Recommendations for coronavirus infection in rheumatic diseases treated with biologic therapy
Identifieur interne : 001814 ( Pmc/Corpus ); précédent : 001813; suivant : 001815Recommendations for coronavirus infection in rheumatic diseases treated with biologic therapy
Auteurs : Angela Ceribelli ; Francesca Motta ; Maria De Santis ; Aftab A. Ansari ; William M. Ridgway ; M. Eric Gershwin ; Carlo SelmiSource :
- Journal of Autoimmunity [ 0896-8411 ] ; 2020.
Abstract
The Coronavirus-associated disease, that was first identified in 2019 in China (CoViD-19), is a pandemic caused by a bat-derived beta-coronavirus, named SARS-CoV2. It shares homology with SARS and MERS-CoV, responsible for past outbreaks in China and in Middle East. SARS-CoV2 spread from China where the first infections were described in December 2019 and is responsible for the respiratory symptoms that can lead to acute respiratory distress syndrome. A cytokine storm has been shown in patients who develop fatal complications, as observed in past coronavirus infections. The management includes ventilatory support and broad-spectrum antiviral drugs, empirically utilized, as a targeted therapy and vaccines have not been developed. Based upon our limited knowledge on the pathogenesis of CoViD-19, a potential role of some anti-rheumatic drugs may be hypothesized, acting as direct antivirals or targeting host immune response. Antimalarial drugs, commonly used in rheumatology, may alter the lysosomal proteases that mediates the viral entry into the cell and have demonstrated efficacy in improving the infection. Anti-IL-1 and anti-IL-6 may interfere with the cytokine storm in severe cases and use of tocilizumab has shown good outcomes in a small cohort. Baricitinib has both antiviral and anti-inflammatory properties. Checkpoints inhibitors such as anti-CD200 and anti-PD1 could have a role in the treatment of CoViD-19. Rheumatic disease patients taking immunosuppressive drugs should be recommended to maintain the chronic therapy, prevent infection by avoiding social contacts and pausing immunosuppressants in case of infection. National and international registries are being created to collect data on rheumatic patients with CoViD-19.
Url:
DOI: 10.1016/j.jaut.2020.102442
PubMed: 32253068
PubMed Central: 7127009
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Recommendations for coronavirus infection in rheumatic diseases treated with biologic therapy</title><author><name sortKey="Ceribelli, Angela" sort="Ceribelli, Angela" uniqKey="Ceribelli A" first="Angela" last="Ceribelli">Angela Ceribelli</name><affiliation><nlm:aff id="aff1">Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy</nlm:aff></affiliation></author><author><name sortKey="Motta, Francesca" sort="Motta, Francesca" uniqKey="Motta F" first="Francesca" last="Motta">Francesca Motta</name><affiliation><nlm:aff id="aff2">Humanitas University, Department of Biomedical Sciences, Via Rita Levi Montalcini 4, 20090 Pieve Emanuele Milan, Italy</nlm:aff></affiliation></author><author><name sortKey="De Santis, Maria" sort="De Santis, Maria" uniqKey="De Santis M" first="Maria" last="De Santis">Maria De Santis</name><affiliation><nlm:aff id="aff1">Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy</nlm:aff></affiliation></author><author><name sortKey="Ansari, Aftab A" sort="Ansari, Aftab A" uniqKey="Ansari A" first="Aftab A." last="Ansari">Aftab A. Ansari</name><affiliation><nlm:aff id="aff3">Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA</nlm:aff></affiliation></author><author><name sortKey="Ridgway, William M" sort="Ridgway, William M" uniqKey="Ridgway W" first="William M." last="Ridgway">William M. Ridgway</name><affiliation><nlm:aff id="aff3">Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA</nlm:aff></affiliation></author><author><name sortKey="Gershwin, M Eric" sort="Gershwin, M Eric" uniqKey="Gershwin M" first="M. Eric" last="Gershwin">M. Eric Gershwin</name><affiliation><nlm:aff id="aff3">Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA</nlm:aff></affiliation></author><author><name sortKey="Selmi, Carlo" sort="Selmi, Carlo" uniqKey="Selmi C" first="Carlo" last="Selmi">Carlo Selmi</name><affiliation><nlm:aff id="aff1">Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Humanitas University, Department of Biomedical Sciences, Via Rita Levi Montalcini 4, 20090 Pieve Emanuele Milan, Italy</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">32253068</idno><idno type="pmc">7127009</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7127009</idno><idno type="RBID">PMC:7127009</idno><idno type="doi">10.1016/j.jaut.2020.102442</idno><date when="2020">2020</date><idno type="wicri:Area/Pmc/Corpus">001814</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001814</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Recommendations for coronavirus infection in rheumatic diseases treated with biologic therapy</title><author><name sortKey="Ceribelli, Angela" sort="Ceribelli, Angela" uniqKey="Ceribelli A" first="Angela" last="Ceribelli">Angela Ceribelli</name><affiliation><nlm:aff id="aff1">Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy</nlm:aff></affiliation></author><author><name sortKey="Motta, Francesca" sort="Motta, Francesca" uniqKey="Motta F" first="Francesca" last="Motta">Francesca Motta</name><affiliation><nlm:aff id="aff2">Humanitas University, Department of Biomedical Sciences, Via Rita Levi Montalcini 4, 20090 Pieve Emanuele Milan, Italy</nlm:aff></affiliation></author><author><name sortKey="De Santis, Maria" sort="De Santis, Maria" uniqKey="De Santis M" first="Maria" last="De Santis">Maria De Santis</name><affiliation><nlm:aff id="aff1">Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy</nlm:aff></affiliation></author><author><name sortKey="Ansari, Aftab A" sort="Ansari, Aftab A" uniqKey="Ansari A" first="Aftab A." last="Ansari">Aftab A. Ansari</name><affiliation><nlm:aff id="aff3">Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA</nlm:aff></affiliation></author><author><name sortKey="Ridgway, William M" sort="Ridgway, William M" uniqKey="Ridgway W" first="William M." last="Ridgway">William M. Ridgway</name><affiliation><nlm:aff id="aff3">Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA</nlm:aff></affiliation></author><author><name sortKey="Gershwin, M Eric" sort="Gershwin, M Eric" uniqKey="Gershwin M" first="M. Eric" last="Gershwin">M. Eric Gershwin</name><affiliation><nlm:aff id="aff3">Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA</nlm:aff></affiliation></author><author><name sortKey="Selmi, Carlo" sort="Selmi, Carlo" uniqKey="Selmi C" first="Carlo" last="Selmi">Carlo Selmi</name><affiliation><nlm:aff id="aff1">Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Humanitas University, Department of Biomedical Sciences, Via Rita Levi Montalcini 4, 20090 Pieve Emanuele Milan, Italy</nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Autoimmunity</title><idno type="ISSN">0896-8411</idno><idno type="eISSN">1095-9157</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The Coronavirus-associated disease, that was first identified in 2019 in China (CoViD-19), is a pandemic caused by a bat-derived beta-coronavirus, named SARS-CoV2. It shares homology with SARS and MERS-CoV, responsible for past outbreaks in China and in Middle East. SARS-CoV2 spread from China where the first infections were described in December 2019 and is responsible for the respiratory symptoms that can lead to acute respiratory distress syndrome. A cytokine storm has been shown in patients who develop fatal complications, as observed in past coronavirus infections. The management includes ventilatory support and broad-spectrum antiviral drugs, empirically utilized, as a targeted therapy and vaccines have not been developed. Based upon our limited knowledge on the pathogenesis of CoViD-19, a potential role of some anti-rheumatic drugs may be hypothesized, acting as direct antivirals or targeting host immune response. Antimalarial drugs, commonly used in rheumatology, may alter the lysosomal proteases that mediates the viral entry into the cell and have demonstrated efficacy in improving the infection. Anti-IL-1 and anti-IL-6 may interfere with the cytokine storm in severe cases and use of tocilizumab has shown good outcomes in a small cohort. Baricitinib has both antiviral and anti-inflammatory properties. Checkpoints inhibitors such as anti-CD200 and anti-PD1 could have a role in the treatment of CoViD-19. Rheumatic disease patients taking immunosuppressive drugs should be recommended to maintain the chronic therapy, prevent infection by avoiding social contacts and pausing immunosuppressants in case of infection. National and international registries are being created to collect data on rheumatic patients with CoViD-19.