Mol Life Sci</source> (<year>2012</year>) <volume>69</volume>(<issue>14</issue>):<fpage>2327</fpage>–<lpage>43</lpage>.<pub-id pub-id-type="doi">10.1007/s00018-012-1010-9</pub-id><pub-id pub-id-type="pmid">22648375</pub-id></mixed-citation></ref><ref id="B182"><label>182</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Heumuller</surname><given-names>S</given-names></name><name><surname>Wind</surname><given-names>S</given-names></name><name><surname>Barbosa-Sicard</surname><given-names>E</given-names></name><name><surname>Schmidt</surname><given-names>HH</given-names></name><name><surname>Busse</surname><given-names>R</given-names></name><name><surname>Schroder</surname><given-names>K</given-names></name><etal></etal></person-group><article-title>Apocynin is not an inhibitor of vascular NADPH oxidases but an antioxidant</article-title>. <source>Hypertension</source> (<year>2008</year>) <volume>51</volume>(<issue>2</issue>):<fpage>211</fpage>–<lpage>7</lpage>.<pub-id pub-id-type="doi">10.1161/HYPERTENSIONAHA.107.100214</pub-id><pub-id pub-id-type="pmid">18086956</pub-id></mixed-citation></ref><ref id="B183"><label>183</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Vlahos</surname><given-names>R</given-names></name><name><surname>Stambas</surname><given-names>J</given-names></name><name><surname>Bozinovski</surname><given-names>S</given-names></name><name><surname>Broughton</surname><given-names>BR</given-names></name><name><surname>Drummond</surname><given-names>GR</given-names></name><name><surname>Selemidis</surname><given-names>S</given-names></name></person-group>. <article-title>Inhibition of Nox2 oxidase activity ameliorates influenza A virus-induced lung inflammation</article-title>. <source>PLoS Pathog</source> (<year>2011</year>) <volume>7</volume>(<issue>2</issue>):<fpage>e1001271</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.1001271</pub-id><pub-id pub-id-type="pmid">21304882</pub-id></mixed-citation></ref><ref id="B184"><label>184</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Oostwoud</surname><given-names>LC</given-names></name><name><surname>Gunasinghe</surname><given-names>P</given-names></name><name><surname>Seow</surname><given-names>HJ</given-names></name><name><surname>Ye</surname><given-names>JM</given-names></name><name><surname>Selemidis</surname><given-names>S</given-names></name><name><surname>Bozinovski</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>Apocynin and ebselen reduce influenza A virus-induced lung inflammation in cigarette smoke-exposed mice</article-title>. <source>Sci Rep</source> (<year>2016</year>) <volume>6</volume>:<fpage>20983</fpage>.<pub-id pub-id-type="doi">10.1038/srep20983</pub-id><pub-id pub-id-type="pmid">26877172</pub-id></mixed-citation></ref><ref id="B185"><label>185</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>Q</given-names></name><name><surname>Zhou</surname><given-names>YH</given-names></name><name><surname>Yang</surname><given-names>ZQ</given-names></name></person-group>. <article-title>The cytokine storm of severe influenza and development of immunomodulatory therapy</article-title>. <source>Cell Mol Immunol</source> (<year>2016</year>) <volume>13</volume>(<issue>1</issue>):<fpage>3</fpage>–<lpage>10</lpage>.<pub-id pub-id-type="doi">10.1038/cmi.2015.74</pub-id><pub-id pub-id-type="pmid">26189369</pub-id></mixed-citation></ref><ref id="B186"><label>186</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Betakova</surname><given-names>T</given-names></name><name><surname>Kostrabova</surname><given-names>A</given-names></name><name><surname>Lachova</surname><given-names>V</given-names></name><name><surname>Turianova</surname><given-names>L</given-names></name></person-group>. <article-title>Cytokines induced during influenza virus infection</article-title>. <source>Curr Pharm Des</source> (<year>2017</year>) <volume>23</volume>(<issue>18</issue>):<fpage>2616</fpage>–<lpage>22</lpage>.<pub-id pub-id-type="doi">10.2174/1381612823666170316123736</pub-id><pub-id pub-id-type="pmid">28302021</pub-id></mixed-citation></ref><ref id="B187"><label>187</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Julkunen</surname><given-names>I</given-names></name><name><surname>Sareneva</surname><given-names>T</given-names></name><name><surname>Pirhonen</surname><given-names>J</given-names></name><name><surname>Ronni</surname><given-names>T</given-names></name><name><surname>Melen</surname><given-names>K</given-names></name><name><surname>Matikainen</surname><given-names>S</given-names></name></person-group>. <article-title>Molecular pathogenesis of influenza A virus infection and virus-induced regulation of cytokine gene expression</article-title>. <source>Cytokine Growth Factor Rev</source> (<year>2001</year>) <volume>12</volume>(<issue>2–3</issue>):<fpage>171</fpage>–<lpage>80</lpage>.<pub-id pub-id-type="doi">10.1016/S1359-6101(00)00026-5</pub-id><pub-id pub-id-type="pmid">11325600</pub-id></mixed-citation></ref><ref id="B188"><label>188</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Iwai</surname><given-names>A</given-names></name><name><surname>Shiozaki</surname><given-names>T</given-names></name><name><surname>Miyazaki</surname><given-names>T</given-names></name></person-group>. <article-title>Relevance of signaling molecules for apoptosis induction on influenza A virus replication</article-title>. <source>Biochem Biophys Res Commun</source> (<year>2013</year>) <volume>441</volume>(<issue>3</issue>):<fpage>531</fpage>–<lpage>7</lpage>.<pub-id pub-id-type="doi">10.1016/j.bbrc.2013.10.100</pub-id><pub-id pub-id-type="pmid">24177013</pub-id></mixed-citation></ref><ref id="B189"><label>189</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhou</surname><given-names>X</given-names></name><name><surname>Jiang</surname><given-names>W</given-names></name><name><surname>Liu</surname><given-names>Z</given-names></name><name><surname>Liu</surname><given-names>S</given-names></name><name><surname>Liang</surname><given-names>X</given-names></name></person-group><article-title>Virus infection and death receptor-mediated apoptosis</article-title>. <source>Viruses</source> (<year>2017</year>) <volume>9</volume>(<issue>11</issue>):<fpage>E316</fpage><pub-id pub-id-type="doi">10.3390/v9110316</pub-id><pub-id pub-id-type="pmid">29077026</pub-id></mixed-citation></ref><ref id="B190"><label>190</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>To</surname><given-names>KK</given-names></name><name><surname>Lau</surname><given-names>CC</given-names></name><name><surname>Woo</surname><given-names>PC</given-names></name><name><surname>Lau</surname><given-names>SK</given-names></name><name><surname>Chan</surname><given-names>JF</given-names></name><name><surname>Chan</surname><given-names>KH</given-names></name><etal></etal></person-group><article-title>Human H7N9 virus induces a more pronounced pro-inflammatory cytokine but an attenuated interferon response in human bronchial epithelial cells when compared with an epidemiologically-linked chicken H7N9 virus</article-title>. <source>Virol J</source> (<year>2016</year>) <volume>13</volume>:<fpage>42</fpage>.<pub-id pub-id-type="doi">10.1186/s12985-016-0498-2</pub-id><pub-id pub-id-type="pmid">26975414</pub-id></mixed-citation></ref><ref id="B191"><label>191</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Quinn</surname><given-names>KM</given-names></name><name><surname>Kan</surname><given-names>WT</given-names></name><name><surname>Watson</surname><given-names>KA</given-names></name><name><surname>Liddicoat</surname><given-names>BJ</given-names></name><name><surname>Swan</surname><given-names>NG</given-names></name><name><surname>McQuilten</surname><given-names>H</given-names></name><etal></etal></person-group><article-title>Extrinsically derived TNF is primarily responsible for limiting antiviral CD8+ T cell response magnitude</article-title>. <source>PLoS One</source> (<year>2017</year>) <volume>12</volume>(<issue>9</issue>):<fpage>e0184732</fpage>.<pub-id pub-id-type="doi">10.1371/journal.pone.0184732</pub-id><pub-id pub-id-type="pmid">28886201</pub-id></mixed-citation></ref><ref id="B192"><label>192</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>DeBerge</surname><given-names>MP</given-names></name><name><surname>Ely</surname><given-names>KH</given-names></name><name><surname>Enelow</surname><given-names>RI</given-names></name></person-group><article-title>Soluble, but not transmembrane, TNF-α is required during influenza infection to limit the magnitude of immune responses and the extent of immunopathology</article-title>. <source>J Immunol</source> (<year>2014</year>) <volume>192</volume>(<issue>12</issue>):<fpage>5839</fpage>–<lpage>51</lpage>.