Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections
Identifieur interne : 000126 ( Istex/Corpus ); précédent : 000125; suivant : 000127Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections
Auteurs : Tamaki Okabayashi ; Hiroaki Kariwa ; Shin-Ichi Yokota ; Shigeo Iki ; Tomokazu Indoh ; Noriko Yokosawa ; Ikuo Takashima ; Hiroyuki Tsutsumi ; Nobuhiro FujiiSource :
- Journal of Medical Virology [ 0146-6615 ] ; 2006-04.
English descriptors
- Teeft :
- Ace2, Antiviral, Biochem biophys, Caco2, Caco2 cells, Cell lines, Chan, Clinical progression, Coronavirus, Culture medium, Cytokine, Cytokine production, Cytokine regulation, Distress syndrome, Fluav, Gapdh, Gapdh mrna, Hokkaido, Hpiv2, Hpiv2 infections, Human virus type, Ifns, Important role, Induction, Induction levels, Infection, Interferon, Irf7, Isgs, Less induction, Many viruses, Mrna, Negative regulator, Pathway, Post infection, Protein level, Rantes, Receptor, Regulator, Replication, Respir crit care, Respiratory syncytial virus, Respiratory syndrome, Sars, Sars coronavirus, Sars patients, Signal transduction, Signal transduction pathway, Siha cells, Socs family, Socs3, Stat3, Syncytial, Syndrome, Transduction, University school, Viral, Virol, Virus, Virus infection, Zhang.
Abstract
The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS‐CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS‐CoV infection. Therefore, SARS‐CoV replication was suppressed by pretreatment with IFN. SARS‐CoV and RSV induced high levels of IL‐6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling‐3 (SOCS3) by SARS‐CoV was significantly lower than that by RSV in spite of the significant production of IL‐6. Toll‐like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS‐CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with “severe” inflammation in SARS. J. Med. Virol. 78:417–424, 2006. © 2006 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jmv.20556
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ISTEX:F17D45D4C06BEA8CE19CAA34D56E1870ED79FE3ALe document en format XML
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first="Shin-Ichi" last="Yokota">Shin-Ichi Yokota</name><affiliation><mods:affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</mods:affiliation></affiliation></author><author><name sortKey="Iki, Shigeo" sort="Iki, Shigeo" uniqKey="Iki S" first="Shigeo" last="Iki">Shigeo Iki</name><affiliation><mods:affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</mods:affiliation></affiliation></author><author><name sortKey="Indoh, Tomokazu" sort="Indoh, Tomokazu" uniqKey="Indoh T" first="Tomokazu" last="Indoh">Tomokazu Indoh</name><affiliation><mods:affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</mods:affiliation></affiliation></author><author><name sortKey="Yokosawa, Noriko" sort="Yokosawa, Noriko" uniqKey="Yokosawa N" first="Noriko" last="Yokosawa">Noriko Yokosawa</name><affiliation><mods:affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</mods:affiliation></affiliation></author><author><name sortKey="Takashima, Ikuo" sort="Takashima, Ikuo" uniqKey="Takashima I" first="Ikuo" last="Takashima">Ikuo Takashima</name><affiliation><mods:affiliation>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Hokkaido, Japan</mods:affiliation></affiliation></author><author><name sortKey="Tsutsumi, Hiroyuki" sort="Tsutsumi, Hiroyuki" uniqKey="Tsutsumi H" first="Hiroyuki" last="Tsutsumi">Hiroyuki Tsutsumi</name><affiliation><mods:affiliation>Department of Pediatrics, Sapporo Medical University School of Medicine, Hokkaido, Japan</mods:affiliation></affiliation></author><author><name sortKey="Fujii, Nobuhiro" sort="Fujii, Nobuhiro" uniqKey="Fujii N" first="Nobuhiro" last="Fujii">Nobuhiro Fujii</name><affiliation><mods:affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: fujii@sapmed.ac.jp</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence address: Department of Microbiology, Sapporo Medical University School of Medicine, South‐1, West‐17, Chuo‐ku, Sapporo 060‐8556, Hokkaido, Japan.===</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Medical Virology</title><title level="j" type="alt">JOURNAL OF MEDICAL VIROLOGY</title><idno type="ISSN">0146-6615</idno><idno type="eISSN">1096-9071</idno><imprint><biblScope unit="vol">78</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="417">417</biblScope><biblScope unit="page" to="424">424</biblScope><biblScope unit="page-count">8</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-04">2006-04</date></imprint><idno type="ISSN">0146-6615</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0146-6615</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Ace2</term><term>Antiviral</term><term>Biochem biophys</term><term>Caco2</term><term>Caco2 cells</term><term>Cell lines</term><term>Chan</term><term>Clinical progression</term><term>Coronavirus</term><term>Culture medium</term><term>Cytokine</term><term>Cytokine production</term><term>Cytokine regulation</term><term>Distress syndrome</term><term>Fluav</term><term>Gapdh</term><term>Gapdh mrna</term><term>Hokkaido</term><term>Hpiv2</term><term>Hpiv2 infections</term><term>Human virus type</term><term>Ifns</term><term>Important role</term><term>Induction</term><term>Induction levels</term><term>Infection</term><term>Interferon</term><term>Irf7</term><term>Isgs</term><term>Less induction</term><term>Many viruses</term><term>Mrna</term><term>Negative regulator</term><term>Pathway</term><term>Post infection</term><term>Protein level</term><term>Rantes</term><term>Receptor</term><term>Regulator</term><term>Replication</term><term>Respir crit care</term><term>Respiratory syncytial virus</term><term>Respiratory syndrome</term><term>Sars</term><term>Sars coronavirus</term><term>Sars patients</term><term>Signal transduction</term><term>Signal transduction pathway</term><term>Siha cells</term><term>Socs family</term><term>Socs3</term><term>Stat3</term><term>Syncytial</term><term>Syndrome</term><term>Transduction</term><term>University school</term><term>Viral</term><term>Virol</term><term>Virus</term><term>Virus infection</term><term>Zhang</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS‐CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS‐CoV infection. Therefore, SARS‐CoV replication was suppressed by pretreatment with IFN. SARS‐CoV and RSV induced high levels of IL‐6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling‐3 (SOCS3) by SARS‐CoV was significantly lower than that by RSV in spite of the significant production of IL‐6. Toll‐like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS‐CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with “severe” inflammation in SARS. J. Med. Virol. 78:417–424, 2006. © 2006 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>cytokine</json:string><json:string>sars</json:string><json:string>mrna</json:string><json:string>socs3</json:string><json:string>fluav</json:string><json:string>hpiv2</json:string><json:string>pathway</json:string><json:string>caco2</json:string><json:string>virol</json:string><json:string>interferon</json:string><json:string>caco2 cells</json:string><json:string>receptor</json:string><json:string>stat3</json:string><json:string>coronavirus</json:string><json:string>ifns</json:string><json:string>isgs</json:string><json:string>antiviral</json:string><json:string>transduction</json:string><json:string>rantes</json:string><json:string>syncytial</json:string><json:string>irf7</json:string><json:string>ace2</json:string><json:string>chan</json:string><json:string>viral</json:string><json:string>zhang</json:string><json:string>virus 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Japan</json:string></affiliations></json:item><json:item><name>Shin‐ichi Yokota</name><affiliations><json:string>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</json:string></affiliations></json:item><json:item><name>Shigeo Iki</name><affiliations><json:string>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</json:string></affiliations></json:item><json:item><name>Tomokazu Indoh</name><affiliations><json:string>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</json:string></affiliations></json:item><json:item><name>Noriko Yokosawa</name><affiliations><json:string>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</json:string></affiliations></json:item><json:item><name>Ikuo Takashima</name><affiliations><json:string>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Hokkaido, Japan</json:string></affiliations></json:item><json:item><name>Hiroyuki Tsutsumi</name><affiliations><json:string>Department of Pediatrics, Sapporo Medical University School of Medicine, Hokkaido, Japan</json:string></affiliations></json:item><json:item><name>Nobuhiro Fujii</name><affiliations><json:string>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</json:string><json:string>E-mail: fujii@sapmed.ac.jp</json:string><json:string>Correspondence address: Department of Microbiology, Sapporo Medical University School of Medicine, South‐1, West‐17, Chuo‐ku, Sapporo 060‐8556, Hokkaido, Japan.===</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>SARS‐CoV</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SOCS3</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cytokine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>IL‐6</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>IFN</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>TLR</value></json:item></subject><articleId><json:string>JMV20556</json:string></articleId><arkIstex>ark:/67375/WNG-FQB1SXHD-6</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS‐CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS‐CoV infection. Therefore, SARS‐CoV replication was suppressed by pretreatment with IFN. SARS‐CoV and RSV induced high levels of IL‐6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling‐3 (SOCS3) by SARS‐CoV was significantly lower than that by RSV in spite of the significant production of IL‐6. Toll‐like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS‐CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with “severe” inflammation in SARS. J. Med. Virol. 78:417–424, 2006. © 2006 Wiley‐Liss, Inc.