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Lu, R" uniqKey="Lu R">R. Lu</name></author><author><name sortKey="Zhao, X" uniqKey="Zhao X">X. Zhao</name></author><author><name sortKey="Li, J" uniqKey="Li J">J. Li</name></author><author><name sortKey="Niu, P" uniqKey="Niu P">P. Niu</name></author><author><name sortKey="Yang, B" uniqKey="Yang B">B. Yang</name></author><author><name sortKey="Wu, H" uniqKey="Wu H">H. Wu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xu, X" uniqKey="Xu X">X. Xu</name></author><author><name sortKey="Yu, C" uniqKey="Yu C">C. Yu</name></author><author><name sortKey="Qu, J" uniqKey="Qu J">J. Qu</name></author><author><name sortKey="Zhang, L" uniqKey="Zhang L">L. Zhang</name></author><author><name sortKey="Jiang, S" uniqKey="Jiang S">S. Jiang</name></author><author><name sortKey="Huang, D" uniqKey="Huang D">D. Huang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Han, Q" uniqKey="Han Q">Q. Han</name></author><author><name sortKey="Lin, Q" uniqKey="Lin Q">Q. Lin</name></author><author><name sortKey="Jin, S" uniqKey="Jin S">S. Jin</name></author><author><name sortKey="You, L" uniqKey="You L">L. You</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wu, Z" uniqKey="Wu Z">Z. Wu</name></author><author><name sortKey="Mcgoogan, J M" uniqKey="Mcgoogan J">J.M. McGoogan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rothan, H A" uniqKey="Rothan H">H.A. Rothan</name></author><author><name sortKey="Byrareddy, S N" uniqKey="Byrareddy S">S.N. Byrareddy</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chen, J" uniqKey="Chen J">J. Chen</name></author><author><name sortKey="Subbarao, K" uniqKey="Subbarao K">K. Subbarao</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zheng, Y" uniqKey="Zheng Y">Y. Zheng</name></author><author><name sortKey="Shang, J" uniqKey="Shang J">J. Shang</name></author><author><name sortKey="Yang, Y" uniqKey="Yang Y">Y. Yang</name></author><author><name sortKey="Liu, C" uniqKey="Liu C">C. Liu</name></author><author><name sortKey="Wan, Y" uniqKey="Wan Y">Y. Wan</name></author><author><name sortKey="Geng, Q" uniqKey="Geng Q">Q. Geng</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gao, J" uniqKey="Gao J">J. Gao</name></author><author><name sortKey="Tian, Z" uniqKey="Tian Z">Z. Tian</name></author><author><name sortKey="Breakthrough, Yang X" uniqKey="Breakthrough Y">Yang X. Breakthrough</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yao, X" uniqKey="Yao X">X. Yao</name></author><author><name sortKey="Ye, F" uniqKey="Ye F">F. Ye</name></author><author><name sortKey="Zhang, M" uniqKey="Zhang M">M. Zhang</name></author><author><name sortKey="Cui, C" uniqKey="Cui C">C. Cui</name></author><author><name sortKey="Huang, B" uniqKey="Huang B">B. Huang</name></author><author><name sortKey="Niu, P" uniqKey="Niu P">P. Niu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Channappanavar, R" uniqKey="Channappanavar R">R. Channappanavar</name></author><author><name sortKey="Perlman, S" uniqKey="Perlman S">S. Perlman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yoshikawa, T" uniqKey="Yoshikawa T">T. Yoshikawa</name></author><author><name sortKey="Hill, T" uniqKey="Hill T">T. Hill</name></author><author><name sortKey="Li, K" uniqKey="Li K">K. Li</name></author><author><name sortKey="Peters, C J" uniqKey="Peters C">C.J. Peters</name></author><author><name sortKey="Tseng, C T K" uniqKey="Tseng C">C.-T.K. Tseng</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Le, R Q" uniqKey="Le R">R.Q. Le</name></author><author><name sortKey="Li, L" uniqKey="Li L">L. Li</name></author><author><name sortKey="Yuan, W" uniqKey="Yuan W">W. Yuan</name></author><author><name sortKey="Shord, S S" uniqKey="Shord S">S.S. Shord</name></author><author><name sortKey="Nie, L" uniqKey="Nie L">L. Nie</name></author><author><name sortKey="Habtemariam, B A" uniqKey="Habtemariam B">B.A. Habtemariam</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xu Xh, M" uniqKey="Xu Xh M">M. Xu Xh</name></author><author><name sortKey="Li, T" uniqKey="Li T">T. Li</name></author><author><name sortKey="Sun, W" uniqKey="Sun W">W. Sun</name></author><author><name sortKey="Wang, D" uniqKey="Wang D">D. Wang</name></author><author><name sortKey="Fu, B" uniqKey="Fu B">B. Fu</name></author><author><name sortKey="Zhou, Y" uniqKey="Zhou Y">Y. Zhou</name></author><author><name sortKey="Zheng, X" uniqKey="Zheng X">X. Zheng</name></author><author><name sortKey="Yang, Y" uniqKey="Yang Y">Y. Yang</name></author><author><name sortKey="Li, X" uniqKey="Li X">X. Li</name></author><author><name sortKey="Zhang, X" uniqKey="Zhang X">X. Zhang</name></author><author><name sortKey="Pan, A" uniqKey="Pan A">A. Pan</name></author><author><name sortKey="Wei, H" uniqKey="Wei H">H. Wei</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, Y" uniqKey="Yang Y">Y. Yang</name></author><author><name sortKey="Peng, F" uniqKey="Peng F">F. Peng</name></author><author><name sortKey="Wang, R" uniqKey="Wang R">R. Wang</name></author><author><name sortKey="Guan, K" uniqKey="Guan K">K. Guan</name></author><author><name sortKey="Jiang, T" uniqKey="Jiang T">T. Jiang</name></author><author><name sortKey="Xu, G" uniqKey="Xu G">G. Xu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Richardson, P" uniqKey="Richardson P">P. Richardson</name></author><author><name sortKey="Griffin, I" uniqKey="Griffin I">I. Griffin</name></author><author><name sortKey="Tucker, C" uniqKey="Tucker C">C. Tucker</name></author><author><name sortKey="Smith, D" uniqKey="Smith D">D. Smith</name></author><author><name sortKey="Oechsle, O" uniqKey="Oechsle O">O. Oechsle</name></author><author><name sortKey="Phelan, A" uniqKey="Phelan A">A. Phelan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Channappanavar, R" uniqKey="Channappanavar R">R. Channappanavar</name></author><author><name sortKey="Fehr, A R" uniqKey="Fehr A">A.R. Fehr</name></author><author><name sortKey="Vijay, R" uniqKey="Vijay R">R. Vijay</name></author><author><name sortKey="Mack, M" uniqKey="Mack M">M. Mack</name></author><author><name sortKey="Zhao, J" uniqKey="Zhao J">J. Zhao</name></author><author><name sortKey="Meyerholz, D K" uniqKey="Meyerholz D">D.K. Meyerholz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zheng, J" uniqKey="Zheng J">J. Zheng</name></author><author><name sortKey="Perlman, S" uniqKey="Perlman S">S. Perlman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cameron, M J" uniqKey="Cameron M">M.J. Cameron</name></author><author><name sortKey="Ran, L" uniqKey="Ran L">L. Ran</name></author><author><name sortKey="Xu, L" uniqKey="Xu L">L. Xu</name></author><author><name sortKey="Danesh, A" uniqKey="Danesh A">A. Danesh</name></author><author><name sortKey="Bermejo Martin, J F" uniqKey="Bermejo Martin J">J.F. Bermejo-Martin</name></author><author><name sortKey="Cameron, C M" uniqKey="Cameron C">C.M. Cameron</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Vaine, C A" uniqKey="Vaine C">C.A. Vaine</name></author><author><name sortKey="Soberman, R J" uniqKey="Soberman R">R.J. Soberman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Karnam, G" uniqKey="Karnam G">G. Karnam</name></author><author><name sortKey="Rygiel, T P" uniqKey="Rygiel T">T.P. Rygiel</name></author><author><name sortKey="Raaben, M" uniqKey="Raaben M">M. Raaben</name></author><author><name sortKey="Grinwis, G C M" uniqKey="Grinwis G">G.C.M. Grinwis</name></author><author><name sortKey="Coenjaerts, F E" uniqKey="Coenjaerts F">F.E. Coenjaerts</name></author><author><name sortKey="Ressing, M E" uniqKey="Ressing M">M.E. Ressing</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hayakawa, K" uniqKey="Hayakawa K">K. Hayakawa</name></author><author><name sortKey="Pham, L D D" uniqKey="Pham L">L.