<pub-id pub-id-type="doi">10.4049/jimmunol.1302729</pub-id><pub-id pub-id-type="pmid">24790150</pub-id></mixed-citation></ref><ref id="B193"><label>193</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>van de Sandt</surname><given-names>CE</given-names></name><name><surname>Barcena</surname><given-names>M</given-names></name><name><surname>Koster</surname><given-names>AJ</given-names></name><name><surname>Kasper</surname><given-names>J</given-names></name><name><surname>Kirkpatrick</surname><given-names>CJ</given-names></name><name><surname>Scott</surname><given-names>DP</given-names></name><etal></etal></person-group><article-title>Human CD8(+) T cells damage noninfected epithelial cells during influenza virus infection in vitro</article-title>. <source>Am J Respir Cell Mol Biol</source> (<year>2017</year>) <volume>57</volume>(<issue>5</issue>):<fpage>536</fpage>–<lpage>46</lpage>.<pub-id pub-id-type="doi">10.1165/rcmb.2016-0377OC</pub-id><pub-id pub-id-type="pmid">28613916</pub-id></mixed-citation></ref><ref id="B194"><label>194</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Brincks</surname><given-names>EL</given-names></name><name><surname>Woodland</surname><given-names>DL</given-names></name></person-group>. <article-title>Novel roles for IL-15 in T cell survival</article-title>. <source>F1000 Biol Rep</source> (<year>2010</year>) <volume>2</volume>:<fpage>67</fpage>.<pub-id pub-id-type="doi">10.3410/B2-67</pub-id><pub-id pub-id-type="pmid">21173876</pub-id></mixed-citation></ref><ref id="B195"><label>195</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gagnon</surname><given-names>J</given-names></name><name><surname>Ramanathan</surname><given-names>S</given-names></name><name><surname>Leblanc</surname><given-names>C</given-names></name><name><surname>Cloutier</surname><given-names>A</given-names></name><name><surname>McDonald</surname><given-names>PP</given-names></name><name><surname>Ilangumaran</surname><given-names>S</given-names></name></person-group><article-title>IL-6, in synergy with IL-7 or IL-15, stimulates TCR-independent proliferation and functional differentiation of CD8+ T lymphocytes</article-title>. <source>J Immunol</source> (<year>2008</year>) <volume>180</volume>(<issue>12</issue>):<fpage>7958</fpage>–<lpage>68</lpage>.<pub-id pub-id-type="doi">10.4049/jimmunol.180.12.7958</pub-id><pub-id pub-id-type="pmid">18523259</pub-id></mixed-citation></ref><ref id="B196"><label>196</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Damjanovic</surname><given-names>D</given-names></name><name><surname>Divangahi</surname><given-names>M</given-names></name><name><surname>Kugathasan</surname><given-names>K</given-names></name><name><surname>Small</surname><given-names>CL</given-names></name><name><surname>Zganiacz</surname><given-names>A</given-names></name><name><surname>Brown</surname><given-names>EG</given-names></name><etal></etal></person-group><article-title>Negative regulation of lung inflammation and immunopathology by TNF-alpha during acute influenza infection</article-title>. <source>Am J Pathol</source> (<year>2011</year>) <volume>179</volume>(<issue>6</issue>):<fpage>2963</fpage>–<lpage>76</lpage>.<pub-id pub-id-type="doi">10.1016/j.ajpath.2011.09.003</pub-id><pub-id pub-id-type="pmid">22001698</pub-id></mixed-citation></ref><ref id="B197"><label>197</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>G</given-names></name><name><surname>Hamacher</surname><given-names>J</given-names></name><name><surname>Gorshkov</surname><given-names>B</given-names></name><name><surname>White</surname><given-names>R</given-names></name><name><surname>Sridhar</surname><given-names>S</given-names></name><name><surname>Verin</surname><given-names>A</given-names></name><etal></etal></person-group><article-title>The dual role of TNF in pulmonary edema</article-title>. <source>J Cardiovas Dis Res</source> (<year>2010</year>) <volume>1</volume>(<issue>1</issue>):<fpage>29</fpage>–<lpage>36</lpage>.<pub-id pub-id-type="doi">10.4103/0975-3583.59983</pub-id><pub-id pub-id-type="pmid">21188088</pub-id></mixed-citation></ref><ref id="B198"><label>198</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>DeBerge</surname><given-names>MP</given-names></name><name><surname>Ely</surname><given-names>KH</given-names></name><name><surname>Cheng</surname><given-names>GS</given-names></name><name><surname>Enelow</surname><given-names>RI</given-names></name></person-group>. <article-title>ADAM17-mediated processing of TNF-α expressed by antiviral effector CD8+ T cells is required for severe T-cell-mediated lung injury</article-title>. <source>PLoS One</source> (<year>2013</year>) <volume>8</volume>(<issue>11</issue>):<fpage>e79340</fpage>.<pub-id pub-id-type="doi">10.1371/journal.pone.0079340</pub-id><pub-id pub-id-type="pmid">24223177</pub-id></mixed-citation></ref><ref id="B199"><label>199</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hasegawa</surname><given-names>S</given-names></name><name><surname>Matsushige</surname><given-names>T</given-names></name><name><surname>Inoue</surname><given-names>H</given-names></name><name><surname>Shirabe</surname><given-names>K</given-names></name><name><surname>Fukano</surname><given-names>R</given-names></name><name><surname>Ichiyama</surname><given-names>T</given-names></name></person-group>. <article-title>Serum and cerebrospinal fluid cytokine profile of patients with 2009 pandemic H1N1 influenza virus-associated encephalopathy</article-title>. <source>Cytokine</source> (<year>2011</year>) <volume>54</volume>(<issue>2</issue>):<fpage>167</fpage>–<lpage>72</lpage>.<pub-id pub-id-type="doi">10.1016/j.cyto.2011.01.006</pub-id><pub-id pub-id-type="pmid">21371904</pub-id></mixed-citation></ref><ref id="B200"><label>200</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ichiyama</surname><given-names>T</given-names></name><name><surname>Nishikawa</surname><given-names>M</given-names></name><name><surname>Yoshitomi</surname><given-names>T</given-names></name><name><surname>Hayashi</surname><given-names>T</given-names></name><name><surname>Furukawa</surname><given-names>S</given-names></name></person-group>. <article-title>Tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6 in cerebrospinal fluid from children with prolonged febrile seizures. Comparison with acute encephalitis/encephalopathy</article-title>. <source>Neurology</source> (<year>1998</year>) <volume>50</volume>(<issue>2</issue>):<fpage>407</fpage>–<lpage>11</lpage>.<pub-id pub-id-type="doi">10.1212/WNL.50.2.407</pub-id><pub-id pub-id-type="pmid">9484363</pub-id></mixed-citation></ref><ref id="B201"><label>201</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ito</surname><given-names>Y</given-names></name><name><surname>Ichiyama</surname><given-names>T</given-names></name><name><surname>Kimura</surname><given-names>H</given-names></name><name><surname>Shibata</surname><given-names>M</given-names></name><name><surname>Ishiwada</surname><given-names>N</given-names></name><name><surname>Kuroki</surname><given-names>H</given-names></name><etal></etal></person-group><article-title>Detection of influenza virus RNA by reverse transcription-PCR and proinflammatory cytokines in influenza-virus-associated encephalopathy</article-title>. <source>J Med Virol</source> (<year>1999</year>) <volume>58</volume>(<issue>4</issue>):<fpage>420</fpage>–<lpage>5</lpage>.<pub-id pub-id-type="doi">10.1002/(SICI)1096-9071(199908)58:4<420::AID-JMV16>3.0.CO;2-T</pub-id><pub-id pub-id-type="pmid">10421411</pub-id></mixed-citation></ref><ref id="B202"><label>202</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lv</surname><given-names>S</given-names></name><name><surname>Song</surname><given-names>HL</given-names></name><name><surname>Zhou</surname><given-names>Y</given-names></name><name><surname>Li</surname><given-names>LX</given-names></name><name><surname>Cui</surname><given-names>W</given-names></name><name><surname>Wang</surname><given-names>W</given-names></name><etal></etal></person-group><article-title>Tumour necrosis factor-alpha affects blood-brain barrier permeability and tight junction-associated occludin in acute liver failure</article-title>. <source>Liver Int</source> (<year>2010</year>) <volume>30</volume>(<issue>8</issue>):<fpage>1198</fpage>–<lpage>210</lpage>.