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>167</abstractWordCount><abstractCharCount>1193</abstractCharCount><keywordCount>6</keywordCount><score>9.004</score><pdfWordCount>5471</pdfWordCount><pdfCharCount>35567</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>8</pdfPageCount><pdfPageSize>594 x 792 pts</pdfPageSize><pdfWordsPerPage>684</pdfWordsPerPage><pdfText>true</pdfText></qualityIndicators><title>Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections</title><pmid><json:string>16482545</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Journal of Medical Virology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1002/(ISSN)1096-9071</json:string></doi><issn><json:string>0146-6615</json:string></issn><eissn><json:string>1096-9071</json:string></eissn><publisherId><json:string>JMV</json:string></publisherId><volume>78</volume><issue>4</issue><pages><first>417</first><last>424</last><total>8</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Research Article</value></json:item></subject></host><namedEntities><unitex><date><json:string>2006</json:string></date><geogName></geogName><orgName><json:string>Department of Microbiology, Sapporo Medical University School of Medicine and Laboratory</json:string><json:string>Genzyme-Techne</json:string><json:string>Department of Pediatrics, Sapporo Medical University School of Medicine, Hokkaido, Japan</json:string><json:string>Serotec</json:string><json:string>Hokkaido University</json:string><json:string>Department of Microbiology, Sapporo Medical University School of Medicine, South</json:string><json:string>Japan Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Hokkaido, Japan</json:string><json:string>Wiley-Liss, Inc</json:string><json:string>LISS, INC.</json:string><json:string>Mie University</json:string><json:string>American Type Culture Collection</json:string><json:string>Nagasaki University, Japan</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>I. 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[2000]</json:string><json:string>Kubo et al., 2003</json:string><json:string>Tsutsumi et al., 1989</json:string><json:string>Yang et al., 2003</json:string><json:string>Morgenstern et al., 2005</json:string><json:string>Spiegel et al. [2005]</json:string><json:string>Sen and Ransohoff, 1993</json:string><json:string>Andrejeva et al., 2002</json:string><json:string>Lund et al., 2004</json:string><json:string>Okabayashi et al.</json:string><json:string>Cinatl et al., 2004</json:string><json:string>Hemmi et al., 2000</json:string><json:string>Chollet-Martin et al., 1996</json:string><json:string>Sigurs et al., 2000</json:string><json:string>Poole et al., 2002</json:string><json:string>Nicholls et al., 2003</json:string><json:string>Cheung et al., 2005</json:string><json:string>Peiris et al., 2003</json:string><json:string>Monick et al., 2003</json:string><json:string>Yasukawa et al., 2003</json:string><json:string>Hornsleth et al., 1998</json:string><json:string>Kariwa et al., 2004</json:string><json:string>Fujii et al., 2004</json:string><json:string>Huang et al., 2005</json:string><json:string>Talon et al., 2000</json:string><json:string>Island et al., 2002</json:string><json:string>Gongora et al., 1997</json:string><json:string>Zhang et al., 2004</json:string><json:string>Sung et al., 2001</json:string><json:string>Li et al., 2003</json:string><json:string>Hong et al., 2004</json:string><json:string>Ramaswamy et al., 2004</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-FQB1SXHD-6</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - virology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - virology</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Infectious Diseases</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Virology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et 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type="first">Tamaki</forename><surname>Okabayashi</surname></persName><affiliation><orgName type="department">Department of Microbiology</orgName><orgName type="institution">Sapporo Medical University School of Medicine</orgName><address><addrLine>Chuo‐ku</addrLine><addrLine>Sapporo, Hokkaido, Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Hiroaki</forename><surname>Kariwa</surname></persName><affiliation><orgName type="laboratory">Laboratory of Public Health</orgName><orgName type="division">Department of Environmental Veterinary Sciences</orgName><orgName type="department">Graduate School of Veterinary Medicine</orgName><orgName type="institution">Hokkaido University</orgName><address><addrLine>Hokkaido</addrLine><addrLine>Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Shin‐ichi</forename><surname>Yokota</surname></persName><affiliation><orgName type="department">Department of Microbiology</orgName><orgName type="institution">Sapporo Medical University School of Medicine</orgName><address><addrLine>Chuo‐ku</addrLine><addrLine>Sapporo, Hokkaido, Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Shigeo</forename><surname>Iki</surname></persName><affiliation><orgName type="department">Department of Microbiology</orgName><orgName type="institution">Sapporo Medical University School of Medicine</orgName><address><addrLine>Chuo‐ku</addrLine><addrLine>Sapporo, Hokkaido, Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Tomokazu</forename><surname>Indoh</surname></persName><affiliation><orgName type="department">Department of 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type="main">Abstract</title><p>The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS‐CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS‐CoV infection. Therefore, SARS‐CoV replication was suppressed by pretreatment with IFN. SARS‐CoV and RSV induced high levels of IL‐6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling‐3 (SOCS3) by SARS‐CoV was significantly lower than that by RSV in spite of the significant production of IL‐6. Toll‐like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS‐CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with “severe” inflammation in SARS. <i>J. Med. Virol.</i> 78:417–424, 2006. © 2006 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>This work was performed at Department of Microbiology, Sapporo Medical University School of Medicine, Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, and Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>SARS‐CoV and Cytokines</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections</title></titleInfo><name type="personal"><namePart type="given">Tamaki</namePart><namePart type="family">Okabayashi</namePart><affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hiroaki</namePart><namePart type="family">Kariwa</namePart><affiliation>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shin‐ichi</namePart><namePart type="family">Yokota</namePart><affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shigeo</namePart><namePart type="family">Iki</namePart><affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tomokazu</namePart><namePart type="family">Indoh</namePart><affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Noriko</namePart><namePart type="family">Yokosawa</namePart><affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ikuo</namePart><namePart type="family">Takashima</namePart><affiliation>Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hiroyuki</namePart><namePart type="family">Tsutsumi</namePart><affiliation>Department of Pediatrics, Sapporo Medical University School of Medicine, Hokkaido, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nobuhiro</namePart><namePart type="family">Fujii</namePart><affiliation>Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan</affiliation><affiliation>E-mail: fujii@sapmed.ac.jp</affiliation><affiliation>Correspondence address: Department of Microbiology, Sapporo Medical University School of Medicine, South‐1, West‐17, Chuo‐ku, Sapporo 060‐8556, Hokkaido, Japan.===</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2006-04</dateIssued><dateValid encoding="w3cdtf">2005-12-12</dateValid><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">5</extent><extent unit="tables">2</extent><extent unit="references">51</extent><extent unit="words">1531</extent></physicalDescription><abstract lang="en">The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS‐CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS‐CoV infection. Therefore, SARS‐CoV replication was suppressed by pretreatment with IFN. SARS‐CoV and RSV induced high levels of IL‐6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling‐3 (SOCS3) by SARS‐CoV was significantly lower than that by RSV in spite of the significant production of IL‐6. Toll‐like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS‐CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with “severe” inflammation in SARS. J. Med. Virol. 78:417–424, 2006. © 2006 Wiley‐Liss, Inc.</abstract><note type="content">*This work was performed at Department of Microbiology, Sapporo Medical University School of Medicine, Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, and Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases.</note><subject lang="en"><genre>keywords</genre><topic>SARS‐CoV</topic><topic>SOCS3</topic><topic>cytokine</topic><topic>IL‐6</topic><topic>IFN</topic><topic>TLR</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Medical Virology</title></titleInfo><titleInfo type="abbreviated"><title>J. Med. Virol.</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>article-category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0146-6615</identifier><identifier type="eISSN">1096-9071</identifier><identifier type="DOI">10.1002/(ISSN)1096-9071</identifier><identifier type="PublisherID">JMV</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>78</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>417</start><end>424</end><total>8</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>Degradation of STAT1 and STAT2 by the V proteins of simian virus 5 and human parainfluenza virus type 2, respectively: Consequences for virus replication in the presence of alpha/beta and gamma interferons</title></titleInfo><name type="personal"><namePart type="given">J</namePart><namePart type="family">Andrejeva</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DF</namePart><namePart type="family">Young</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Goodbourn</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RE</namePart><namePart type="family">Randall</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Andrejeva J, Young DF, Goodbourn S, Randall RE. 2002. Degradation of STAT1 and STAT2 by the V proteins of simian virus 5 and human parainfluenza virus type 2, respectively: Consequences for virus replication in the presence of alpha/beta and gamma interferons. J Virol 76: 2159–2167.