-D.D. Pham</name></author><author><name sortKey="Seo, J H" uniqKey="Seo J">J.H. Seo</name></author><author><name sortKey="Miyamoto, N" uniqKey="Miyamoto N">N. Miyamoto</name></author><author><name sortKey="Maki, T" uniqKey="Maki T">T. Maki</name></author><author><name sortKey="Terasaki, Y" uniqKey="Terasaki Y">Y. Terasaki</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Seeds, R E" uniqKey="Seeds R">R.E. Seeds</name></author><author><name sortKey="Mukhopadhyay, S" uniqKey="Mukhopadhyay S">S. Mukhopadhyay</name></author><author><name sortKey="Jones, I M" uniqKey="Jones I">I.M. Jones</name></author><author><name sortKey="Gordon, S" uniqKey="Gordon S">S. Gordon</name></author><author><name sortKey="Miller, J L" uniqKey="Miller J">J.L. Miller</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jani, M" uniqKey="Jani M">M. Jani</name></author><author><name sortKey="Barton, A" uniqKey="Barton A">A. Barton</name></author><author><name sortKey="Hyrich, K" uniqKey="Hyrich K">K. Hyrich</name></author></analytic></biblStruct></listBibl></div1></back></TEI><pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Autoimmun</journal-id><journal-id journal-id-type="iso-abbrev">J. Autoimmun</journal-id><journal-title-group><journal-title>Journal of Autoimmunity</journal-title></journal-title-group><issn pub-type="ppub">0896-8411</issn><issn pub-type="epub">1095-9157</issn><publisher><publisher-name>Published by Elsevier Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">32253068</article-id><article-id pub-id-type="pmc">7127009</article-id><article-id pub-id-type="publisher-id">S0896-8411(20)30055-X</article-id><article-id pub-id-type="doi">10.1016/j.jaut.2020.102442</article-id><article-id pub-id-type="publisher-id">102442</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Recommendations for coronavirus infection in rheumatic diseases treated with biologic therapy</article-title></title-group><contrib-group><contrib contrib-type="author" id="au1"><name><surname>Ceribelli</surname><given-names>Angela</given-names></name><xref rid="aff1" ref-type="aff">a</xref><xref rid="fn1" ref-type="fn">1</xref></contrib><contrib contrib-type="author" id="au2"><name><surname>Motta</surname><given-names>Francesca</given-names></name><xref rid="aff2" ref-type="aff">b</xref><xref rid="fn1" ref-type="fn">1</xref></contrib><contrib contrib-type="author" id="au3"><name><surname>De Santis</surname><given-names>Maria</given-names></name><xref rid="aff1" ref-type="aff">a</xref></contrib><contrib contrib-type="author" id="au4"><name><surname>Ansari</surname><given-names>Aftab A.</given-names></name><xref rid="aff3" ref-type="aff">c</xref></contrib><contrib contrib-type="author" id="au5"><name><surname>Ridgway</surname><given-names>William M.</given-names></name><xref rid="aff3" ref-type="aff">c</xref></contrib><contrib contrib-type="author" id="au6"><name><surname>Gershwin</surname><given-names>M. Eric</given-names></name><email>megershwin@ucdavis.edu</email><xref rid="aff3" ref-type="aff">c</xref><xref rid="cor2" ref-type="corresp">∗∗</xref></contrib><contrib contrib-type="author" id="au7"><name><surname>Selmi</surname><given-names>Carlo</given-names></name><email>carlo.selmi@hunimed.eu</email><xref rid="aff1" ref-type="aff">a</xref><xref rid="aff2" ref-type="aff">b</xref><xref rid="cor1" ref-type="corresp">∗</xref></contrib></contrib-group><aff id="aff1"><label>a</label>Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center - IRCCS, Via Manzoni 56, 20089 Rozzano (Mi) , Italy</aff><aff id="aff2"><label>b</label>Humanitas University, Department of Biomedical Sciences, Via Rita Levi Montalcini 4, 20090 Pieve Emanuele Milan, Italy</aff><aff id="aff3"><label>c</label>Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA</aff><author-notes><corresp id="cor1"><label>∗</label>Corresponding author. Rheumatology and Clinical Immunology; Humanitas Research Hospital, Humanitas University, Via A. Manzoni 113, 20089, Rozzano, Milan, Italy. <email>carlo.selmi@hunimed.eu</email></corresp><corresp id="cor2"><label>∗∗</label>Corresponding author. Rheumatology, Allergy and Clinical Immunology, University of California Davis, Davis, CA, 95616, USA. <email>megershwin@ucdavis.edu</email></corresp><fn id="fn1"><label>1</label><p id="ntpara0010">These authors contributed equally to this manuscript.</p></fn></author-notes><pub-date pub-type="pmc-release"><day>2</day><month>4</month><year>2020</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>5</month><year>2020</year></pub-date><pub-date pub-type="epub"><day>2</day><month>4</month><year>2020</year></pub-date><volume>109</volume><fpage>102442</fpage><lpage>102442</lpage><history><date date-type="received"><day>18</day><month>3</month><year>2020</year></date><date date-type="accepted"><day>22</day><month>3</month><year>2020</year></date></history><permissions><copyright-statement>© 2020 Published by Elsevier Ltd.</copyright-statement><copyright-year>2020</copyright-year><copyright-holder></copyright-holder><license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p></license></permissions><abstract id="abs0010"><p>The Coronavirus-associated disease, that was first identified in 2019 in China (CoViD-19), is a pandemic caused by a bat-derived beta-coronavirus, named SARS-CoV2. It shares homology with SARS and MERS-CoV, responsible for past outbreaks in China and in Middle East. SARS-CoV2 spread from China where the first infections were described in December 2019 and is responsible for the respiratory symptoms that can lead to acute respiratory distress syndrome. A cytokine storm has been shown in patients who develop fatal complications, as observed in past coronavirus infections. The management includes ventilatory support and broad-spectrum antiviral drugs, empirically utilized, as a targeted therapy and vaccines have not been developed. Based upon our limited knowledge on the pathogenesis of CoViD-19, a potential role of some anti-rheumatic drugs may be hypothesized, acting as direct antivirals or targeting host immune response. Antimalarial drugs, commonly used in rheumatology, may alter the lysosomal proteases that mediates the viral entry into the cell and have demonstrated efficacy in improving the infection. Anti-IL-1 and anti-IL-6 may interfere with the cytokine storm in severe cases and use of tocilizumab has shown good outcomes in a small cohort. Baricitinib has both antiviral and anti-inflammatory properties. Checkpoints inhibitors such as anti-CD200 and anti-PD1 could have a role in the treatment of CoViD-19. Rheumatic disease patients taking immunosuppressive drugs should be recommended to maintain the chronic therapy, prevent infection by avoiding social contacts and pausing immunosuppressants in case of infection. National and international registries are being created to collect data on rheumatic patients with CoViD-19.</p></abstract><abstract abstract-type="author-highlights" id="abs0015"><title>Highlights</title><p><list list-type="simple" id="ulist0010"><list-item id="u0010"><label>•</label><p id="p0010">CoViD-19 is a pandemic caused by SARS-CoV2, that can lead to acute respiratory distress syndrome.</p></list-item><list-item id="u0015"><label>•</label><p id="p0015">Antimalarial drugs, anti-IL-1 and anti-IL-6 may be used in severe cases targeting the cytokine storm induced by CoViD-19.</p></list-item><list-item id="u0040"><label>•</label><p id="p0040">Recommendations for rheumatic disease patients include the prevention of infection by avoiding social contacts.