<pub-id pub-id-type="doi">10.1111/j.1478-3231.2010.02211.x</pub-id><pub-id pub-id-type="pmid">20492508</pub-id></mixed-citation></ref><ref id="B203"><label>203</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tsuge</surname><given-names>M</given-names></name><name><surname>Yasui</surname><given-names>K</given-names></name><name><surname>Ichiyawa</surname><given-names>T</given-names></name><name><surname>Saito</surname><given-names>Y</given-names></name><name><surname>Nagaoka</surname><given-names>Y</given-names></name><name><surname>Yashiro</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>Increase of tumor necrosis factor-alpha in the blood induces early activation of matrix metalloproteinase-9 in the brain</article-title>. <source>Microbiol Immunol</source> (<year>2010</year>) <volume>54</volume>(<issue>7</issue>):<fpage>417</fpage>–<lpage>24</lpage>.<pub-id pub-id-type="doi">10.1111/j.1348-0421.2010.00226.x</pub-id><pub-id pub-id-type="pmid">20618688</pub-id></mixed-citation></ref><ref id="B204"><label>204</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kuperberg</surname><given-names>SJ</given-names></name><name><surname>Wadgaonkar</surname><given-names>R</given-names></name></person-group>. <article-title>Sepsis-associated encephalopathy: the blood-brain barrier and the sphingolipid rheostat</article-title>. <source>Front Immunol</source> (<year>2017</year>) <volume>8</volume>:<fpage>597</fpage>.<pub-id pub-id-type="doi">10.3389/fimmu.2017.00597</pub-id><pub-id pub-id-type="pmid">28670310</pub-id></mixed-citation></ref><ref id="B205"><label>205</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shi</surname><given-names>X</given-names></name><name><surname>Zhou</surname><given-names>W</given-names></name><name><surname>Huang</surname><given-names>H</given-names></name><name><surname>Zhu</surname><given-names>H</given-names></name><name><surname>Zhou</surname><given-names>P</given-names></name><name><surname>Zhu</surname><given-names>H</given-names></name><etal></etal></person-group><article-title>Inhibition of the inflammatory cytokine tumor necrosis factor-alpha with etanercept provides protection against lethal H1N1 influenza infection in mice</article-title>. <source>Crit Care</source> (<year>2013</year>) <volume>17</volume>(<issue>6</issue>):<fpage>R301</fpage>.<pub-id pub-id-type="doi">10.1186/cc13171</pub-id><pub-id pub-id-type="pmid">24373231</pub-id></mixed-citation></ref><ref id="B206"><label>206</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dienz</surname><given-names>O</given-names></name><name><surname>Rud</surname><given-names>JG</given-names></name><name><surname>Eaton</surname><given-names>SM</given-names></name><name><surname>Lanthier</surname><given-names>PA</given-names></name><name><surname>Burg</surname><given-names>E</given-names></name><name><surname>Drew</surname><given-names>A</given-names></name><etal></etal></person-group><article-title>Essential role of IL-6 in protection against H1N1 influenza virus by promoting neutrophil survival in the lung</article-title>. <source>Mucosal Immunol</source> (<year>2012</year>) <volume>5</volume>(<issue>3</issue>):<fpage>258</fpage>–<lpage>66</lpage>.<pub-id pub-id-type="doi">10.1038/mi.2012.2</pub-id><pub-id pub-id-type="pmid">22294047</pub-id></mixed-citation></ref><ref id="B207"><label>207</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>ML</given-names></name><name><surname>Wang</surname><given-names>CT</given-names></name><name><surname>Yang</surname><given-names>SJ</given-names></name><name><surname>Leu</surname><given-names>CH</given-names></name><name><surname>Chen</surname><given-names>SH</given-names></name><name><surname>Wu</surname><given-names>CL</given-names></name><etal></etal></person-group><article-title>IL-6 ameliorates acute lung injury in influenza virus infection</article-title>. <source>Sci Rep</source> (<year>2017</year>) <volume>7</volume>:<fpage>43829</fpage>.<pub-id pub-id-type="doi">10.1038/srep43829</pub-id><pub-id pub-id-type="pmid">28262742</pub-id></mixed-citation></ref><ref id="B208"><label>208</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pyle</surname><given-names>CJ</given-names></name><name><surname>Uwadiae</surname><given-names>FI</given-names></name><name><surname>Swieboda</surname><given-names>DP</given-names></name><name><surname>Harker</surname><given-names>JA</given-names></name></person-group>. <article-title>Early IL-6 signalling promotes IL-27 dependent maturation of regulatory T cells in the lungs and resolution of viral immunopathology</article-title>. <source>PLoS Pathog</source> (<year>2017</year>) <volume>13</volume>(<issue>9</issue>):<fpage>e1006640</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.1006640</pub-id><pub-id pub-id-type="pmid">28953978</pub-id></mixed-citation></ref><ref id="B209"><label>209</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Aiba</surname><given-names>H</given-names></name><name><surname>Mochizuki</surname><given-names>M</given-names></name><name><surname>Kimura</surname><given-names>M</given-names></name><name><surname>Hojo</surname><given-names>H</given-names></name></person-group>. <article-title>Predictive value of serum interleukin-6 level in influenza virus-associated encephalopathy</article-title>. <source>Neurology</source> (<year>2001</year>) <volume>57</volume>(<issue>2</issue>):<fpage>295</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.1212/WNL.57.2.295</pub-id><pub-id pub-id-type="pmid">11468315</pub-id></mixed-citation></ref><ref id="B210"><label>210</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Fukumoto</surname><given-names>Y</given-names></name><name><surname>Okumura</surname><given-names>A</given-names></name><name><surname>Hayakawa</surname><given-names>F</given-names></name><name><surname>Suzuki</surname><given-names>M</given-names></name><name><surname>Kato</surname><given-names>T</given-names></name><name><surname>Watanabe</surname><given-names>K</given-names></name><etal></etal></person-group><article-title>Serum levels of cytokines and EEG findings in children with influenza associated with mild neurological complications</article-title>. <source>Brain Dev</source> (<year>2007</year>) <volume>29</volume>(<issue>7</issue>):<fpage>425</fpage>–<lpage>30</lpage>.<pub-id pub-id-type="doi">10.1016/j.braindev.2006.12.005</pub-id><pub-id pub-id-type="pmid">17287101</pub-id></mixed-citation></ref><ref id="B211"><label>211</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cohen</surname><given-names>SS</given-names></name><name><surname>Min</surname><given-names>M</given-names></name><name><surname>Cummings</surname><given-names>EE</given-names></name><name><surname>Chen</surname><given-names>X</given-names></name><name><surname>Sadowska</surname><given-names>GB</given-names></name><name><surname>Sharma</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>Effects of interleukin-6 on the expression of tight junction proteins in isolated cerebral microvessels from yearling and adult sheep</article-title>. <source>Neuroimmunomodulation</source> (<year>2013</year>) <volume>20</volume>(<issue>5</issue>):<fpage>264</fpage>–<lpage>73</lpage>.<pub-id pub-id-type="doi">10.1159/000350470</pub-id><pub-id pub-id-type="pmid">23867217</pub-id></mixed-citation></ref><ref id="B212"><label>212</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Song</surname><given-names>M</given-names></name><name><surname>Winchester</surname><given-names>J</given-names></name><name><surname>Albright</surname><given-names>RL</given-names></name><name><surname>Capponi</surname><given-names>VJ</given-names></name><name><surname>Choquette</surname><given-names>MD</given-names></name><name><surname>Kellum</surname><given-names>JA</given-names></name></person-group>. <article-title>Cytokine removal with a novel adsorbent polymer</article-title>. <source>Blood Purif</source> (<year>2004</year>) <volume>22</volume>(<issue>5</issue>):<fpage>428</fpage>–<lpage>34</lpage>.<pub-id pub-id-type="doi">10.1159/000080235</pub-id><pub-id pub-id-type="pmid">15316198</pub-id></mixed-citation></ref><ref id="B213"><label>213</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lees</surname><given-names>NJ</given-names></name><name><surname>Rosenberg</surname><given-names>A</given-names></name><name><surname>Hurtado-Doce</surname><given-names>AI</given-names></name><name><surname>Jones</surname><given-names>J</given-names></name><name><surname>Marczin</surname><given-names>N</given-names></name><name><surname>Zeriouh</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>Combination of ECMO and cytokine adsorption therapy for severe sepsis with cardiogenic shock and ARDS due to Panton-Valentine leukocidin-positive <italic>Staphylococcus aureus</italic> pneumonia and H1N1</article-title>. <source>J Artif Organs</source> (<year>2016</year>) <volume>19</volume>(<issue>4</issue>):<fpage>399</fpage>–<lpage>402</lpage>.