</note><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>76</number></detail><extent unit="pages"><start>2159</start><end>2167</end></extent></part><relatedItem type="host"><titleInfo><title>J Virol</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>76</number></detail><extent unit="pages"><start>2159</start><end>2167</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit2"><titleInfo><title>Interaction between neutrophils and chemokines in blood and alveolar spaces during ARDS</title></titleInfo><name type="personal"><namePart type="given">S</namePart><namePart type="family">Chollet‐Martin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Jourdain</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Gibert</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Elbim</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Chastre</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MA</namePart><namePart type="family">Gougerot‐Pocidalo</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Chollet‐Martin S, Jourdain B, Gibert C, Elbim C, Chastre J, Gougerot‐Pocidalo MA. 1996. Interaction between neutrophils and chemokines in blood and alveolar spaces during ARDS. Am J Respir Crit Care Med 154: 594–601.</note><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>154</number></detail><extent unit="pages"><start>594</start><end>601</end></extent></part><relatedItem type="host"><titleInfo><title>Am J Respir Crit Care Med</title></titleInfo><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>154</number></detail><extent unit="pages"><start>594</start><end>601</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit3"><titleInfo><title>Role of interferons in the treatment of severe acute respiratory syndrome</title></titleInfo><name type="personal"><namePart type="given">J</namePart><namePart type="family">Cinatl Jr.</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Michaelis</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Scholz</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HW</namePart><namePart type="family">Doerr</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Cinatl J, Jr., Michaelis M, Scholz M, Doerr HW. 2004. Role of interferons in the treatment of severe acute respiratory syndrome. Expert Opin Biol Ther 4: 827–836.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>827</start><end>836</end></extent></part><relatedItem type="host"><titleInfo><title>Expert Opin Biol Ther</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>827</start><end>836</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit4"><titleInfo><title>2‐5A and virus infection</title></titleInfo><name type="personal"><namePart type="given">N</namePart><namePart type="family">Fujii</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Fujii N. 1994. 2‐5A and virus infection. Prog Mol Subcell Biol 14: 150–175.</note><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>14</number></detail><extent unit="pages"><start>150</start><end>175</end></extent></part><relatedItem type="host"><titleInfo><title>Prog Mol Subcell Biol</title></titleInfo><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>14</number></detail><extent unit="pages"><start>150</start><end>175</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit5"><titleInfo><title>Current concepts in SARS treatment</title></titleInfo><name type="personal"><namePart type="given">T</namePart><namePart type="family">Fujii</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Nakamura</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Iwamoto</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Fujii T, Nakamura T, Iwamoto A. 2004. Current concepts in SARS treatment. J Infect Chemother 10: 1–7.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>1</start><end>7</end></extent></part><relatedItem type="host"><titleInfo><title>J Infect Chemother</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>1</start><end>7</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit6"><titleInfo><title>Relationships among specific viral pathogens, virus‐induced interleukin‐8, and respiratory symptoms in infancy</title></titleInfo><name type="personal"><namePart type="given">JE</namePart><namePart type="family">Gern</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MS</namePart><namePart type="family">Martin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KA</namePart><namePart type="family">Anklam</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Shen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KA</namePart><namePart type="family">Roberg</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KT</namePart><namePart type="family">Carlson‐Dakes</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Adler</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Gilbertson‐White</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Hamilton</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PA</namePart><namePart type="family">Shult</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CJ</namePart><namePart type="family">Kirk</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DF</namePart><namePart type="family">Da Silva</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SA</namePart><namePart type="family">Sund</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MR</namePart><namePart type="family">Kosorok</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RF</namePart><namePart type="family">Lemanske Jr.</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Gern JE, Martin MS, Anklam KA, Shen K, Roberg KA, Carlson‐Dakes KT, Adler K, Gilbertson‐White S, Hamilton R, Shult PA, Kirk CJ, Da Silva DF, Sund SA, Kosorok MR, Lemanske RF, Jr. 2002. Relationships among specific viral pathogens, virus‐induced interleukin‐8, and respiratory symptoms in infancy. Pediatr Allergy Immunol 13: 386–393.</note><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>386</start><end>393</end></extent></part><relatedItem type="host"><titleInfo><title>Pediatr Allergy Immunol</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>386</start><end>393</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit7"><titleInfo><title>Molecular cloning of a new interferon‐induced PML nuclear body‐associated protein</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Gongora</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">David</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Pintard</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Tissot</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">TD</namePart><namePart type="family">Hua</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Dejean</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Mechti</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Gongora C, David G, Pintard L, Tissot C, Hua TD, Dejean A, Mechti N. 1997. Molecular cloning of a new interferon‐induced PML nuclear body‐associated protein. J Biol Chem 272: 19457–19463.</note><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>272</number></detail><extent unit="pages"><start>19457</start><end>19463</end></extent></part><relatedItem type="host"><titleInfo><title>J Biol Chem</title></titleInfo><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>272</number></detail><extent unit="pages"><start>19457</start><end>19463</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit8"><titleInfo><title>Interferons: Cell signalling, immune modulation, antiviral response and virus countermeasures</title></titleInfo><name type="personal"><namePart type="given">S</namePart><namePart type="family">Goodbourn</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Didcock</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RE</namePart><namePart type="family">Randall</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Goodbourn S, Didcock L, Randall RE. 2000. Interferons: Cell signalling, immune modulation, antiviral response and virus countermeasures. J Gen Virol 81: 2341–2364.</note><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>81</number></detail><extent unit="pages"><start>2341</start><end>2364</end></extent></part><relatedItem type="host"><titleInfo><title>J Gen Virol</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>81</number></detail><extent unit="pages"><start>2341</start><end>2364</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit9"><titleInfo><title>A Toll‐like receptor recognizes bacterial DNA</title></titleInfo><name type="personal"><namePart type="given">H</namePart><namePart type="family">Hemmi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O</namePart><namePart type="family">Takeuchi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Kawai</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Kaisho</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Sato</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Sanjo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Matsumoto</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Hoshino</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Wagner</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Takeda</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Akira</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Hemmi H, Takeuchi O, Kawai T, Kaisho T, Sato S, Sanjo H, Matsumoto M, Hoshino K, Wagner H, Takeda K, Akira S. 2000. A Toll‐like receptor recognizes bacterial DNA. Nature 408: 740–745.</note><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>408</number></detail><extent unit="pages"><start>740</start><end>745</end></extent></part><relatedItem type="host"><titleInfo><title>Nature</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>408</number></detail><extent unit="pages"><start>740</start><end>745</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit10"><titleInfo><title>Cytokine responses in sever acute respiratory syndrome coronavirus‐infected macrophages in vitro: Possible relevance to pathogenesis</title></titleInfo><name type="personal"><namePart type="given">CY</namePart><namePart type="family">Heung</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LLM</namePart><namePart type="family">Poon</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">IHY</namePart><namePart type="family">Ng</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Luk</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Sia</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MHS</namePart><namePart type="family">Wu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Chan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Yuen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Gordon</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Guan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JSM</namePart><namePart type="family">Peiris</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Heung CY, Poon LLM, Ng IHY, Luk W, Sia S, Wu MHS, Chan K, Yuen K, Gordon S, Guan Y, Peiris JSM. 2005. Cytokine responses in sever acute respiratory syndrome coronavirus‐infected macrophages in vitro: Possible relevance to pathogenesis. J Virol 79: 7819–7826.