</p></list-item><list-item id="u0045"><label>•</label><p id="p0045">Patients should also continue their ongoing therapy except in the case of overt infection.</p></list-item></list></p></abstract><kwd-group id="kwrds0010"><title>Keywords</title><kwd>CoViD-19</kwd><kwd>SARS-CoV2</kwd><kwd>Rheumatic diseases</kwd><kwd>Antimalarials</kwd><kwd>Tocilizumab</kwd><kwd>Baricitinib</kwd></kwd-group></article-meta></front><body><sec id="sec1"><label>1</label><title>SARS-CoV2 and the acute respiratory distress syndrome</title><p id="p0050">Coronavirus Disease-2019 (CoViD-19) has emerged over the past months as a clinical syndrome caused by a novel beta-Coronavirus, named Severe Acute Respiratory Syndrome (SARS)-CoV2. It was first reported in late December 2019 in Wuhan, China and the disease was officially named CoViD-19 by the World Health Organization (WHO) on February 11th<sup>,</sup> 2020 following an outbreak of acute respiratory illness in the Hubei province. Since these earliest reports, this infection has spread in many countries worldwide with a significant rate of infection in Italy that currently accounts for more than 110,000 infected cases associated with 13,155 fatalities. The WHO declared CoViD-19 a pandemic on March 11th. The CoViD-19 pandemic has important implications for patients with rheumatic diseases, particularly those undergoing a variety of immunosuppressive therapies. As it seems obvious that immunosuppressive therapy increases their risk of severe disease if infected with CoViD-19, many patients have the tendency to stop their immunosuppressive treatments, especially in highly impacted areas such as the Italian Lombardy region. However, it is important to note that many commonly used immunosuppressive drugs such as JAK kinase inhibitors and tocilizumab have been proposed and/or used for the treatment of select patients who develop a frequently fatal clinical sequalae known as Cytokine Release Syndrome (CRS) (also referred to as “cytokine storm”) following CoViD-19 infection. While data are changing rapidly and the disease trajectories can only be hypothesized, the issue whether to continue treating rheumatic disease patients needs to be addressed by the field of Rheumatology and other medical subspecialties, since some of these agents may be beneficial for specific phases or complications of the disease. SARS-CoV2 is a positive single strand 30,000 nucleotide RNA virus that includes 14 open reading frames that encode 27 proteins and belongs to the <italic>Coronaviridae</italic> family. Its phylogenetic data are consistent with the presence of a bat reservoir and subsequent spill over into the human population. Sequencing data shows that SARS-CoV2 shares a high degree of sequence homology with a betacoronavirus isolated from bats termed Bat-CoV-RaTG13, suggesting that the Chinese chrysanthemum bat is the likely origin of SARS-CoV2. Nonetheless, an unknown animal sold at the seafood market in Wuhan has been hypothesized to act as the intermediate host, as the first cases had common contacts in a market where no bats were present (bats hibernate in December). In addition, SARS-CoV2 shares 79% and 50% gene homologies with the SARS Coronavirus (SARS-CoV) that was responsible for an outbreak in 2002 and with the Middle East Respiratory Syndrome (MERS)-CoV responsible for infections in Saudi Arabia in 2012, respectively. Both these viruses had intermediate hosts that included the civet and camel, respectively, with humans serving as terminal hosts [<xref rid="bib1" ref-type="bibr">1</xref>].""</p><p id="p0055">Person-to-person transmission has already been established for SARS-CoV2 infection and reasoned to be mediated by respiratory droplets. The current data also suggests that the elderly and patients with a compromised immune system are at a significantly higher risk and higher mortality.</p><p id="p0060">The CoViD-19 infection is suspected when patients develop fever, cough, myalgia and fatigue, with bilateral interstitial pneumonia diagnosed in most patients (up to 76% in the earliest series) by ground glass opacity and patchy infiltrates in the chest as visualized by computerized tomography. Around 20% of cases rapidly worsen into respiratory failure or acute respiratory distress syndrome (ARDS), requiring admission to the intensive care unit (ICU) with a mortality rate of approximately 2–3%, being highest in older age patients particularly those with chronic diseases and who are currently hospitalized in ICUs (up to 38%) [<xref rid="bib2" ref-type="bibr">[2]</xref>, <xref rid="bib3" ref-type="bibr">[3]</xref>, <xref rid="bib4" ref-type="bibr">[4]</xref>]. Currently there are no specific drugs and/or vaccines for SARS-CoV2 infection, prompting the use of several broad-spectrum antiviral molecules. In addition, an animal model to study the disease and test potential vaccines is at present missing [<xref rid="bib5" ref-type="bibr">5</xref>].</p></sec><sec id="sec2"><label>2</label><title>Anti-rheumatic drugs as possible therapies: antimalarials, anti-IL6, anti-IL1 and baricitinib</title><p id="p0065">Some drugs usually used in rheumatologic field and targeting the host and its immune response seem to have the potential to interfere with CoViD-19 infection and their potential benefit is being studied in patients (<xref rid="fig1" ref-type="fig">Fig. 1</xref>). The pathogenesis of CoViD-19 remains unclear, but modelling assays revealed a high degree of homology in the receptor binding domains between SARS-CoV2 and SARS-CoV. All coronaviruses express a surface glycoprotein termed a “spike” which bind to the host receptor for viral entry that has been identified as angiotensin-converting enzyme 2 receptors (ACE2r) [<xref rid="bib1" ref-type="bibr">1</xref>], expressed by mature lung epithelial cells, enterocytes, kidney proximal tubular cells and endothelial cells [<xref rid="bib6" ref-type="bibr">6</xref>]. After receptor binding, lysosomal proteases cleave the spike protein releasing the signal peptide that facilitates viral entry into the cell [<xref rid="bib7" ref-type="bibr">7</xref>]. These mechanisms may be targeted and interrupted by therapies such as chloroquine, an antimalarial drug, and preliminary data demonstrate that it may have clinical benefit in the management of CoViD-19 infected patients as determined by improved imaging and shortening of the diseases course [<xref rid="bib8" ref-type="bibr">8</xref>]. We should note that hydroxychloroquine, which shares the same mechanism of action as chloroquine but has a better safety profile and is frequently used particularly in connective tissue disease, has a more potent anti-viral effect than chloroquine in vitro. From the results of physiologically-based pharmacokinetic models, a loading dose of 800 mg orally followed by 400 mg daily for four days reaches three times the potency of chloroquine and is therefore a promising drug for both the prevention and the treatment of CoViD-19, with low risk of toxicity [<xref rid="bib9" ref-type="bibr">9</xref>]. These findings have led to several clinical trials that are ongoing to study the efficacy of chloroquine or hydroxychloroquine in CoViD-19 patients. Hydroxychloroquine is thus being used in Italy for the treatment of CoViD-19 patients despite the absence of efficacy data in the clinical setting. In light of these data, the recommendation for rheumatic patients chronically taking antimalarial drugs is to not discontinue them, considering the antiviral efficacy and the immunomodulatory rather than immunosuppressive effect.<fig id="fig1"><label>Fig. 1</label><caption><p>Representation of possible mechanisms of action of anti-rheumatic drugs in coronavirus infection. AAK1 = AP2-associated protein kinase 1; SARS = severe acute respiratory syndrome.