<pub-id pub-id-type="doi">10.1007/s10047-016-0915-8</pub-id><pub-id pub-id-type="pmid">27436098</pub-id></mixed-citation></ref><ref id="B214"><label>214</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>FD</given-names></name><name><surname>Kenngott</surname><given-names>EE</given-names></name><name><surname>Schroter</surname><given-names>MF</given-names></name><name><surname>Kuhl</surname><given-names>A</given-names></name><name><surname>Jennrich</surname><given-names>S</given-names></name><name><surname>Watzlawick</surname><given-names>R</given-names></name><etal></etal></person-group><article-title>Timed action of IL-27 protects from immunopathology while preserving defense in influenza</article-title>. <source>PLoS Pathog</source> (<year>2014</year>) <volume>10</volume>(<issue>5</issue>):<fpage>e1004110</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.1004110</pub-id><pub-id pub-id-type="pmid">24809349</pub-id></mixed-citation></ref><ref id="B215"><label>215</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Robinson</surname><given-names>KM</given-names></name><name><surname>Lee</surname><given-names>B</given-names></name><name><surname>Scheller</surname><given-names>EV</given-names></name><name><surname>Mandalapu</surname><given-names>S</given-names></name><name><surname>Enelow</surname><given-names>RI</given-names></name><name><surname>Kolls</surname><given-names>JK</given-names></name><etal></etal></person-group><article-title>The role of IL-27 in susceptibility to post-influenza <italic>Staphylococcus aureus</italic> pneumonia</article-title>. <source>Respir Res</source> (<year>2015</year>) <volume>16</volume>:<fpage>10</fpage>.<pub-id pub-id-type="doi">10.1186/s12931-015-0168-8</pub-id><pub-id pub-id-type="pmid">25651926</pub-id></mixed-citation></ref><ref id="B216"><label>216</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Krug</surname><given-names>RM</given-names></name></person-group>. <article-title>Functions of the influenza A virus NS1 protein in antiviral defense</article-title>. <source>Curr Opin Virol</source> (<year>2015</year>) <volume>12</volume>:<fpage>1</fpage>–<lpage>6</lpage>.<pub-id pub-id-type="doi">10.1016/j.coviro.2015.01.007</pub-id><pub-id pub-id-type="pmid">25638592</pub-id></mixed-citation></ref><ref id="B217"><label>217</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jureka</surname><given-names>AS</given-names></name><name><surname>Kleinpeter</surname><given-names>AB</given-names></name><name><surname>Cornilescu</surname><given-names>G</given-names></name><name><surname>Cornilescu</surname><given-names>CC</given-names></name><name><surname>Petit</surname><given-names>CM</given-names></name></person-group>. <article-title>Structural basis for a novel interaction between the NS1 protein derived from the 1918 influenza virus and RIG-I</article-title>. <source>Structure</source> (<year>2015</year>) <volume>23</volume>(<issue>11</issue>):<fpage>2001</fpage>–<lpage>10</lpage>.<pub-id pub-id-type="doi">10.1016/j.str.2015.08.007</pub-id><pub-id pub-id-type="pmid">26365801</pub-id></mixed-citation></ref><ref id="B218"><label>218</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ciancanelli</surname><given-names>MJ</given-names></name><name><surname>Huang</surname><given-names>SX</given-names></name><name><surname>Luthra</surname><given-names>P</given-names></name><name><surname>Garner</surname><given-names>H</given-names></name><name><surname>Itan</surname><given-names>Y</given-names></name><name><surname>Volpi</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>Infectious disease. Life-threatening influenza and impaired interferon amplification in human IRF7 deficiency</article-title>. <source>Science</source> (<year>2015</year>) <volume>348</volume>(<issue>6233</issue>):<fpage>448</fpage>–<lpage>53</lpage>.<pub-id pub-id-type="doi">10.1126/science.aaa1578</pub-id><pub-id pub-id-type="pmid">25814066</pub-id></mixed-citation></ref><ref id="B219"><label>219</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Davidson</surname><given-names>S</given-names></name><name><surname>Maini</surname><given-names>MK</given-names></name><name><surname>Wack</surname><given-names>A</given-names></name></person-group>. <article-title>Disease-promoting effects of type I interferons in viral, bacterial, and coinfections</article-title>. <source>J Interferon Cytokine Res</source> (<year>2015</year>) <volume>35</volume>(<issue>4</issue>):<fpage>252</fpage>–<lpage>64</lpage>.<pub-id pub-id-type="doi">10.1089/jir.2014.0227</pub-id><pub-id pub-id-type="pmid">25714109</pub-id></mixed-citation></ref><ref id="B220"><label>220</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Beilharz</surname><given-names>MW</given-names></name><name><surname>Cummins</surname><given-names>JM</given-names></name><name><surname>Bennett</surname><given-names>AL</given-names></name></person-group>. <article-title>Protection from lethal influenza virus challenge by oral type 1 interferon</article-title>. <source>Biochem Biophys Res Commun</source> (<year>2007</year>) <volume>355</volume>(<issue>3</issue>):<fpage>740</fpage>–<lpage>4</lpage>.<pub-id pub-id-type="doi">10.1016/j.bbrc.2007.02.019</pub-id><pub-id pub-id-type="pmid">17316562</pub-id></mixed-citation></ref><ref id="B221"><label>221</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bennett</surname><given-names>AL</given-names></name><name><surname>Smith</surname><given-names>DW</given-names></name><name><surname>Cummins</surname><given-names>MJ</given-names></name><name><surname>Jacoby</surname><given-names>PA</given-names></name><name><surname>Cummins</surname><given-names>JM</given-names></name><name><surname>Beilharz</surname><given-names>MW</given-names></name></person-group>. <article-title>Low-dose oral interferon alpha as prophylaxis against viral respiratory illness: a double-blind, parallel controlled trial during an influenza pandemic year</article-title>. <source>Influenza Other Respi Viruses</source> (<year>2013</year>) <volume>7</volume>(<issue>5</issue>):<fpage>854</fpage>–<lpage>62</lpage>.<pub-id pub-id-type="doi">10.1111/irv.12094</pub-id><pub-id pub-id-type="pmid">23398960</pub-id></mixed-citation></ref><ref id="B222"><label>222</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Davidson</surname><given-names>S</given-names></name><name><surname>McCabe</surname><given-names>TM</given-names></name><name><surname>Crotta</surname><given-names>S</given-names></name><name><surname>Gad</surname><given-names>HH</given-names></name><name><surname>Hessel</surname><given-names>EM</given-names></name><name><surname>Beinke</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>IFNlambda is a potent anti-influenza therapeutic without the inflammatory side effects of IFNalpha treatment</article-title>. <source>EMBO Mol Med</source> (<year>2016</year>) <volume>8</volume>(<issue>9</issue>):<fpage>1099</fpage>–<lpage>112</lpage>.<pub-id pub-id-type="doi">10.15252/emmm.201606413</pub-id><pub-id pub-id-type="pmid">27520969</pub-id></mixed-citation></ref><ref id="B223"><label>223</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Davidson</surname><given-names>S</given-names></name><name><surname>Crotta</surname><given-names>S</given-names></name><name><surname>McCabe</surname><given-names>TM</given-names></name><name><surname>Wack</surname><given-names>A</given-names></name></person-group><article-title>Pathogenic potential of interferon alphabeta in acute influenza infection</article-title>. <source>Nat Commun</source> (<year>2014</year>) <volume>5</volume>:<fpage>3864</fpage><pub-id pub-id-type="doi">10.1038/ncomms4864</pub-id><pub-id pub-id-type="pmid">24844667</pub-id></mixed-citation></ref><ref id="B224"><label>224</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kim</surname><given-names>S</given-names></name><name><surname>Kim</surname><given-names>MJ</given-names></name><name><surname>Kim</surname><given-names>CH</given-names></name><name><surname>Kang</surname><given-names>JW</given-names></name><name><surname>Shin</surname><given-names>HK</given-names></name><name><surname>Kim</surname><given-names>DY</given-names></name><etal></etal></person-group><article-title>The superiority of IFN-lambda as a therapeutic candidate to control acute influenza viral lung infection</article-title>. <source>Am J Respir Cell Mol Biol</source> (<year>2017</year>) <volume>56</volume>(<issue>2</issue>):<fpage>202</fpage>–<lpage>12</lpage>.