</note><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>79</number></detail><extent unit="pages"><start>7819</start><end>7826</end></extent></part><relatedItem type="host"><titleInfo><title>J Virol</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>79</number></detail><extent unit="pages"><start>7819</start><end>7826</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit11"><titleInfo><title>Interactions between respiratory tract infections and atopy in the aetiology of asthma</title></titleInfo><name type="personal"><namePart type="given">PG</namePart><namePart type="family">Holt</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PD</namePart><namePart type="family">Sly</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Holt PG, Sly PD. 2002. Interactions between respiratory tract infections and atopy in the aetiology of asthma. Eur Respir J 19: 538–545.</note><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>19</number></detail><extent unit="pages"><start>538</start><end>545</end></extent></part><relatedItem type="host"><titleInfo><title>Eur Respir J</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>19</number></detail><extent unit="pages"><start>538</start><end>545</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit12"><titleInfo><title>Development and evaluation of a novel loop‐mediated isothermal amplification method for rapid detection of severe acute respiratory syndrome coronavirus</title></titleInfo><name type="personal"><namePart type="given">TC</namePart><namePart type="family">Hong</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">QL</namePart><namePart type="family">Mai</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DV</namePart><namePart type="family">Cuong</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Parida</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Minekawa</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Notomi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Hasebe</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Morita</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Hong TC, Mai QL, Cuong DV, Parida M, Minekawa H, Notomi T, Hasebe F, Morita K. 2004. Development and evaluation of a novel loop‐mediated isothermal amplification method for rapid detection of severe acute respiratory syndrome coronavirus. J Clin Microbiol 42: 1956–1961.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>42</number></detail><extent unit="pages"><start>1956</start><end>1961</end></extent></part><relatedItem type="host"><titleInfo><title>J Clin Microbiol</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>42</number></detail><extent unit="pages"><start>1956</start><end>1961</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit13"><titleInfo><title>Severity of respiratory syncytial virus disease related to type and genotype of virus and to cytokine values in nasopharyngeal secretions</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Hornsleth</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Klug</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Nir</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Johansen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KS</namePart><namePart type="family">Hansen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LS</namePart><namePart type="family">Christensen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LB</namePart><namePart type="family">Larsen</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Hornsleth A, Klug B, Nir M, Johansen J, Hansen KS, Christensen LS, Larsen LB. 1998. Severity of respiratory syncytial virus disease related to type and genotype of virus and to cytokine values in nasopharyngeal secretions. Pediatr Infect Dis J 17: 1114–1121.</note><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>1114</start><end>1121</end></extent></part><relatedItem type="host"><titleInfo><title>Pediatr Infect Dis J</title></titleInfo><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>1114</start><end>1121</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit14"><titleInfo><title>An interferon‐gamma‐related cytokine storm in SARS patients</title></titleInfo><name type="personal"><namePart type="given">KJ</namePart><namePart type="family">Huang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">IJ</namePart><namePart type="family">Su</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Theron</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YC</namePart><namePart type="family">Wu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SK</namePart><namePart type="family">Lai</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CC</namePart><namePart type="family">Liu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HY</namePart><namePart type="family">Lei</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Huang KJ, Su IJ, Theron M, Wu YC, Lai SK, Liu CC, Lei HY. 2005. An interferon‐gamma‐related cytokine storm in SARS patients. J Med Virol 75: 185–194.</note><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>75</number></detail><extent unit="pages"><start>185</start><end>194</end></extent></part><relatedItem type="host"><titleInfo><title>J Med Virol</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>75</number></detail><extent unit="pages"><start>185</start><end>194</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit15"><titleInfo><title>Repression by homeoprotein pitx1 of virus‐induced interferon a promoters is mediated by physical interaction and trans repression of IRF3 and IRF7</title></titleInfo><name type="personal"><namePart type="given">ML</namePart><namePart type="family">Island</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Mesplede</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Darracq</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MT</namePart><namePart type="family">Bandu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Christeff</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Djian</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Drouin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Navarro</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Island ML, Mesplede T, Darracq N, Bandu MT, Christeff N, Djian P, Drouin J, Navarro S. 2002. Repression by homeoprotein pitx1 of virus‐induced interferon a promoters is mediated by physical interaction and trans repression of IRF3 and IRF7. Mol Cell Biol 22: 7120–7133.</note><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><extent unit="pages"><start>7120</start><end>7133</end></extent></part><relatedItem type="host"><titleInfo><title>Mol Cell Biol</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><extent unit="pages"><start>7120</start><end>7133</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit16"><titleInfo><title>Inactivation of SARS coronavirus by means of povidone‐iodine, physical conditions, and chemical reagents</title></titleInfo><name type="personal"><namePart type="given">H</namePart><namePart type="family">Kariwa</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Fujii</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I</namePart><namePart type="family">Takashima</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Kariwa H, Fujii N, Takashima I. 2004. Inactivation of SARS coronavirus by means of povidone‐iodine, physical conditions, and chemical reagents. Jpn J Vet Res 52: 105–112.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>52</number></detail><extent unit="pages"><start>105</start><end>112</end></extent></part><relatedItem type="host"><titleInfo><title>Jpn J Vet Res</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>52</number></detail><extent unit="pages"><start>105</start><end>112</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit17"><titleInfo><title>Suppressors of cytokine signaling and immunity</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Kubo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Hanada</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Yoshimura</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Kubo M, Hanada T, Yoshimura A. 2003. Suppressors of cytokine signaling and immunity. Nat Immunol 4: 1169–1176.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>1169</start><end>1176</end></extent></part><relatedItem type="host"><titleInfo><title>Nat Immunol</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>1169</start><end>1176</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit18"><titleInfo><title>SOCS3 regulates the plasticity of gp130 signaling</title></titleInfo><name type="personal"><namePart type="given">R</namePart><namePart type="family">Lang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AL</namePart><namePart type="family">Pauleau</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Parganas</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Takahashi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Mages</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JN</namePart><namePart type="family">Ihle</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Rutschman</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PJ</namePart><namePart type="family">Murray</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Lang R, Pauleau AL, Parganas E, Takahashi Y, Mages J, Ihle JN, Rutschman R, Murray PJ. 2003. SOCS3 regulates the plasticity of gp130 signaling. Nat Immunol 4: 546–550.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>546</start><end>550</end></extent></part><relatedItem type="host"><titleInfo><title>Nat Immunol</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>546</start><end>550</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit19"><titleInfo><title>Enteric involvement of severe acute respiratory syndrome‐associated coronavirus infection</title></titleInfo><name type="personal"><namePart type="given">WK</namePart><namePart type="family">Leung</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KF</namePart><namePart type="family">To</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PK</namePart><namePart type="family">Chan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HL</namePart><namePart type="family">Chan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AK</namePart><namePart type="family">Wu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Lee</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KY</namePart><namePart type="family">Yuen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JJ</namePart><namePart type="family">Sung</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Leung WK, To KF, Chan PK, Chan HL, Wu AK, Lee N, Yuen KY, Sung JJ. 2003. Enteric involvement of severe acute respiratory syndrome‐associated coronavirus infection. Gastroenterology 125: 1011–1017.