</p></caption><alt-text id="alttext0010">Fig. 1</alt-text><graphic xlink:href="gr1_lrg"></graphic></fig></p><p id="p0070">The pulmonary complications in human CoViD-19 patients are due to an exuberant local inflammatory response with diffuse alveolar damage. Patients dying because of SARS have lung consolidation, edema and mucopurulent material in the bronchial tree. At microscopic examination, alterations such as diffuse alveolar damage, hyaline membrane and fibrin formation, neutrophils and macrophages infiltrates were detected in the interstitium and alveoli. Similar features were noted in the only human autopsy report available of MERS infection. Cytokines and chemokines play a key role in the immune response against viral infections, and their altered production has been demonstrated in both SARS and MERS coronavirus infections. Such altered levels have been shown to be likely due to the low synthesis of antiviral cytokines such as interferons (IFN)α or β and in concert increased levels of other pro-inflammatory cytokines/chemokines that have pathogenic consequences. Among them, interleukin (IL)-1, IL-6 and other pro-inflammatory cytokines were shown to be significantly more elevated in patients with severe compared to uncomplicated SARS or MERS infection [<xref rid="bib10" ref-type="bibr">10</xref>,<xref rid="bib11" ref-type="bibr">11</xref>]. Recent preliminary data from China reported high plasma levels of cytokines including IL-6, related to the severity and the prognosis of the disease with a clear implication for the occurrence of “cytokine storm” and CRS. Tocilizumab, an anti-IL-6 receptor antibody that has been used clinically to treat rheumatoid arthritis and other autoimmune diseases, has been used and approved for treatment of a variety of clinical conditions that include CRS. These have included clinical conditions such as those associated with chimeric antigen receptor T-cell (CAR-T) therapy that appears to induce severe or life-threatening cytokine release syndrome [<xref rid="bib12" ref-type="bibr">12</xref>]. A single dose of tocilizumab was used in 21 patients in China suffering from severe respiratory syndrome during CoViD-19 infection, at the dosage of 400 mg intravenously, in addition to routine therapy. In a few days, 90% of patients recovered and lung opacities disappeared [<xref rid="bib13" ref-type="bibr">13</xref>], suggesting that anti-IL-6 might be a powerful potential rescue therapy in respiratory distress syndrome of CoViD-19.</p><p id="p0075">A potential role for anti-IL1 biologics could be hypothesized from data showing an activation of the NLRP3 inflammasome by SARS-CoV, with secretion of IL-1β. Studies have demonstrated that inflammasome activation also occurs in SARS-CoV2 infection, especially within lymphoid cells and patients have increased serum IL-1β [<xref rid="bib14" ref-type="bibr">14</xref>]. Another potential treatment under evaluation for SARS-CoV2 related acute respiratory disease is baricitinib, an oral drug used to treat rheumatoid arthritis patients that functions as a blocker of Janus Kinases (JAK) 1 and 2, enzymes associated with intracellular signaling, including Type I and type II IFN signaling. One rationale for its use is based on the fact that viruses such as SARS-CoV2 utilize a protein expressed on its spike to bind to the ACE2 receptor and enter cells through a mechanism of receptor-mediated endocytosis. One of the known regulators of receptor mediated endocytosis is a kinase termed the AP2-associated protein kinase 1 (AAK1). Baricitinib has high affinity for AAK1. Inhibition of AAK1 is reasoned to not only inhibit receptor mediated endocytosis (blocking intracellular entry of the virus) but it may also function in the intracellular assembly of virus particles [<xref rid="bib15" ref-type="bibr">15</xref>]. The plasma concentration of baricitinib at its current therapeutic dosage (2 or 4 mg orally once daily) is sufficient to inhibit AAK1, thus it may be able to reduce both the viral entry and the inflammation characteristic of CoViD-19 patients.</p><p id="p0080">Another important aspect in CoViD-19 is that patients are not able to initiate a valid and rapid type I IFN response [<xref rid="bib10" ref-type="bibr">10</xref>], but the mechanisms underlying this defective response are not completely clear. In SARS, macrophages and dendritic cells are only abortively infected and natural killer cells are not activated by the virus, thus suggesting a defective innate immune response with an altered virus clearance [<xref rid="bib6" ref-type="bibr">6</xref>]. In a mouse model using the related coronavirus, delayed type-I IFN responses (with IFN levels peaking later in the immune response and remaining elevated) were associated with mortality from severe lung disease, due to recruitment of highly inflammatory macrophages into the lung [<xref rid="bib16" ref-type="bibr">16</xref>,<xref rid="bib17" ref-type="bibr">17</xref>]. Studies of human SARS-CoV infections also strongly suggest that dysregulated and persistently elevated type-I IFN responses are associated with severe human lung disease [<xref rid="bib18" ref-type="bibr">18</xref>]. In the mouse model, absence of Type-I IFN signaling (achieved by knockout of the IFN-receptor) abolished lung mediated lethality. These data also suggest a second possible explanation for a therapeutic effect of JAK inhibitors such as baricitinib, since they block the downstream signaling of alpha and beta IFN receptors. The situation is complicated by the finding that very early administration of IFN-β in the mouse model also decreased lung disease, suggesting that timing and duration of type-I IFN responses is critical to whether the outcome is helpful or deleterious [<xref rid="bib16" ref-type="bibr">16</xref>]. What does this imply for patients on JAK inhibition therapy? They may have a decreased IFN response to the virus, which would cause excess virus replication, but they also might have less risk of severe lung disease due to downregulation of the IFN signaling pathway. This illustrates the difficult balance between an adequate immune response to prevent viral replication and an over-exuberant immune response that causes severe lung pathology [<xref rid="bib17" ref-type="bibr">17</xref>]. The role of type I IFN in SARS-CoV2 and the role of blocking IFN-I pathways therefore requires more detailed studies.</p></sec><sec id="sec3"><label>3</label><title>The role of the checkpoints inhibitors</title><p id="p0085">The evasion of the immune system checkpoints are often used by both malignant cancer cells and pathogens to escape immune surveillance. One of the most interesting checkpoint inhibitors is the CD200-CD200R1 system (<xref rid="fig1" ref-type="fig">Fig. 1</xref>). This checkpoint negatively regulates the immune response with the aim to prevent an excessive inflammatory response to different triggers [<xref rid="bib19" ref-type="bibr">19</xref>]. Thus, it has been shown to down-modulate TLR7 (single strand RNA virus sensor) in plasmacytoid dendritic cells of a mouse model of coronavirus infection [<xref rid="bib20" ref-type="bibr">20</xref>] and to down-modulate macrophage activation [<xref rid="bib21" ref-type="bibr">21</xref>]. Interestingly, the inhibition of CD200-CD200R1 has positive effects on coronavirus infection [<xref rid="bib19" ref-type="bibr">19</xref>,<xref rid="bib20" ref-type="bibr">20</xref>,<xref rid="bib22" ref-type="bibr">22</xref>], restoring IFN production and increasing virus clearance. Checkpoint inhibitors are currently and effectively used as therapeutic agents for a variety of cancers, but have only minimally been studied in human infectious diseases, although their function was clearly defined using the murine model of LCMV infection. A CD200-Fc fusion protein has been successfully used in experimental settings [<xref rid="bib21" ref-type="bibr">21</xref>] and trials on inhibitory antibody targeting of CD200 has been tested for the treatment of human cancer [<xref rid="bib19" ref-type="bibr">19</xref>], thus suggesting the intriguing possibility to use currently available checkpoint inhibitors for the treatment of CoViD-19. A trial with another checkpoint inhibitor, anti-PD1, is also ongoing in CoViD-19 patients.