<pub-id pub-id-type="doi">10.1165/rcmb.2016-0174OC</pub-id><pub-id pub-id-type="pmid">27632156</pub-id></mixed-citation></ref><ref id="B225"><label>225</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>W</given-names></name><name><surname>Moltedo</surname><given-names>B</given-names></name><name><surname>Moran</surname><given-names>TM</given-names></name></person-group><article-title>Type I interferon induction during influenza virus infection increases susceptibility to secondary <italic>Streptococcus pneumoniae</italic> infection by negative regulation of gammadelta T cells</article-title>. <source>J Virol</source> (<year>2012</year>) <volume>86</volume>(<issue>22</issue>):<fpage>12304</fpage>–<lpage>12</lpage>.<pub-id pub-id-type="doi">10.1128/JVI.01269-12</pub-id><pub-id pub-id-type="pmid">22951826</pub-id></mixed-citation></ref><ref id="B226"><label>226</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Galani</surname><given-names>IE</given-names></name><name><surname>Triantafyllia</surname><given-names>V</given-names></name><name><surname>Eleminiadou</surname><given-names>EE</given-names></name><name><surname>Koltsida</surname><given-names>O</given-names></name><name><surname>Stavropoulos</surname><given-names>A</given-names></name><name><surname>Manioudaki</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>Interferon-lambda mediates non-redundant front-line antiviral protection against influenza virus infection without compromising host fitness</article-title>. <source>Immunity</source> (<year>2017</year>) <volume>46</volume>(<issue>5</issue>):<fpage>875</fpage>–<lpage>890.e6</lpage>.<pub-id pub-id-type="doi">10.1016/j.immuni.2017.04.025</pub-id><pub-id pub-id-type="pmid">28514692</pub-id></mixed-citation></ref><ref id="B227"><label>227</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Coch</surname><given-names>C</given-names></name><name><surname>Stumpel</surname><given-names>JP</given-names></name><name><surname>Lilien-Waldau</surname><given-names>V</given-names></name><name><surname>Wohlleber</surname><given-names>D</given-names></name><name><surname>Kummerer</surname><given-names>BM</given-names></name><name><surname>Bekeredjian-Ding</surname><given-names>I</given-names></name><etal></etal></person-group><article-title>RIG-I activation protects and rescues from lethal influenza virus infection and bacterial superinfection</article-title>. <source>Mol Ther</source> (<year>2017</year>) <volume>25</volume>(<issue>9</issue>):<fpage>2093</fpage>–<lpage>103</lpage>.<pub-id pub-id-type="doi">10.1016/j.ymthe.2017.07.003</pub-id><pub-id pub-id-type="pmid">28760668</pub-id></mixed-citation></ref><ref id="B228"><label>228</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lee</surname><given-names>SM</given-names></name><name><surname>Gai</surname><given-names>WW</given-names></name><name><surname>Cheung</surname><given-names>TK</given-names></name><name><surname>Peiris</surname><given-names>JS</given-names></name></person-group>. <article-title>Antiviral effect of a selective COX-2 inhibitor on H5N1 infection in vitro</article-title>. <source>Antiviral Res</source> (<year>2011</year>) <volume>91</volume>(<issue>3</issue>):<fpage>330</fpage>–<lpage>4</lpage>.<pub-id pub-id-type="doi">10.1016/j.antiviral.2011.07.011</pub-id><pub-id pub-id-type="pmid">21798291</pub-id></mixed-citation></ref><ref id="B229"><label>229</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>C</given-names></name><name><surname>Li</surname><given-names>C</given-names></name><name><surname>Zhang</surname><given-names>AJ</given-names></name><name><surname>To</surname><given-names>KK</given-names></name><name><surname>Lee</surname><given-names>AC</given-names></name><name><surname>Zhu</surname><given-names>H</given-names></name><etal></etal></person-group><article-title>Avian influenza A H7N9 virus induces severe pneumonia in mice without prior adaptation and responds to a combination of zanamivir and COX-2 inhibitor</article-title>. <source>PLoS One</source> (<year>2014</year>) <volume>9</volume>(<issue>9</issue>):<fpage>e107966</fpage>.<pub-id pub-id-type="doi">10.1371/journal.pone.0107966</pub-id><pub-id pub-id-type="pmid">25232731</pub-id></mixed-citation></ref><ref id="B230"><label>230</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lee</surname><given-names>MY</given-names></name><name><surname>Cheung</surname><given-names>CY</given-names></name><name><surname>Peiris</surname><given-names>JS</given-names></name></person-group>. <article-title>Role of cyclooxygenase-2 in H5N1 viral pathogenesis and the potential use of its inhibitors</article-title>. <source>Hong Kong Med J</source> (<year>2013</year>) <volume>19</volume>(<issue>Suppl 4</issue>):<fpage>S29</fpage>–<lpage>35</lpage>.<pub-id pub-id-type="pmid">23775184</pub-id></mixed-citation></ref><ref id="B231"><label>231</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Coulombe</surname><given-names>F</given-names></name><name><surname>Jaworska</surname><given-names>J</given-names></name><name><surname>Verway</surname><given-names>M</given-names></name><name><surname>Tzelepis</surname><given-names>F</given-names></name><name><surname>Massoud</surname><given-names>A</given-names></name><name><surname>Gillard</surname><given-names>J</given-names></name><etal></etal></person-group><article-title>Targeted prostaglandin E2 inhibition enhances antiviral immunity through induction of type I interferon and apoptosis in macrophages</article-title>. <source>Immunity</source> (<year>2014</year>) <volume>40</volume>(<issue>4</issue>):<fpage>554</fpage>–<lpage>68</lpage>.<pub-id pub-id-type="doi">10.1016/j.immuni.2014.02.013</pub-id><pub-id pub-id-type="pmid">24726877</pub-id></mixed-citation></ref><ref id="B232"><label>232</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chen</surname><given-names>L</given-names></name><name><surname>Fan</surname><given-names>J</given-names></name><name><surname>Li</surname><given-names>Y</given-names></name><name><surname>Shi</surname><given-names>X</given-names></name><name><surname>Ju</surname><given-names>D</given-names></name><name><surname>Yan</surname><given-names>Q</given-names></name><etal></etal></person-group><article-title>Modified Jiu Wei Qiang Huo decoction improves dysfunctional metabolomics in influenza A pneumonia-infected mice</article-title>. <source>Biomed Chromatogr</source> (<year>2014</year>) <volume>28</volume>(<issue>4</issue>):<fpage>468</fpage>–<lpage>74</lpage>.<pub-id pub-id-type="doi">10.1002/bmc.3055</pub-id><pub-id pub-id-type="pmid">24132661</pub-id></mixed-citation></ref><ref id="B233"><label>233</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Takeuchi</surname><given-names>O</given-names></name><name><surname>Akira</surname><given-names>S</given-names></name></person-group><article-title>Pattern recognition receptors and inflammation</article-title>. <source>Cell</source> (<year>2010</year>) <volume>140</volume>(<issue>6</issue>):<fpage>805</fpage>–<lpage>20</lpage>.<pub-id pub-id-type="doi">10.1016/j.cell.2010.01.022</pub-id><pub-id pub-id-type="pmid">20303872</pub-id></mixed-citation></ref><ref id="B234"><label>234</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Le Goffic</surname><given-names>R</given-names></name><name><surname>Pothlichet</surname><given-names>J</given-names></name><name><surname>Vitour</surname><given-names>D</given-names></name><name><surname>Fujita</surname><given-names>T</given-names></name><name><surname>Meurs</surname><given-names>E</given-names></name><name><surname>Chignard</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>Cutting edge: influenza A virus activates TLR3-dependent inflammatory and RIG-I-dependent antiviral responses in human lung epithelial cells</article-title>. <source>J Immunol</source> (<year>2007</year>) <volume>178</volume>(<issue>6</issue>):<fpage>3368</fpage>–<lpage>72</lpage>.<pub-id pub-id-type="doi">10.4049/jimmunol.178.6.3368</pub-id><pub-id pub-id-type="pmid">17339430</pub-id></mixed-citation></ref><ref id="B235"><label>235</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lee</surname><given-names>SM</given-names></name><name><surname>Kok</surname><given-names>KH</given-names></name><name><surname>Jaume</surname><given-names>M</given-names></name><name><surname>Cheung</surname><given-names>TK</given-names></name><name><surname>Yip</surname><given-names>TF</given-names></name><name><surname>Lai</surname><given-names>JC</given-names></name><etal></etal></person-group><article-title>Toll-like receptor 10 is involved in induction of innate immune responses to influenza virus infection</article-title>. <source>Proc Natl Acad Sci U S A</source> (<year>2014</year>) <volume>111</volume>(<issue>10</issue>):<fpage>3793</fpage>–<lpage>8</lpage>.