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>125</number></detail><extent unit="pages"><start>1011</start><end>1017</end></extent></part><relatedItem type="host"><titleInfo><title>Gastroenterology</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>125</number></detail><extent unit="pages"><start>1011</start><end>1017</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit20"><titleInfo><title>Angiotensin‐converting enzyme 2 is a functional receptor for the SARS coronavirus</title></titleInfo><name type="personal"><namePart type="given">W</namePart><namePart type="family">Li</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MJ</namePart><namePart type="family">Moore</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Vasilieva</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Sui</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SK</namePart><namePart type="family">Wong</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MA</namePart><namePart type="family">Berne</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Somasundaran</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Sullivan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Luzuriaga</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">TC</namePart><namePart type="family">Greenough</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Choe</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Farzan</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Li W, Moore MJ, Vasilieva N, Sui J, Wong SK, Berne MA, Somasundaran M, Sullivan JL, Luzuriaga K, Greenough TC, Choe H, Farzan M. 2003. Angiotensin‐converting enzyme 2 is a functional receptor for the SARS coronavirus. Nature 426: 450–454.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>426</number></detail><extent unit="pages"><start>450</start><end>454</end></extent></part><relatedItem type="host"><titleInfo><title>Nature</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>426</number></detail><extent unit="pages"><start>450</start><end>454</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit21"><titleInfo><title>Recognition of single‐stranded RNA viruses by Toll‐like receptor 7</title></titleInfo><name type="personal"><namePart type="given">JM</namePart><namePart type="family">Lund</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Alexopoulou</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Sato</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Karow</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">NC</namePart><namePart type="family">Adams</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">NW</namePart><namePart type="family">Gale</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Iwasaki</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RA</namePart><namePart type="family">Flavell</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Lund JM, Alexopoulou L, Sato A, Karow M, Adams NC, Gale NW, Iwasaki A, Flavell RA. 2004. Recognition of single‐stranded RNA viruses by Toll‐like receptor 7. Proc Natl Acad Sci USA 101: 5598–5603.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>101</number></detail><extent unit="pages"><start>5598</start><end>5603</end></extent></part><relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>101</number></detail><extent unit="pages"><start>5598</start><end>5603</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit22"><titleInfo><title>Tyrosine dephosphorylation of STAT3 in SARS coronavirus‐infected Vero E6 cells</title></titleInfo><name type="personal"><namePart type="given">T</namePart><namePart type="family">Mizutani</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Fukushi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Murakami</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Hirano</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Saijo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I</namePart><namePart type="family">Kurane</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Morikawa</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Mizutani T, Fukushi S, Murakami M, Hirano T, Saijo M, Kurane I, Morikawa S. 2004a. Tyrosine dephosphorylation of STAT3 in SARS coronavirus‐infected Vero E6 cells. FEBS Lett 577: 187–192.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>577</number></detail><extent unit="pages"><start>187</start><end>192</end></extent></part><relatedItem type="host"><titleInfo><title>FEBS Lett</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>577</number></detail><extent unit="pages"><start>187</start><end>192</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit23"><titleInfo><title>Importance of Akt signaling pathway for apoptosis in SARS‐CoV‐infected Vero E6 cells</title></titleInfo><name type="personal"><namePart type="given">T</namePart><namePart type="family">Mizutani</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Fukushi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Saijo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I</namePart><namePart type="family">Kurane</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Morikawa</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Mizutani T, Fukushi S, Saijo M, Kurane I, Morikawa S. 2004b. Importance of Akt signaling pathway for apoptosis in SARS‐CoV‐infected Vero E6 cells. Virology 327: 169–174.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>327</number></detail><extent unit="pages"><start>169</start><end>174</end></extent></part><relatedItem type="host"><titleInfo><title>Virology</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>327</number></detail><extent unit="pages"><start>169</start><end>174</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit24"><titleInfo><title>Phosphorylation of p38 MAPK and its downstream targets in SARS coronavirus‐infected cells</title></titleInfo><name type="personal"><namePart type="given">T</namePart><namePart type="family">Mizutani</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Fukushi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Saijo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I</namePart><namePart type="family">Kurane</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Morikawa</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Mizutani T, Fukushi S, Saijo M, Kurane I, Morikawa S. 2004c. Phosphorylation of p38 MAPK and its downstream targets in SARS coronavirus‐infected cells. Biochem Biophys Res Commun 319: 1228–1234.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>319</number></detail><extent unit="pages"><start>1228</start><end>1234</end></extent></part><relatedItem type="host"><titleInfo><title>Biochem Biophys Res Commun</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>319</number></detail><extent unit="pages"><start>1228</start><end>1234</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit25"><titleInfo><title>Respiratory syncytial virus up‐regulates TLR4 and sensitizes airway epithelial cells to endotoxin</title></titleInfo><name type="personal"><namePart type="given">MM</namePart><namePart type="family">Monick</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">TO</namePart><namePart type="family">Yarovinsky</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LS</namePart><namePart type="family">Powers</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">NS</namePart><namePart type="family">Butler</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AB</namePart><namePart type="family">Carter</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Gudmundsson</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GW</namePart><namePart type="family">Hunninghake</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Monick MM, Yarovinsky TO, Powers LS, Butler NS, Carter AB, Gudmundsson G, Hunninghake GW. 2003. Respiratory syncytial virus up‐regulates TLR4 and sensitizes airway epithelial cells to endotoxin. J Biol Chem 278: 53035–53044.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>278</number></detail><extent unit="pages"><start>53035</start><end>53044</end></extent></part><relatedItem type="host"><titleInfo><title>J Biol Chem</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>278</number></detail><extent unit="pages"><start>53035</start><end>53044</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit26"><titleInfo><title>Ribavirin and interferon‐beta synergistically inhibit SARS‐associated coronavirus replication in animal and human cell lines</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Morgenstern</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Michaelis</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PC</namePart><namePart type="family">Baer</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HW</namePart><namePart type="family">Doerr</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Cinatl Jr.</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Morgenstern B, Michaelis M, Baer PC, Doerr HW, Cinatl J, Jr. 2005. Ribavirin and interferon‐beta synergistically inhibit SARS‐associated coronavirus replication in animal and human cell lines. Biochem Biophys Res Commun 326: 905–908.</note><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>326</number></detail><extent unit="pages"><start>905</start><end>908</end></extent></part><relatedItem type="host"><titleInfo><title>Biochem Biophys Res Commun</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>326</number></detail><extent unit="pages"><start>905</start><end>908</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit27"><titleInfo><title>Lung pathology of fatal severe acute respiratory syndrome</title></titleInfo><name type="personal"><namePart type="given">JM</namePart><namePart type="family">Nicholls</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LL</namePart><namePart type="family">Poon</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KC</namePart><namePart type="family">Lee</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">WF</namePart><namePart type="family">Ng</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ST</namePart><namePart type="family">Lai</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CY</namePart><namePart type="family">Leung</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CM</namePart><namePart type="family">Chu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PK</namePart><namePart type="family">Hui</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KL</namePart><namePart type="family">Mak</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Lim</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KW</namePart><namePart type="family">Yan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KH</namePart><namePart type="family">Chan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">NC</namePart><namePart type="family">Tsang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Guan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KY</namePart><namePart type="family">Yuen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JS</namePart><namePart type="family">Peiris</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Nicholls JM, Poon LL, Lee KC, Ng WF, Lai ST, Leung CY, Chu CM, Hui PK, Mak KL, Lim W, Yan KW, Chan KH, Tsang NC, Guan Y, Yuen KY, Peiris JS. 2003. Lung pathology of fatal severe acute respiratory syndrome. Lancet 361: 1773–1778.