</p></sec><sec id="sec4"><label>4</label><title>Management of rheumatic patients during the CoViD-19 pandemic</title><p id="p0090">The scientific research on SARS-CoV2 and its possible therapies are based on the knowledge of previous coronaviruses and on data recently made available by the Chinese scientific society. Likewise, social and health policy, information and containment measures are based on what has been learned from previous epidemics, in order to optimize the current measures. From the epidemiology of SARS-CoV and SARS-CoV2 in China we have learned how fundamental are measures such as early recognition of the problem, strict infection control and identification of infected patients, isolation measures, inclusion and formation of new medical and sanitary staff in the health system, designation of new hospital wards with appropriate equipment and information through the mass and social media [<xref rid="bib14" ref-type="bibr">14</xref>]. As part of these measures, recently, the Italian Society of Rheumatology has proposed a set of practical recommendations to improve the management of CoViD-19 patients and to decrease the risk of acquiring this infection in particular in rheumatic patients undergoing immunosuppressive therapies (<xref rid="tbl1" ref-type="table">Table 1</xref>). In general, the interruption of therapies used in rheumatic patients is not advised, as it may be responsible for the onset of clinical flares of the rheumatic disease with subsequent use of other immunosuppressants such as oral glucocorticoids that may be equally unsafe for patients in case of acquired CoViD-19. Although the data are at present unavailable, it appears important to maintain chronic therapies and to have a strict control of each patient in order to evaluate specific clinical needs. In fact, the infection risk in rheumatic diseases such as rheumatoid arthritis is also related to disease activity and a flare due to therapy discontinuation would confer a higher risk of infection [<xref rid="bib23" ref-type="bibr">23</xref>].<table-wrap position="float" id="tbl1"><label>Table 1</label><caption><p>Recommendations proposed for rheumatic diseases during CoViD-19 pandemic.</p></caption><alt-text id="alttext0015">Table 1</alt-text><table frame="hsides" rules="groups"><tbody><tr><td align="left">1- Do not discontinue immunosuppressive treatment</td></tr><tr><td align="left">2- Follow the recommendations for infection prevention suggested by the Italian Ministry of Health, in particular avoid contact with crowded places. Smart working is encouraged.</td></tr><tr><td align="left">3- Chloroquine and hydroxychloroquine seem to have some efficacy on SARS-CoV2 infection.</td></tr><tr><td align="left">4- Chronic immunomodulatory therapies, including biologic drugs, must be guaranteed for rheumatic patients. This includes tocilizumab and baricitinib availability for patients chronically taking these compounds, as they may start to be used to treat CoViD-19 severe pneumonia cases.</td></tr><tr><td align="left">5- Outpatients clinics, albeit with limited activity, should be guaranteed for biologic therapies, as the National Health System has authorized people to move for very specific reasons such as health issues. For all patients, consulting should be made available using media that exclude a person-to-person relationship.</td></tr></tbody></table></table-wrap></p><p id="p0095">For the same reason, rheumatic patients on long term oral glucocorticoid treatment should not only never stop these abruptly but in addition it should be kept in mind that ending of such therapy may also lead to adrenal crisis. Prevention measures suggested by the Italian Ministry of Health must be applied to everyone, in particular by rheumatic patients undergoing immunosuppressive therapies. Patients are therefore strongly encouraged to avoid social contact and maintain isolation. Chronic therapies will be guaranteed for rheumatic patients also in these weeks of CoViD-19 outbreak in which the routine outpatient clinics are closed, as the National Health System has authorized people to move for very specific reasons such as health issues and the need for biologic therapies which are available only in some hospitals. As tocilizumab and baricitinib may start to be used to treat CoViD-19 severe pneumonia cases, their availability must be guaranteed for the treatment of rheumatic patients who are using these compounds. If a rheumatic patient develops symptoms of any infection, it is important to follow the guidelines suggested by the rheumatology community and immunosuppressive therapy should be paused for the duration of the infection. The one exception is hydroxychloroquine, which may have therapeutic potential for CoViD-19 infection and should therefore not be stopped in patients who have been taking it for a rheumatic disease. As mentioned above, it is possible that IL-6 blockade and the use of JAK inhibitors could have beneficial effects on severe lung disease, but we don't yet know enough to recommend continuing these agents, since they could adversely affect viral clearance. Much more study of the kinetics of SARS-CoV2 in the lung, and the relation of the immune response to the onset of CRS, is therefore needed to clarify recommendations for patients on these agents.</p><p id="p0100">The epidemiological scenario is rapidly changing daily and we still have no knowledge about the infection rate and course of CoViD-19 in rheumatologic conditions. Therefore, a national or international registry is strongly encouraged to understand the impact of the infection on specific rheumatic diseases or treatments and the risk factors for poor outcomes. The Italian Society of Rheumatology has established such a registry in March 2020 and data are being collected. Although our observations have no epidemiological grounds, we are quite surprised by the limited number of rheumatic patients contacting us because of a CoViD-19 infection. Furthermore, an international registry supported by America College of Rheumatology, European League Against Rheumatism and other rheumatologic societies worldwide is being launched.</p><p id="p0105">In the meantime, it is important that patients are reassured and consultations made available using media that exclude a person-to-person relationship to minimize the risk of infection.</p></sec></body><back><ref-list id="cebib0010"><title>References</title><ref id="bib1"><label>1</label><element-citation publication-type="journal" id="sref1"><person-group person-group-type="author"><name><surname>Lu</surname><given-names>R.</given-names></name><name><surname>Zhao</surname><given-names>X.</given-names></name><name><surname>Li</surname><given-names>J.</given-names></name><name><surname>Niu</surname><given-names>P.</given-names></name><name><surname>Yang</surname><given-names>B.</given-names></name><name><surname>Wu</surname><given-names>H.</given-names></name></person-group><article-title>Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding</article-title><source>Lancet (London, England)</source><volume>395</volume><issue>10224</issue><year>2020</year><fpage>565</fpage><lpage>574</lpage><comment>Epub 2020/01/30</comment></element-citation></ref><ref id="bib2"><label>2</label><element-citation publication-type="journal" id="sref2"><person-group person-group-type="author"><name><surname>Xu</surname><given-names>X.</given-names></name><name><surname>Yu</surname><given-names>C.</given-names></name><name><surname>Qu</surname><given-names>J.</given-names></name><name><surname>Zhang</surname><given-names>L.</given-names></name><name><surname>Jiang</surname><given-names>S.</given-names></name><name><surname>Huang</surname><given-names>D.</given-names></name></person-group><article-title>Imaging and clinical features of patients with 2019 novel coronavirus SARS-CoV-2</article-title><source>Eur. J. Nucl. Med. Mol. Imag.