<pub-id pub-id-type="doi">10.1073/pnas.1324266111</pub-id><pub-id pub-id-type="pmid">24567377</pub-id></mixed-citation></ref><ref id="B236"><label>236</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wu</surname><given-names>W</given-names></name><name><surname>Zhang</surname><given-names>W</given-names></name><name><surname>Duggan</surname><given-names>ES</given-names></name><name><surname>Booth</surname><given-names>JL</given-names></name><name><surname>Zou</surname><given-names>MH</given-names></name><name><surname>Metcalf</surname><given-names>JP</given-names></name></person-group>. <article-title>RIG-I and TLR3 are both required for maximum interferon induction by influenza virus in human lung alveolar epithelial cells</article-title>. <source>Virology</source> (<year>2015</year>) <volume>482</volume>:<fpage>181</fpage>–<lpage>8</lpage>.<pub-id pub-id-type="doi">10.1016/j.virol.2015.03.048</pub-id><pub-id pub-id-type="pmid">25880109</pub-id></mixed-citation></ref><ref id="B237"><label>237</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Patel</surname><given-names>JR</given-names></name><name><surname>Garcia-Sastre</surname><given-names>A</given-names></name></person-group>. <article-title>Activation and regulation of pathogen sensor RIG-I</article-title>. <source>Cytokine Growth Factor Rev</source> (<year>2014</year>) <volume>25</volume>(<issue>5</issue>):<fpage>513</fpage>–<lpage>23</lpage>.<pub-id pub-id-type="doi">10.1016/j.cytogfr.2014.08.005</pub-id><pub-id pub-id-type="pmid">25212896</pub-id></mixed-citation></ref><ref id="B238"><label>238</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Weber-Gerlach</surname><given-names>M</given-names></name><name><surname>Weber</surname><given-names>F</given-names></name></person-group>. <article-title>Standing on three legs: antiviral activities of RIG-I against influenza viruses</article-title>. <source>Curr Opin Immunol</source> (<year>2016</year>) <volume>42</volume>:<fpage>71</fpage>–<lpage>5</lpage>.<pub-id pub-id-type="doi">10.1016/j.coi.2016.05.016</pub-id><pub-id pub-id-type="pmid">27318973</pub-id></mixed-citation></ref><ref id="B239"><label>239</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yoneyama</surname><given-names>M</given-names></name><name><surname>Onomoto</surname><given-names>K</given-names></name><name><surname>Jogi</surname><given-names>M</given-names></name><name><surname>Akaboshi</surname><given-names>T</given-names></name><name><surname>Fujita</surname><given-names>T</given-names></name></person-group>. <article-title>Viral RNA detection by RIG-I-like receptors</article-title>. <source>Curr Opin Immunol</source> (<year>2015</year>) <volume>32</volume>:<fpage>48</fpage>–<lpage>53</lpage>.<pub-id pub-id-type="doi">10.1016/j.coi.2014.12.012</pub-id><pub-id pub-id-type="pmid">25594890</pub-id></mixed-citation></ref><ref id="B240"><label>240</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>De Nardo</surname><given-names>D</given-names></name></person-group>. <article-title>Toll-like receptors: activation, signalling and transcriptional modulation</article-title>. <source>Cytokine</source> (<year>2015</year>) <volume>74</volume>(<issue>2</issue>):<fpage>181</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.1016/j.cyto.2015.02.025</pub-id><pub-id pub-id-type="pmid">25846205</pub-id></mixed-citation></ref><ref id="B241"><label>241</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kagan</surname><given-names>JC</given-names></name><name><surname>Su</surname><given-names>T</given-names></name><name><surname>Horng</surname><given-names>T</given-names></name><name><surname>Chow</surname><given-names>A</given-names></name><name><surname>Akira</surname><given-names>S</given-names></name><name><surname>Medzhitov</surname><given-names>R</given-names></name></person-group>. <article-title>TRAM couples endocytosis of toll-like receptor 4 to the induction of interferon-beta</article-title>. <source>Nat Immunol</source> (<year>2008</year>) <volume>9</volume>(<issue>4</issue>):<fpage>361</fpage>–<lpage>8</lpage>.<pub-id pub-id-type="doi">10.1038/ni1569</pub-id><pub-id pub-id-type="pmid">18297073</pub-id></mixed-citation></ref><ref id="B242"><label>242</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Oosting</surname><given-names>M</given-names></name><name><surname>Cheng</surname><given-names>SC</given-names></name><name><surname>Bolscher</surname><given-names>JM</given-names></name><name><surname>Vestering-Stenger</surname><given-names>R</given-names></name><name><surname>Plantinga</surname><given-names>TS</given-names></name><name><surname>Verschueren</surname><given-names>IC</given-names></name><etal></etal></person-group><article-title>Human TLR10 is an anti-inflammatory pattern-recognition receptor</article-title>. <source>Proc Natl Acad Sci U S A</source> (<year>2014</year>) <volume>111</volume>(<issue>42</issue>):<fpage>E4478</fpage>–<lpage>84</lpage>.<pub-id pub-id-type="doi">10.1073/pnas.1410293111</pub-id><pub-id pub-id-type="pmid">25288745</pub-id></mixed-citation></ref><ref id="B243"><label>243</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jiang</surname><given-names>S</given-names></name><name><surname>Li</surname><given-names>X</given-names></name><name><surname>Hess</surname><given-names>NJ</given-names></name><name><surname>Guan</surname><given-names>Y</given-names></name><name><surname>Tapping</surname><given-names>RI</given-names></name></person-group>. <article-title>TLR10 is a negative regulator of both MyD88-dependent and -independent TLR signaling</article-title>. <source>J Immunol</source> (<year>2016</year>) <volume>196</volume>(<issue>9</issue>):<fpage>3834</fpage>–<lpage>41</lpage>.<pub-id pub-id-type="doi">10.4049/jimmunol.1502599</pub-id><pub-id pub-id-type="pmid">27022193</pub-id></mixed-citation></ref><ref id="B244"><label>244</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lee</surname><given-names>SMY</given-names></name><name><surname>Yip</surname><given-names>TF</given-names></name><name><surname>Yan</surname><given-names>S</given-names></name><name><surname>Jin</surname><given-names>DY</given-names></name><name><surname>Wei</surname><given-names>HL</given-names></name><name><surname>Guo</surname><given-names>RT</given-names></name><etal></etal></person-group><article-title>Recognition of double-stranded RNA and regulation of interferon pathway by toll-like receptor 10</article-title>. <source>Front Immunol</source> (<year>2018</year>) <volume>9</volume>:<fpage>516</fpage>.<pub-id pub-id-type="doi">10.3389/fimmu.2018.00516</pub-id><pub-id pub-id-type="pmid">29616030</pub-id></mixed-citation></ref><ref id="B245"><label>245</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Imai</surname><given-names>Y</given-names></name><name><surname>Kuba</surname><given-names>K</given-names></name><name><surname>Neely</surname><given-names>GG</given-names></name><name><surname>Yaghubian-Malhami</surname><given-names>R</given-names></name><name><surname>Perkmann</surname><given-names>T</given-names></name><name><surname>van Loo</surname><given-names>G</given-names></name><etal></etal></person-group><article-title>Identification of oxidative stress and toll-like receptor 4 signaling as a key pathway of acute lung injury</article-title>. <source>Cell</source> (<year>2008</year>) <volume>133</volume>(<issue>2</issue>):<fpage>235</fpage>–<lpage>49</lpage>.