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>361</number></detail><extent unit="pages"><start>1773</start><end>1778</end></extent></part><relatedItem type="host"><titleInfo><title>Lancet</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>361</number></detail><extent unit="pages"><start>1773</start><end>1778</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit28"><titleInfo><title>Clinical progression and viral load in a community outbreak of coronavirus‐associated SARS pneumonia: A prospective study</title></titleInfo><name type="personal"><namePart type="given">JS</namePart><namePart type="family">Peiris</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CM</namePart><namePart type="family">Chu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">VC</namePart><namePart type="family">Cheng</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KS</namePart><namePart type="family">Chan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">IF</namePart><namePart type="family">Hung</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LL</namePart><namePart type="family">Poon</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KI</namePart><namePart type="family">Law</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">BS</namePart><namePart type="family">Tang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">TY</namePart><namePart type="family">Hon</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CS</namePart><namePart type="family">Chan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KH</namePart><namePart type="family">Chan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JS</namePart><namePart type="family">Ng</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">BJ</namePart><namePart type="family">Zheng</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">WL</namePart><namePart type="family">Ng</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RW</namePart><namePart type="family">Lai</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Guan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KY</namePart><namePart type="family">Yuen</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Peiris JS, Chu CM, Cheng VC, Chan KS, Hung IF, Poon LL, Law KI, Tang BS, Hon TY, Chan CS, Chan KH, Ng JS, Zheng BJ, Ng WL, Lai RW, Guan Y, Yuen KY. 2003. Clinical progression and viral load in a community outbreak of coronavirus‐associated SARS pneumonia: A prospective study. Lancet 361: 1767–1772.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>361</number></detail><extent unit="pages"><start>1767</start><end>1772</end></extent></part><relatedItem type="host"><titleInfo><title>Lancet</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>361</number></detail><extent unit="pages"><start>1767</start><end>1772</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit29"><titleInfo><title>Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: Mutations in Tlr4 gene</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Poltorak</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">X</namePart><namePart type="family">He</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I</namePart><namePart type="family">Smirnova</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MY</namePart><namePart type="family">Liu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Van Huffel</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">X</namePart><namePart type="family">Du</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Birdwell</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Alejos</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Silva</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Galanos</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Freudenberg</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Ricciardi‐Castagnoli</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Layton</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Beutler</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Poltorak A, He X, Smirnova I, Liu MY, Van Huffel C, Du X, Birdwell D, Alejos E, Silva M, Galanos C, Freudenberg M, Ricciardi‐Castagnoli P, Layton B, Beutler B. 1998. Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: Mutations in Tlr4 gene. Science 282: 2085–2088.</note><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>282</number></detail><extent unit="pages"><start>2085</start><end>2088</end></extent></part><relatedItem type="host"><titleInfo><title>Science</title></titleInfo><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>282</number></detail><extent unit="pages"><start>2085</start><end>2088</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit30"><titleInfo><title>The V proteins of simian virus 5 and other paramyxoviruses inhibit induction of interferon‐beta</title></titleInfo><name type="personal"><namePart type="given">E</namePart><namePart type="family">Poole</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">He</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RA</namePart><namePart type="family">Lamb</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RE</namePart><namePart type="family">Randall</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Goodbourn</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Poole E, He B, Lamb RA, Randall RE, Goodbourn S. 2002. The V proteins of simian virus 5 and other paramyxoviruses inhibit induction of interferon‐beta. Virology 303: 33–46.</note><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>303</number></detail><extent unit="pages"><start>33</start><end>46</end></extent></part><relatedItem type="host"><titleInfo><title>Virology</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>303</number></detail><extent unit="pages"><start>33</start><end>46</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit31"><titleInfo><title>Specific inhibition of type I interferon signal transduction by respiratory syncytial virus</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Ramaswamy</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Shi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MM</namePart><namePart type="family">Monick</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GW</namePart><namePart type="family">Hunninghake</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DC</namePart><namePart type="family">Look</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Ramaswamy M, Shi L, Monick MM, Hunninghake GW, Look DC. 2004. Specific inhibition of type I interferon signal transduction by respiratory syncytial virus. Am J Respir Cell Mol Biol 30: 893–900.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>30</number></detail><extent unit="pages"><start>893</start><end>900</end></extent></part><relatedItem type="host"><titleInfo><title>Am J Respir Cell Mol Biol</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>30</number></detail><extent unit="pages"><start>893</start><end>900</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit32"><titleInfo><title>Interferon‐beta and interferon‐gamma synergistically inhibit the replication of severe acute respiratory syndrome‐associated coronavirus (SARS‐CoV)</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Sainz Jr.</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">EC</namePart><namePart type="family">Mossel</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CJ</namePart><namePart type="family">Peters</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RF</namePart><namePart type="family">Garry</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Sainz B, Jr., Mossel EC, Peters CJ, Garry RF. 2004. Interferon‐beta and interferon‐gamma synergistically inhibit the replication of severe acute respiratory syndrome‐associated coronavirus (SARS‐CoV). Virology 329: 11–17.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>329</number></detail><extent unit="pages"><start>11</start><end>17</end></extent></part><relatedItem type="host"><titleInfo><title>Virology</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>329</number></detail><extent unit="pages"><start>11</start><end>17</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit33"><titleInfo><title>Antiviral actions of interferon. Interferon‐regulated cellular proteins and their surprisingly selective antiviral activities</title></titleInfo><name type="personal"><namePart type="given">CE</namePart><namePart type="family">Samuel</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Samuel CE. 1991. Antiviral actions of interferon. Interferon‐regulated cellular proteins and their surprisingly selective antiviral activities. Virology 183: 1–11.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>183</number></detail><extent unit="pages"><start>1</start><end>11</end></extent></part><relatedItem type="host"><titleInfo><title>Virology</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>183</number></detail><extent unit="pages"><start>1</start><end>11</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit34"><titleInfo><title>Distinct and essential roles of transcription factors IRF‐3 and IRF‐7 in response to viruses for IFN‐alpha/beta gene induction</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Sato</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Suemori</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Hata</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Asagiri</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Ogasawara</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Nakao</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Nakaya</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Katsuki</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Noguchi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Tanaka</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Taniguchi</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Sato M, Suemori H, Hata N, Asagiri M, Ogasawara K, Nakao K, Nakaya T, Katsuki M, Noguchi S, Tanaka N, Taniguchi T. 2000. Distinct and essential roles of transcription factors IRF‐3 and IRF‐7 in response to viruses for IFN‐alpha/beta gene induction. Immunity 13: 539–548.