</source><year>2020</year></element-citation></ref><ref id="bib3"><label>3</label><element-citation publication-type="journal" id="sref3"><person-group person-group-type="author"><name><surname>Han</surname><given-names>Q.</given-names></name><name><surname>Lin</surname><given-names>Q.</given-names></name><name><surname>Jin</surname><given-names>S.</given-names></name><name><surname>You</surname><given-names>L.</given-names></name></person-group><article-title>Recent insights into 2019-nCoV: a brief but comprehensive review</article-title><source>J. Infect.</source><volume>S0163–4453</volume><issue>20</issue><year>2020</year><comment>30087-6</comment></element-citation></ref><ref id="bib4"><label>4</label><element-citation publication-type="journal" id="sref4"><person-group person-group-type="author"><name><surname>Wu</surname><given-names>Z.</given-names></name><name><surname>McGoogan</surname><given-names>J.M.</given-names></name></person-group><article-title>Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: summary of a report of 72 314 cases from the Chinese center for disease control and prevention</article-title><source>J. Am. Med. Assoc.</source><year>2020</year></element-citation></ref><ref id="bib5"><label>5</label><element-citation publication-type="journal" id="sref5"><person-group person-group-type="author"><name><surname>Rothan</surname><given-names>H.A.</given-names></name><name><surname>Byrareddy</surname><given-names>S.N.</given-names></name></person-group><article-title>The epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak</article-title><source>J. Autoimmun.</source><year>2020</year><fpage>102433</fpage><pub-id pub-id-type="pmid">32113704</pub-id></element-citation></ref><ref id="bib6"><label>6</label><element-citation publication-type="journal" id="sref6"><person-group person-group-type="author"><name><surname>Chen</surname><given-names>J.</given-names></name><name><surname>Subbarao</surname><given-names>K.</given-names></name></person-group><article-title>The immunobiology of SARS*</article-title><source>Annu. Rev. Immunol.</source><volume>25</volume><year>2007</year><fpage>443</fpage><lpage>472</lpage><pub-id pub-id-type="pmid">17243893</pub-id></element-citation></ref><ref id="bib7"><label>7</label><element-citation publication-type="journal" id="sref7"><person-group person-group-type="author"><name><surname>Zheng</surname><given-names>Y.</given-names></name><name><surname>Shang</surname><given-names>J.</given-names></name><name><surname>Yang</surname><given-names>Y.</given-names></name><name><surname>Liu</surname><given-names>C.</given-names></name><name><surname>Wan</surname><given-names>Y.</given-names></name><name><surname>Geng</surname><given-names>Q.</given-names></name></person-group><article-title>Lysosomal proteases are a determinant of coronavirus tropism</article-title><source>J. Virol.</source><volume>92</volume><issue>24</issue><year>2018</year><fpage>e01504</fpage><lpage>e01518</lpage><pub-id pub-id-type="pmid">30258004</pub-id></element-citation></ref><ref id="bib8"><label>8</label><element-citation publication-type="journal" id="sref8"><person-group person-group-type="author"><name><surname>Gao</surname><given-names>J.</given-names></name><name><surname>Tian</surname><given-names>Z.</given-names></name><name><surname>Breakthrough</surname><given-names>Yang X.</given-names></name></person-group><article-title>Chloroquine phosphate has shown apparent efficacy in treatment of COVID-19 associated pneumonia in clinical studies</article-title><source>Biosci Trends</source><year>2020</year></element-citation></ref><ref id="bib9"><label>9</label><element-citation publication-type="journal" id="sref9"><person-group person-group-type="author"><name><surname>Yao</surname><given-names>X.</given-names></name><name><surname>Ye</surname><given-names>F.</given-names></name><name><surname>Zhang</surname><given-names>M.</given-names></name><name><surname>Cui</surname><given-names>C.</given-names></name><name><surname>Huang</surname><given-names>B.</given-names></name><name><surname>Niu</surname><given-names>P.</given-names></name></person-group><article-title>In vitro antiviral activity and projection of optimized dosing design of hydroxychloroquine for the treatment of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)</article-title><source>Clin. Infect. Dis.</source><year>2020</year><fpage>ciaa237</fpage><pub-id pub-id-type="pmid">32150618</pub-id></element-citation></ref><ref id="bib10"><label>10</label><element-citation publication-type="journal" id="sref10"><person-group person-group-type="author"><name><surname>Channappanavar</surname><given-names>R.</given-names></name><name><surname>Perlman</surname><given-names>S.</given-names></name></person-group><article-title>Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology</article-title><source>Semin. Immunopathol.</source><volume>39</volume><issue>5</issue><year>2017</year><fpage>529</fpage><lpage>539</lpage><comment>Epub 2017/05/02</comment><pub-id pub-id-type="pmid">28466096</pub-id></element-citation></ref><ref id="bib11"><label>11</label><element-citation publication-type="journal" id="sref11"><person-group person-group-type="author"><name><surname>Yoshikawa</surname><given-names>T.</given-names></name><name><surname>Hill</surname><given-names>T.</given-names></name><name><surname>Li</surname><given-names>K.</given-names></name><name><surname>Peters</surname><given-names>C.J.</given-names></name><name><surname>Tseng</surname><given-names>C.-T.K.</given-names></name></person-group><article-title>Severe acute respiratory syndrome (SARS) coronavirus-induced lung epithelial cytokines exacerbate SARS pathogenesis by modulating intrinsic functions of monocyte-derived macrophages and dendritic cells</article-title><source>J. Virol.</source><volume>83</volume><issue>7</issue><year>2009</year><fpage>3039</fpage><lpage>3048</lpage><comment>Epub 2008/11/12</comment><pub-id pub-id-type="pmid">19004938</pub-id></element-citation></ref><ref id="bib12"><label>12</label><element-citation publication-type="journal" id="sref12"><person-group person-group-type="author"><name><surname>Le</surname><given-names>R.Q.</given-names></name><name><surname>Li</surname><given-names>L.</given-names></name><name><surname>Yuan</surname><given-names>W.</given-names></name><name><surname>Shord</surname><given-names>S.S.</given-names></name><name><surname>Nie</surname><given-names>L.</given-names></name><name><surname>Habtemariam</surname><given-names>B.A.</given-names></name></person-group><article-title>FDA approval summary: tocilizumab for treatment of chimeric antigen receptor T cell-induced severe or life-threatening cytokine release syndrome</article-title><source>Oncol.</source><volume>23</volume><issue>8</issue><year>2018</year><fpage>943</fpage><lpage>947</lpage><comment>Epub 2018/04/05</comment></element-citation></ref><ref id="bib13"><label>13</label><element-citation publication-type="book" id="sref13"><person-group person-group-type="author"><name><surname>Xu Xh</surname><given-names>M.</given-names></name><name><surname>Li</surname><given-names>T.</given-names></name><name><surname>Sun</surname><given-names>W.</given-names></name><name><surname>Wang</surname><given-names>D.</given-names></name><name><surname>Fu</surname><given-names>B.</given-names></name><name><surname>Zhou</surname><given-names>Y.</given-names></name><name><surname>Zheng</surname><given-names>X.</given-names></name><name><surname>Yang</surname><given-names>Y.</given-names></name><name><surname>Li</surname><given-names>X.</given-names></name><name><surname>Zhang</surname><given-names>X.</given-names></name><name><surname>Pan</surname><given-names>A.</given-names></name><name><surname>Wei</surname><given-names>H.</given-names></name></person-group><chapter-title>Effective Treatment of Severe COVID-19 Patients with Tocilizumab</chapter-title><year>2020;</year><publisher-name>ChinaXiv</publisher-name><comment>20200300026</comment></element-citation></ref><ref id="bib14"><label>14</label><element-citation publication-type="journal" id="sref14"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>Y.