<pub-id pub-id-type="doi">10.1016/j.cell.2008.02.043</pub-id><pub-id pub-id-type="pmid">18423196</pub-id></mixed-citation></ref><ref id="B246"><label>246</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tsai</surname><given-names>SY</given-names></name><name><surname>Segovia</surname><given-names>JA</given-names></name><name><surname>Chang</surname><given-names>TH</given-names></name><name><surname>Morris</surname><given-names>IR</given-names></name><name><surname>Berton</surname><given-names>MT</given-names></name><name><surname>Tessier</surname><given-names>PA</given-names></name><etal></etal></person-group><article-title>DAMP molecule S100A9 acts as a molecular pattern to enhance inflammation during influenza A virus infection: role of DDX21-TRIF-TLR4-MyD88 pathway</article-title>. <source>PLoS Pathog</source> (<year>2014</year>) <volume>10</volume>(<issue>1</issue>):<fpage>e1003848</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.1003848</pub-id><pub-id pub-id-type="pmid">24391503</pub-id></mixed-citation></ref><ref id="B247"><label>247</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Opal</surname><given-names>SM</given-names></name><name><surname>Laterre</surname><given-names>PF</given-names></name><name><surname>Francois</surname><given-names>B</given-names></name><name><surname>LaRosa</surname><given-names>SP</given-names></name><name><surname>Angus</surname><given-names>DC</given-names></name><name><surname>Mira</surname><given-names>JP</given-names></name><etal></etal></person-group><article-title>Effect of eritoran, an antagonist of MD2-TLR4, on mortality in patients with severe sepsis: the ACCESS randomized trial</article-title>. <source>JAMA</source> (<year>2013</year>) <volume>309</volume>(<issue>11</issue>):<fpage>1154</fpage>–<lpage>62</lpage>.<pub-id pub-id-type="doi">10.1001/jama.2013.2194</pub-id><pub-id pub-id-type="pmid">23512062</pub-id></mixed-citation></ref><ref id="B248"><label>248</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shirey</surname><given-names>KA</given-names></name><name><surname>Lai</surname><given-names>W</given-names></name><name><surname>Scott</surname><given-names>AJ</given-names></name><name><surname>Lipsky</surname><given-names>M</given-names></name><name><surname>Mistry</surname><given-names>P</given-names></name><name><surname>Pletneva</surname><given-names>LM</given-names></name><etal></etal></person-group><article-title>The TLR4 antagonist eritoran protects mice from lethal influenza infection</article-title>. <source>Nature</source> (<year>2013</year>) <volume>497</volume>(<issue>7450</issue>):<fpage>498</fpage>–<lpage>502</lpage>.<pub-id pub-id-type="doi">10.1038/nature12118</pub-id><pub-id pub-id-type="pmid">23636320</pub-id></mixed-citation></ref><ref id="B249"><label>249</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Perrin-Cocon</surname><given-names>L</given-names></name><name><surname>Aublin-Gex</surname><given-names>A</given-names></name><name><surname>Sestito</surname><given-names>SE</given-names></name><name><surname>Shirey</surname><given-names>KA</given-names></name><name><surname>Patel</surname><given-names>MC</given-names></name><name><surname>Andre</surname><given-names>P</given-names></name><etal></etal></person-group><article-title>TLR4 antagonist FP7 inhibits LPS-induced cytokine production and glycolytic reprogramming in dendritic cells, and protects mice from lethal influenza infection</article-title>. <source>Sci Rep</source> (<year>2017</year>) <volume>7</volume>:<fpage>40791</fpage>.<pub-id pub-id-type="doi">10.1038/srep40791</pub-id><pub-id pub-id-type="pmid">28106157</pub-id></mixed-citation></ref><ref id="B250"><label>250</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Piao</surname><given-names>W</given-names></name><name><surname>Shirey</surname><given-names>KA</given-names></name><name><surname>Ru</surname><given-names>LW</given-names></name><name><surname>Lai</surname><given-names>W</given-names></name><name><surname>Szmacinski</surname><given-names>H</given-names></name><name><surname>Snyder</surname><given-names>GA</given-names></name><etal></etal></person-group><article-title>A decoy peptide that disrupts TIRAP recruitment to TLRs is protective in a murine model of influenza</article-title>. <source>Cell Rep</source> (<year>2015</year>) <volume>11</volume>(<issue>12</issue>):<fpage>1941</fpage>–<lpage>52</lpage>.<pub-id pub-id-type="doi">10.1016/j.celrep.2015.05.035</pub-id><pub-id pub-id-type="pmid">26095366</pub-id></mixed-citation></ref><ref id="B251"><label>251</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shirey</surname><given-names>KA</given-names></name><name><surname>Lai</surname><given-names>W</given-names></name><name><surname>Patel</surname><given-names>MC</given-names></name><name><surname>Pletneva</surname><given-names>LM</given-names></name><name><surname>Pang</surname><given-names>C</given-names></name><name><surname>Kurt-Jones</surname><given-names>E</given-names></name><etal></etal></person-group><article-title>Novel strategies for targeting innate immune responses to influenza</article-title>. <source>Mucosal Immunol</source> (<year>2016</year>) <volume>9</volume>(<issue>5</issue>):<fpage>1173</fpage>–<lpage>82</lpage>.<pub-id pub-id-type="doi">10.1038/mi.2015.141</pub-id><pub-id pub-id-type="pmid">26813341</pub-id></mixed-citation></ref><ref id="B252"><label>252</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Leung</surname><given-names>YH</given-names></name><name><surname>Nicholls</surname><given-names>JM</given-names></name><name><surname>Ho</surname><given-names>CK</given-names></name><name><surname>Sia</surname><given-names>SF</given-names></name><name><surname>Mok</surname><given-names>CK</given-names></name><name><surname>Valkenburg</surname><given-names>SA</given-names></name><etal></etal></person-group><article-title>Highly pathogenic avian influenza A H5N1 and pandemic H1N1 virus infections have different phenotypes in toll-like receptor 3 knockout mice</article-title>. <source>J Gen Virol</source> (<year>2014</year>) <volume>95</volume>(<issue>Pt 9</issue>):<fpage>1870</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.1099/vir.0.066258-0</pub-id><pub-id pub-id-type="pmid">24878639</pub-id></mixed-citation></ref><ref id="B253"><label>253</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gao</surname><given-names>W</given-names></name><name><surname>Xiong</surname><given-names>Y</given-names></name><name><surname>Li</surname><given-names>Q</given-names></name><name><surname>Yang</surname><given-names>H</given-names></name></person-group>. <article-title>Inhibition of toll-like receptor signaling as a promising therapy for inflammatory diseases: a journey from molecular to nano therapeutics</article-title>. <source>Front Physiol</source> (<year>2017</year>) <volume>8</volume>:<fpage>508</fpage>.<pub-id pub-id-type="doi">10.3389/fphys.2017.00508</pub-id><pub-id pub-id-type="pmid">28769820</pub-id></mixed-citation></ref><ref id="B254"><label>254</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cheng</surname><given-names>K</given-names></name><name><surname>Wang</surname><given-names>X</given-names></name><name><surname>Yin</surname><given-names>H</given-names></name></person-group>. <article-title>Small-molecule inhibitors of the TLR3/dsRNA complex</article-title>. <source>J Am Chem Soc</source> (<year>2011</year>) <volume>133</volume>(<issue>11</issue>):<fpage>3764</fpage>–<lpage>7</lpage>.<pub-id pub-id-type="doi">10.1021/ja111312h</pub-id><pub-id pub-id-type="pmid">21355588</pub-id></mixed-citation></ref><ref id="B255"><label>255</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>Z</given-names></name><name><surname>Li</surname><given-names>L</given-names></name><name><surname>Zhou</surname><given-names>H</given-names></name><name><surname>Zeng</surname><given-names>L</given-names></name><name><surname>Chen</surname><given-names>T</given-names></name><name><surname>Chen</surname><given-names>Q</given-names></name><etal></etal></person-group><article-title>Radix isatidis polysaccharides inhibit influenza a virus and influenza A virus-induced inflammation via suppression of Host TLR3 signaling in vitro</article-title>. <source>Molecules</source> (<year>2017</year>) <volume>22</volume>(<issue>1</issue>):<fpage>E116</fpage>.<pub-id pub-id-type="doi">10.3390/molecules22010116</pub-id><pub-id pub-id-type="pmid">28085062</pub-id></mixed-citation></ref><ref id="B256"><label>256</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tian</surname><given-names>J</given-names></name><name><surname>Jiao</surname><given-names>X</given-names></name><name><surname>Wang</surname><given-names>X</given-names></name><name><surname>Geng</surname><given-names>J</given-names></name><name><surname>Wang</surname><given-names>R</given-names></name><name><surname>Liu</surname><given-names>N</given-names></name><etal></etal></person-group><article-title>Novel effect of methionine enkephalin against influenza A virus infection through inhibiting TLR7-MyD88-TRAF6-NF-kappaB p65 signaling pathway</article-title>. <source>Int Immunopharmacol</source> (<year>2017</year>) <volume>55</volume>:<fpage>38</fpage>–<lpage>48</lpage>.