</note><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>539</start><end>548</end></extent></part><relatedItem type="host"><titleInfo><title>Immunity</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>539</start><end>548</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit35"><titleInfo><title>SOCS‐3 regulates onset and maintenance of T(H)2‐mediated allergic responses</title></titleInfo><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Seki</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Inoue</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Nagata</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Hayashi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Fukuyama</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Matsumoto</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O</namePart><namePart type="family">Komine</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Hamano</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Himeno</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Inagaki‐Ohara</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Cacalano</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">O'Garra</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Oshida</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Saito</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JA</namePart><namePart type="family">Johnston</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Yoshimura</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Kubo</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Seki Y, Inoue H, Nagata N, Hayashi K, Fukuyama S, Matsumoto K, Komine O, Hamano S, Himeno K, Inagaki‐Ohara K, Cacalano N, O'Garra A, Oshida T, Saito H, Johnston JA, Yoshimura A, Kubo M. 2003. SOCS‐3 regulates onset and maintenance of T(H)2‐mediated allergic responses. Nat Med 9: 1047–1054.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>1047</start><end>1054</end></extent></part><relatedItem type="host"><titleInfo><title>Nat Med</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>1047</start><end>1054</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit36"><titleInfo><title>Interferon‐induced antiviral actions and their regulation</title></titleInfo><name type="personal"><namePart type="given">GC</namePart><namePart type="family">Sen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RM</namePart><namePart type="family">Ransohoff</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Sen GC, Ransohoff RM. 1993. Interferon‐induced antiviral actions and their regulation. Adv Virus Res 42: 57–102.</note><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>42</number></detail><extent unit="pages"><start>57</start><end>102</end></extent></part><relatedItem type="host"><titleInfo><title>Adv Virus Res</title></titleInfo><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>42</number></detail><extent unit="pages"><start>57</start><end>102</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit37"><titleInfo><title>Respiratory syncytial virus bronchiolitis in infancy is an important risk factor for asthma and allergy at age 7</title></titleInfo><name type="personal"><namePart type="given">N</namePart><namePart type="family">Sigurs</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Bjarnason</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Sigurbergsson</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Kjellman</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Sigurs N, Bjarnason R, Sigurbergsson F, Kjellman B. 2000. Respiratory syncytial virus bronchiolitis in infancy is an important risk factor for asthma and allergy at age 7. Am J Respir Crit Care Med 161: 1501–1507.</note><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>161</number></detail><extent unit="pages"><start>1501</start><end>1507</end></extent></part><relatedItem type="host"><titleInfo><title>Am J Respir Crit Care Med</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>161</number></detail><extent unit="pages"><start>1501</start><end>1507</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit38"><titleInfo><title>Inhibition of beta interferon induction by severe acute respiratory syndrome coronaviruse suggests a two‐step model for activation of interferon regulatory factor 3</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Spiegel</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Pichlmair</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Martinez‐Sobrido</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Cros</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Garcia‐Sastre</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O</namePart><namePart type="family">Haller</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Weber</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Spiegel M, Pichlmair A, Martinez‐Sobrido L, Cros J, Garcia‐Sastre A, Haller O, Weber F. 2005. Inhibition of beta interferon induction by severe acute respiratory syndrome coronaviruse suggests a two‐step model for activation of interferon regulatory factor 3. J Virol 79: 2079–2086.</note><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>79</number></detail><extent unit="pages"><start>2079</start><end>2086</end></extent></part><relatedItem type="host"><titleInfo><title>J Virol</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>79</number></detail><extent unit="pages"><start>2079</start><end>2086</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit39"><titleInfo><title>How cells respond to interferons</title></titleInfo><name type="personal"><namePart type="given">GR</namePart><namePart type="family">Stark</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">IM</namePart><namePart type="family">Kerr</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">BR</namePart><namePart type="family">Williams</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RH</namePart><namePart type="family">Silverman</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RD</namePart><namePart type="family">Schreiber</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Stark GR, Kerr IM, Williams BR, Silverman RH, Schreiber RD. 1998. How cells respond to interferons. Annu Rev Biochem 67: 227–264.</note><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>67</number></detail><extent unit="pages"><start>227</start><end>264</end></extent></part><relatedItem type="host"><titleInfo><title>Annu Rev Biochem</title></titleInfo><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>67</number></detail><extent unit="pages"><start>227</start><end>264</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit40"><titleInfo><title>A comparison of cytokine responses in respiratory syncytial virus and influenza A infections in infants</title></titleInfo><name type="personal"><namePart type="given">RY</namePart><namePart type="family">Sung</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SH</namePart><namePart type="family">Hui</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CK</namePart><namePart type="family">Wong</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CW</namePart><namePart type="family">Lam</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Yin</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Sung RY, Hui SH, Wong CK, Lam CW, Yin J. 2001. A comparison of cytokine responses in respiratory syncytial virus and influenza A infections in infants. Eur J Pediatr 160: 117–122.</note><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>160</number></detail><extent unit="pages"><start>117</start><end>122</end></extent></part><relatedItem type="host"><titleInfo><title>Eur J Pediatr</title></titleInfo><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>160</number></detail><extent unit="pages"><start>117</start><end>122</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit41"><titleInfo><title>Roles of Toll‐like receptors in innate immune responses</title></titleInfo><name type="personal"><namePart type="given">K</namePart><namePart type="family">Takeda</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Akira</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Takeda K, Akira S. 2001. Roles of Toll‐like receptors in innate immune responses. Genes Cells 6: 733–742.</note><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>6</number></detail><extent unit="pages"><start>733</start><end>742</end></extent></part><relatedItem type="host"><titleInfo><title>Genes Cells</title></titleInfo><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>6</number></detail><extent unit="pages"><start>733</start><end>742</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit42"><titleInfo><title>Activation of interferon regulatory factor 3 is inhibited by the influenza A virus NS1 protein</title></titleInfo><name type="personal"><namePart type="given">J</namePart><namePart type="family">Talon</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CM</namePart><namePart type="family">Horvath</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Polley</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CF</namePart><namePart type="family">Basler</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Muster</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Palese</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Garcia‐Sastre</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Talon J, Horvath CM, Polley R, Basler CF, Muster T, Palese P, Garcia‐Sastre A. 2000. Activation of interferon regulatory factor 3 is inhibited by the influenza A virus NS1 protein. J Virol 74: 7989–7996.</note><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>74</number></detail><extent unit="pages"><start>7989</start><end>7996</end></extent></part><relatedItem type="host"><titleInfo><title>J Virol</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>74</number></detail><extent unit="pages"><start>7989</start><end>7996</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit43"><titleInfo><title>Exploring the pathogenesis of severe acute respiratory syndrome (SARS): The tissue distribution of the coronavirus (SARS‐CoV) and its putative receptor, angiotensin‐converting enzyme 2 (ACE2)</title></titleInfo><name type="personal"><namePart type="given">KF</namePart><namePart type="family">To</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AW</namePart><namePart type="family">Lo</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">To KF, Lo AW. 2004. Exploring the pathogenesis of severe acute respiratory syndrome (SARS): The tissue distribution of the coronavirus (SARS‐CoV) and its putative receptor, angiotensin‐converting enzyme 2 (ACE2). J Pathol 203: 740–743.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>203</number></detail><extent unit="pages"><start>740</start><end>743</end></extent></part><relatedItem type="host"><titleInfo><title>J Pathol</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>203</number></detail><extent unit="pages"><start>740</start><end>743</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit44"><titleInfo><title>Antigenic variation of human RSV strains isolated in Japan</title></titleInfo><name type="personal"><namePart type="given">H</namePart><namePart type="family">Tsutsumi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Nagai</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Suga</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Chiba</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Chiba</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Tsugawa</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PL</namePart><namePart type="family">Ogra</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Tsutsumi H, Nagai K, Suga K, Chiba Y, Chiba S, Tsugawa S, Ogra PL. 1989. Antigenic variation of human RSV strains isolated in Japan. J Med Virol 27: 124–130.