</given-names></name><name><surname>Peng</surname><given-names>F.</given-names></name><name><surname>Wang</surname><given-names>R.</given-names></name><name><surname>Guan</surname><given-names>K.</given-names></name><name><surname>Jiang</surname><given-names>T.</given-names></name><name><surname>Xu</surname><given-names>G.</given-names></name></person-group><article-title>The deadly coronaviruses: the 2003 SARS pandemic and the 2020 novel coronavirus epidemic in China</article-title><source>J. Autoimmun.</source><year>2020</year><fpage>102434</fpage><pub-id pub-id-type="pmid">32143990</pub-id></element-citation></ref><ref id="bib15"><label>15</label><element-citation publication-type="journal" id="sref15"><person-group person-group-type="author"><name><surname>Richardson</surname><given-names>P.</given-names></name><name><surname>Griffin</surname><given-names>I.</given-names></name><name><surname>Tucker</surname><given-names>C.</given-names></name><name><surname>Smith</surname><given-names>D.</given-names></name><name><surname>Oechsle</surname><given-names>O.</given-names></name><name><surname>Phelan</surname><given-names>A.</given-names></name></person-group><article-title>Baricitinib as potential treatment for 2019-nCoV acute respiratory disease</article-title><source>Lancet (London, England)</source><volume>395</volume><issue>10223</issue><year>2020</year><fpage>e30</fpage><lpage>e31</lpage><comment>Epub 2020/02/04</comment></element-citation></ref><ref id="bib16"><label>16</label><element-citation publication-type="journal" id="sref16"><person-group person-group-type="author"><name><surname>Channappanavar</surname><given-names>R.</given-names></name><name><surname>Fehr</surname><given-names>A.R.</given-names></name><name><surname>Vijay</surname><given-names>R.</given-names></name><name><surname>Mack</surname><given-names>M.</given-names></name><name><surname>Zhao</surname><given-names>J.</given-names></name><name><surname>Meyerholz</surname><given-names>D.K.</given-names></name></person-group><article-title>Dysregulated type I interferon and inflammatory monocyte-macrophage responses cause lethal pneumonia in SARS-CoV-infected mice</article-title><source>Cell Host Microbe</source><volume>19</volume><issue>2</issue><year>2016</year><fpage>181</fpage><lpage>193</lpage><pub-id pub-id-type="pmid">26867177</pub-id></element-citation></ref><ref id="bib17"><label>17</label><element-citation publication-type="journal" id="sref17"><person-group person-group-type="author"><name><surname>Zheng</surname><given-names>J.</given-names></name><name><surname>Perlman</surname><given-names>S.</given-names></name></person-group><article-title>Immune responses in influenza A virus and human coronavirus infections: an ongoing battle between the virus and host</article-title><source>Curr. Opin. Virol.</source><volume>28</volume><year>2018</year><fpage>43</fpage><lpage>52</lpage><pub-id pub-id-type="pmid">29172107</pub-id></element-citation></ref><ref id="bib18"><label>18</label><element-citation publication-type="journal" id="sref18"><person-group person-group-type="author"><name><surname>Cameron</surname><given-names>M.J.</given-names></name><name><surname>Ran</surname><given-names>L.</given-names></name><name><surname>Xu</surname><given-names>L.</given-names></name><name><surname>Danesh</surname><given-names>A.</given-names></name><name><surname>Bermejo-Martin</surname><given-names>J.F.</given-names></name><name><surname>Cameron</surname><given-names>C.M.</given-names></name></person-group><article-title>Interferon-mediated immunopathological events are associated with atypical innate and adaptive immune responses in patients with severe acute respiratory syndrome</article-title><source>J. Virol.</source><volume>81</volume><issue>16</issue><year>2007</year><fpage>8692</fpage><lpage>8706</lpage><pub-id pub-id-type="pmid">17537853</pub-id></element-citation></ref><ref id="bib19"><label>19</label><element-citation publication-type="journal" id="sref19"><person-group person-group-type="author"><name><surname>Vaine</surname><given-names>C.A.</given-names></name><name><surname>Soberman</surname><given-names>R.J.</given-names></name></person-group><article-title>The CD200-CD200R1 inhibitory signaling pathway: immune regulation and host-pathogen interactions</article-title><source>Adv. Immunol.</source><volume>121</volume><year>2014</year><fpage>191</fpage><lpage>211</lpage><pub-id pub-id-type="pmid">24388216</pub-id></element-citation></ref><ref id="bib20"><label>20</label><element-citation publication-type="journal" id="sref20"><person-group person-group-type="author"><name><surname>Karnam</surname><given-names>G.</given-names></name><name><surname>Rygiel</surname><given-names>T.P.</given-names></name><name><surname>Raaben</surname><given-names>M.</given-names></name><name><surname>Grinwis</surname><given-names>G.C.M.</given-names></name><name><surname>Coenjaerts</surname><given-names>F.E.</given-names></name><name><surname>Ressing</surname><given-names>M.E.</given-names></name></person-group><article-title>CD200 receptor controls sex-specific TLR7 responses to viral infection</article-title><comment>e1002710-e</comment><source>PLoS Pathog.</source><volume>8</volume><issue>5</issue><year>2012</year><comment>Epub 2012/05/17</comment></element-citation></ref><ref id="bib21"><label>21</label><element-citation publication-type="journal" id="sref21"><person-group person-group-type="author"><name><surname>Hayakawa</surname><given-names>K.</given-names></name><name><surname>Pham</surname><given-names>L.-D.D.</given-names></name><name><surname>Seo</surname><given-names>J.H.</given-names></name><name><surname>Miyamoto</surname><given-names>N.</given-names></name><name><surname>Maki</surname><given-names>T.</given-names></name><name><surname>Terasaki</surname><given-names>Y.</given-names></name></person-group><article-title>CD200 restrains macrophage attack on oligodendrocyte precursors via toll-like receptor 4 downregulation</article-title><source>J. Cerebr. Blood Flow Metabol.</source><volume>36</volume><issue>4</issue><year>2016</year><fpage>781</fpage><lpage>793</lpage><comment>Epub 2015/09/30</comment></element-citation></ref><ref id="bib22"><label>22</label><element-citation publication-type="journal" id="sref22"><person-group person-group-type="author"><name><surname>Seeds</surname><given-names>R.E.</given-names></name><name><surname>Mukhopadhyay</surname><given-names>S.</given-names></name><name><surname>Jones</surname><given-names>I.M.</given-names></name><name><surname>Gordon</surname><given-names>S.</given-names></name><name><surname>Miller</surname><given-names>J.L.</given-names></name></person-group><article-title>The role of myeloid receptors on murine plasmacytoid dendritic cells in induction of type I interferon</article-title><source>Int. Immunopharm.</source><volume>11</volume><issue>7</issue><year>2011</year><fpage>794</fpage><lpage>801</lpage><comment>Epub 2011/01/31</comment></element-citation></ref><ref id="bib23"><label>23</label><element-citation publication-type="journal" id="sref23"><person-group person-group-type="author"><name><surname>Jani</surname><given-names>M.</given-names></name><name><surname>Barton</surname><given-names>A.</given-names></name><name><surname>Hyrich</surname><given-names>K.</given-names></name></person-group><article-title>Prediction of infection risk in rheumatoid arthritis patients treated with biologics: are we any closer to risk stratification?</article-title><source>Curr. Opin. Rheumatol.</source><volume>31</volume><issue>3</issue><year>2019</year><fpage>285</fpage><lpage>292</lpage><pub-id pub-id-type="pmid">30789850</pub-id></element-citation></ref></ref-list></back></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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