<pub-id pub-id-type="doi">10.1016/j.intimp.2017.12.001</pub-id><pub-id pub-id-type="pmid">29220721</pub-id></mixed-citation></ref><ref id="B257"><label>257</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hulme</surname><given-names>KD</given-names></name><name><surname>Gallo</surname><given-names>LA</given-names></name><name><surname>Short</surname><given-names>KR</given-names></name></person-group>. <article-title>Influenza virus and glycemic variability in diabetes: a killer combination?</article-title><source>Front Microbiol</source> (<year>2017</year>) <volume>8</volume>:<fpage>861</fpage>.<pub-id pub-id-type="doi">10.3389/fmicb.2017.00861</pub-id><pub-id pub-id-type="pmid">28588558</pub-id></mixed-citation></ref><ref id="B258"><label>258</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kohio</surname><given-names>HP</given-names></name><name><surname>Adamson</surname><given-names>AL</given-names></name></person-group>. <article-title>Glycolytic control of vacuolar-type ATPase activity: a mechanism to regulate influenza viral infection</article-title>. <source>Virology</source> (<year>2013</year>) <volume>444</volume>(<issue>1–2</issue>):<fpage>301</fpage>–<lpage>9</lpage>.<pub-id pub-id-type="doi">10.1016/j.virol.2013.06.026</pub-id><pub-id pub-id-type="pmid">23876457</pub-id></mixed-citation></ref><ref id="B259"><label>259</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Miyake-Stoner</surname><given-names>SJ</given-names></name><name><surname>O’Shea</surname><given-names>CC</given-names></name></person-group>. <article-title>Metabolism goes viral</article-title>. <source>Cell Metab</source> (<year>2014</year>) <volume>19</volume>(<issue>4</issue>):<fpage>549</fpage>–<lpage>50</lpage>.<pub-id pub-id-type="doi">10.1016/j.cmet.2014.03.022</pub-id><pub-id pub-id-type="pmid">24703688</pub-id></mixed-citation></ref><ref id="B260"><label>260</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Munger</surname><given-names>J</given-names></name><name><surname>Bajad</surname><given-names>SU</given-names></name><name><surname>Coller</surname><given-names>HA</given-names></name><name><surname>Shenk</surname><given-names>T</given-names></name><name><surname>Rabinowitz</surname><given-names>JD</given-names></name></person-group>. <article-title>Dynamics of the cellular metabolome during human cytomegalovirus infection</article-title>. <source>PLoS Pathog</source> (<year>2006</year>) <volume>2</volume>(<issue>12</issue>):<fpage>e132</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.0020132</pub-id><pub-id pub-id-type="pmid">17173481</pub-id></mixed-citation></ref><ref id="B261"><label>261</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Koyuncu</surname><given-names>E</given-names></name><name><surname>Purdy</surname><given-names>JG</given-names></name><name><surname>Rabinowitz</surname><given-names>JD</given-names></name><name><surname>Shenk</surname><given-names>T</given-names></name></person-group>. <article-title>Saturated very long chain fatty acids are required for the production of infectious human cytomegalovirus progeny</article-title>. <source>PLoS Pathog</source> (<year>2013</year>) <volume>9</volume>(<issue>5</issue>):<fpage>e1003333</fpage>.<pub-id pub-id-type="doi">10.1371/journal.ppat.1003333</pub-id><pub-id pub-id-type="pmid">23696731</pub-id></mixed-citation></ref><ref id="B262"><label>262</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Goodwin</surname><given-names>CM</given-names></name><name><surname>Xu</surname><given-names>S</given-names></name><name><surname>Munger</surname><given-names>J</given-names></name></person-group>. <article-title>Stealing the keys to the kitchen: viral manipulation of the host cell metabolic network</article-title>. <source>Trends Microbiol</source> (<year>2015</year>) <volume>23</volume>(<issue>12</issue>):<fpage>789</fpage>–<lpage>98</lpage>.<pub-id pub-id-type="doi">10.1016/j.tim.2015.08.007</pub-id><pub-id pub-id-type="pmid">26439298</pub-id></mixed-citation></ref><ref id="B263"><label>263</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sanchez</surname><given-names>EL</given-names></name><name><surname>Lagunoff</surname><given-names>M</given-names></name></person-group><article-title>Viral activation of cellular metabolism</article-title>. <source>Virology</source> (<year>2015</year>) <volume>47</volume>(<issue>9–480</issue>):<fpage>609</fpage>–<lpage>18</lpage>.<pub-id pub-id-type="doi">10.1016/j.virol.2015.02.038</pub-id></mixed-citation></ref><ref id="B264"><label>264</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Smallwood</surname><given-names>HS</given-names></name><name><surname>Duan</surname><given-names>S</given-names></name><name><surname>Morfouace</surname><given-names>M</given-names></name><name><surname>Rezinciuc</surname><given-names>S</given-names></name><name><surname>Shulkin</surname><given-names>BL</given-names></name><name><surname>Shelat</surname><given-names>A</given-names></name><etal></etal></person-group><article-title>Targeting metabolic reprogramming by influenza infection for therapeutic intervention</article-title>. <source>Cell Rep</source> (<year>2017</year>) <volume>19</volume>(<issue>8</issue>):<fpage>1640</fpage>–<lpage>53</lpage>.<pub-id pub-id-type="doi">10.1016/j.celrep.2017.04.039</pub-id><pub-id pub-id-type="pmid">28538182</pub-id></mixed-citation></ref><ref id="B265"><label>265</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ritter</surname><given-names>JB</given-names></name><name><surname>Wahl</surname><given-names>AS</given-names></name><name><surname>Freund</surname><given-names>S</given-names></name><name><surname>Genzel</surname><given-names>Y</given-names></name><name><surname>Reichl</surname><given-names>U</given-names></name></person-group>. <article-title>Metabolic effects of influenza virus infection in cultured animal cells: Intra- and extracellular metabolite profiling</article-title>. <source>BMC Syst Biol</source> (<year>2010</year>) <volume>4</volume>:<fpage>61</fpage>.<pub-id pub-id-type="doi">10.1186/1752-0509-4-61</pub-id><pub-id pub-id-type="pmid">20465796</pub-id></mixed-citation></ref><ref id="B266"><label>266</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ryan</surname><given-names>DG</given-names></name><name><surname>O’Neill</surname><given-names>LAJ</given-names></name></person-group>. <article-title>Krebs cycle rewired for macrophage and dendritic cell effector functions</article-title>. <source>FEBS Lett</source> (<year>2017</year>) <volume>591</volume>(<issue>19</issue>):<fpage>2992</fpage>–<lpage>3006</lpage>.<pub-id pub-id-type="doi">10.1002/1873-3468.12744</pub-id><pub-id pub-id-type="pmid">28685841</pub-id></mixed-citation></ref><ref id="B267"><label>267</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tannahill</surname><given-names>GM</given-names></name><name><surname>Curtis</surname><given-names>AM</given-names></name><name><surname>Adamik</surname><given-names>J</given-names></name><name><surname>Palsson-McDermott</surname><given-names>EM</given-names></name><name><surname>McGettrick</surname><given-names>AF</given-names></name><name><surname>Goel</surname><given-names>G</given-names></name><etal></etal></person-group><article-title>Succinate is an inflammatory signal that induces IL-1beta through HIF-1alpha</article-title>. <source>Nature</source> (<year>2013</year>) <volume>496</volume>(<issue>7444</issue>):<fpage>238</fpage>–<lpage>42</lpage>.<pub-id pub-id-type="doi">10.1038/nature11986</pub-id><pub-id pub-id-type="pmid">23535595</pub-id></mixed-citation></ref><ref id="B268"><label>268</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mills</surname><given-names>EL</given-names></name><name><surname>Ryan</surname><given-names>DG</given-names></name><name><surname>Prag</surname><given-names>HA</given-names></name><name><surname>Dikovskaya</surname><given-names>D</given-names></name><name><surname>Menon</surname><given-names>D</given-names></name><name><surname>Zaslona</surname><given-names>Z</given-names></name><etal></etal></person-group><article-title>Itaconate is an anti-inflammatory metabolite that activates Nrf2 via alkylation of KEAP1</article-title>. <source>Nature</source> (<year>2018</year>) <volume>556</volume>(<issue>7699</issue>):<fpage>113</fpage>–<lpage>7</lpage>.<pub-id pub-id-type="doi">10.1038/nature25986</pub-id><pub-id pub-id-type="pmid">29590092</pub-id></mixed-citation></ref></ref-list></back></pmc></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/H2N2V1/Data/Pmc/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000D50 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd -nk 000D50 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= H2N2V1
|flux= Pmc
|étape= Corpus
|type= RBID
|clé=
|texte=
}}
| This area was generated with Dilib version V0.6.33. |  |