</note><part><date>1989</date><detail type="volume"><caption>vol.</caption><number>27</number></detail><extent unit="pages"><start>124</start><end>130</end></extent></part><relatedItem type="host"><titleInfo><title>J Med Virol</title></titleInfo><part><date>1989</date><detail type="volume"><caption>vol.</caption><number>27</number></detail><extent unit="pages"><start>124</start><end>130</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit45"><titleInfo><title>GRO alpha and interleukin‐8 in Pneumocystis carinii or bacterial pneumonia and adult respiratory distress syndrome</title></titleInfo><name type="personal"><namePart type="given">J</namePart><namePart type="family">Villard</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Dayer‐Pastore</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Hamacher</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JD</namePart><namePart type="family">Aubert</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Schlegel‐Haueter</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LP</namePart><namePart type="family">Nicod</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Villard J, Dayer‐Pastore F, Hamacher J, Aubert JD, Schlegel‐Haueter S, Nicod LP. 1995. GRO alpha and interleukin‐8 in Pneumocystis carinii or bacterial pneumonia and adult respiratory distress syndrome. Am J Respir Crit Care Med 152: 1549–1554.</note><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>152</number></detail><extent unit="pages"><start>1549</start><end>1554</end></extent></part><relatedItem type="host"><titleInfo><title>Am J Respir Crit Care Med</title></titleInfo><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>152</number></detail><extent unit="pages"><start>1549</start><end>1554</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit46"><titleInfo><title>Interleukin‐6 differentially regulates androgen receptor transactivation via PI3K‐Akt, STAT3, and MAPK, three distinct signal pathways in prostate cancer cells</title></titleInfo><name type="personal"><namePart type="given">L</namePart><namePart type="family">Yang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Wang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HK</namePart><namePart type="family">Lin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PY</namePart><namePart type="family">Kan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Xie</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MY</namePart><namePart type="family">Tsai</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PH</namePart><namePart type="family">Wang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YT</namePart><namePart type="family">Chen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Chang</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Yang L, Wang L, Lin HK, Kan PY, Xie S, Tsai MY, Wang PH, Chen YT, Chang C. 2003. Interleukin‐6 differentially regulates androgen receptor transactivation via PI3K‐Akt, STAT3, and MAPK, three distinct signal pathways in prostate cancer cells. Biochem Biophys Res Commun 305: 462–469.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>305</number></detail><extent unit="pages"><start>462</start><end>469</end></extent></part><relatedItem type="host"><titleInfo><title>Biochem Biophys Res Commun</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>305</number></detail><extent unit="pages"><start>462</start><end>469</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit47"><titleInfo><title>IL‐6 induces an anti‐inflammatory response in the absence of SOCS3 in macrophages</title></titleInfo><name type="personal"><namePart type="given">H</namePart><namePart type="family">Yasukawa</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Ohishi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Mori</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Murakami</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Chinen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Aki</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Hanada</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Takeda</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Akira</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Hoshijima</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Hirano</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KR</namePart><namePart type="family">Chien</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Yoshimura</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Yasukawa H, Ohishi M, Mori H, Murakami M, Chinen T, Aki D, Hanada T, Takeda K, Akira S, Hoshijima M, Hirano T, Chien KR, Yoshimura A. 2003. IL‐6 induces an anti‐inflammatory response in the absence of SOCS3 in macrophages. Nat Immunol 4: 551–556.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>551</start><end>556</end></extent></part><relatedItem type="host"><titleInfo><title>Nat Immunol</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>551</start><end>556</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit48"><titleInfo><title>The CIS family: Negative regulators of JAK‐STAT signaling</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Yoshimura</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Yoshimura A. 1998. The CIS family: Negative regulators of JAK‐STAT signaling. Cytokine Growth Factor Rev 9: 197–204.</note><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>197</start><end>204</end></extent></part><relatedItem type="host"><titleInfo><title>Cytokine Growth Factor Rev</title></titleInfo><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>197</start><end>204</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit49"><titleInfo><title>Paramyxoviridae use distinct virus‐specific mechanisms to circumvent the interferon response</title></titleInfo><name type="personal"><namePart type="given">DF</namePart><namePart type="family">Young</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Didcock</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Goodbourn</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RE</namePart><namePart type="family">Randall</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Young DF, Didcock L, Goodbourn S, Randall RE. 2000. Paramyxoviridae use distinct virus‐specific mechanisms to circumvent the interferon response. Virology 269: 383–390.</note><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>269</number></detail><extent unit="pages"><start>383</start><end>390</end></extent></part><relatedItem type="host"><titleInfo><title>Virology</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>269</number></detail><extent unit="pages"><start>383</start><end>390</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit50"><titleInfo><title>Analysis of serum cytokines in patients with severe acute respiratory syndrome</title></titleInfo><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Zhang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Li</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Zhan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Wu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">X</namePart><namePart type="family">Yu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Zhang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Ye</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Xu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Sun</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Wang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Lou</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Zhang Y, Li J, Zhan Y, Wu L, Yu X, Zhang W, Ye L, Xu S, Sun R, Wang Y, Lou J. 2004. Analysis of serum cytokines in patients with severe acute respiratory syndrome. Infect Immun 72: 4410–4415.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>72</number></detail><extent unit="pages"><start>4410</start><end>4415</end></extent></part><relatedItem type="host"><titleInfo><title>Infect Immun</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>72</number></detail><extent unit="pages"><start>4410</start><end>4415</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit51"><titleInfo><title>Description and clinical treatment of an early outbreak of severe acute respiratory syndrome (SARS) in Guangzhou, PR China</title></titleInfo><name type="personal"><namePart type="given">Z</namePart><namePart type="family">Zhao</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Zhang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Xu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Huang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Zhong</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Cai</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Z</namePart><namePart type="family">Yin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Huang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Z</namePart><namePart type="family">Deng</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Wei</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Xiong</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PM</namePart><namePart type="family">Hawkey</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Zhao Z, Zhang F, Xu M, Huang K, Zhong W, Cai W, Yin Z, Huang S, Deng Z, Wei M, Xiong J, Hawkey PM. 2003. Description and clinical treatment of an early outbreak of severe acute respiratory syndrome (SARS) in Guangzhou, PR China. J Med Microbiol 52: 715–720.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>52</number></detail><extent unit="pages"><start>715</start><end>720</end></extent></part><relatedItem type="host"><titleInfo><title>J Med Microbiol</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>52</number></detail><extent unit="pages"><start>715</start><end>720</end></extent></part></relatedItem></relatedItem><identifier type="istex">F17D45D4C06BEA8CE19CAA34D56E1870ED79FE3A</identifier><identifier type="ark">ark:/67375/WNG-FQB1SXHD-6</identifier><identifier type="DOI">10.1002/jmv.20556</identifier><identifier type="ArticleID">JMV20556</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Converted from (version ) to MODS version 3.6.</recordOrigin><recordCreationDate encoding="w3cdtf">2019-11-15</recordCreationDate></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-FQB1SXHD-6/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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