Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection
Identifieur interne : 000399 ( Istex/Corpus ); précédent : 000398; suivant : 000400Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection
Auteurs : Yao-Hsu Yang ; Yu-Hui Huang ; Ya-Hui Chuang ; Chung-Min Peng ; Li-Chieh Wang ; Yu-Tsan Lin ; Bor-Luen ChiangSource :
- Journal of Medical Virology [ 0146-6615 ] ; 2005-09.
English descriptors
- Teeft :
- Aeca, Aepca, Antibody, Assay, Autoantibody, Cell antibodies, Chan, Clin, Coronavirus, Cytotoxicity, Cytotoxicity index, Elisa, Endothelial, Endothelial cells, Epithelial, Epithelial cells, Healthy controls, Hpec, Human epithelial cells, Human umbilical venous, Huvec, Immunoglobulin, Indirect staining, National taiwan university hospital, Necrotizing pneumonia, Nucleocapsid protein, Peiris, Respiratory syndrome, Room temperature, Sars, Sars patients, Serum levels, Serum samples, Streptococcal necrotizing pneumonia, Syndrome, Systemic vasculitis, Test medium, Ulcerative colitis, Wang.
Abstract
The severe acute respiratory syndrome (SARS) is caused by infection with the SARS‐associated coronavirus (SARS‐CoV) and characterized by severe pulmonary inflammation and fibrosis. In this study, the development of autoantibodies against human epithelial cells and endothelial cells in patients with SARS at different time periods (the first week: phase I, 1 month after the disease onset: phase II/phase III) were investigated. Antibodies in sera of patients and healthy controls against: (1) A549 human pulmonary epithelial cell‐line, (2) human umbilical venous endothelial cells (HUVEC), (3) primary human pulmonary endothelial cells (HPEC) were detected by cell‐based ELISA and indirect immunofluorescence staining. The results revealed that serum levels of IgG anti‐A549 cells antibodies, IgG anti‐HUVEC antibodies, and IgM anti‐HPEC antibodies were significantly higher in SARS patients at phase II/phase III than those in healthy controls. Sera from SARS patients at phase II/phase III could mediate complement dependent cytotoxicity against some A549 cells and HPEC. It is concluded that some autoantibodies against human epithelial cells and endothelial cells would be developed after SARS‐CoV infection and this phenomenon may indicate post‐infectious cellular injury and also induce SARS‐induced immunopathology. J. Med. Virol. 77:1–7, 2005. © 2005 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jmv.20407
Links to Exploration step
ISTEX:6D8019B1F040C7D2802514A11B2E72485323ACE2Le document en format XML
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xml:lang="en"><term>Aeca</term><term>Aepca</term><term>Antibody</term><term>Assay</term><term>Autoantibody</term><term>Cell antibodies</term><term>Chan</term><term>Clin</term><term>Coronavirus</term><term>Cytotoxicity</term><term>Cytotoxicity index</term><term>Elisa</term><term>Endothelial</term><term>Endothelial cells</term><term>Epithelial</term><term>Epithelial cells</term><term>Healthy controls</term><term>Hpec</term><term>Human epithelial cells</term><term>Human umbilical venous</term><term>Huvec</term><term>Immunoglobulin</term><term>Indirect staining</term><term>National taiwan university hospital</term><term>Necrotizing pneumonia</term><term>Nucleocapsid protein</term><term>Peiris</term><term>Respiratory syndrome</term><term>Room temperature</term><term>Sars</term><term>Sars patients</term><term>Serum levels</term><term>Serum samples</term><term>Streptococcal necrotizing pneumonia</term><term>Syndrome</term><term>Systemic vasculitis</term><term>Test medium</term><term>Ulcerative colitis</term><term>Wang</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The severe acute respiratory syndrome (SARS) is caused by infection with the SARS‐associated coronavirus (SARS‐CoV) and characterized by severe pulmonary inflammation and fibrosis. In this study, the development of autoantibodies against human epithelial cells and endothelial cells in patients with SARS at different time periods (the first week: phase I, 1 month after the disease onset: phase II/phase III) were investigated. Antibodies in sera of patients and healthy controls against: (1) A549 human pulmonary epithelial cell‐line, (2) human umbilical venous endothelial cells (HUVEC), (3) primary human pulmonary endothelial cells (HPEC) were detected by cell‐based ELISA and indirect immunofluorescence staining. The results revealed that serum levels of IgG anti‐A549 cells antibodies, IgG anti‐HUVEC antibodies, and IgM anti‐HPEC antibodies were significantly higher in SARS patients at phase II/phase III than those in healthy controls. Sera from SARS patients at phase II/phase III could mediate complement dependent cytotoxicity against some A549 cells and HPEC. It is concluded that some autoantibodies against human epithelial cells and endothelial cells would be developed after SARS‐CoV infection and this phenomenon may indicate post‐infectious cellular injury and also induce SARS‐induced immunopathology. J. Med. Virol. 77:1–7, 2005. © 2005 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>sars</json:string><json:string>autoantibody</json:string><json:string>sars patients</json:string><json:string>epithelial</json:string><json:string>healthy controls</json:string><json:string>respiratory syndrome</json:string><json:string>hpec</json:string><json:string>cell antibodies</json:string><json:string>elisa</json:string><json:string>cytotoxicity</json:string><json:string>endothelial cells</json:string><json:string>aeca</json:string><json:string>huvec</json:string><json:string>peiris</json:string><json:string>wang</json:string><json:string>coronavirus</json:string><json:string>chan</json:string><json:string>clin</json:string><json:string>aepca</json:string><json:string>immunoglobulin</json:string><json:string>endothelial</json:string><json:string>epithelial cells</json:string><json:string>indirect staining</json:string><json:string>cytotoxicity index</json:string><json:string>serum samples</json:string><json:string>syndrome</json:string><json:string>nucleocapsid protein</json:string><json:string>human epithelial cells</json:string><json:string>serum levels</json:string><json:string>assay</json:string><json:string>streptococcal necrotizing pneumonia</json:string><json:string>room temperature</json:string><json:string>national taiwan university hospital</json:string><json:string>necrotizing pneumonia</json:string><json:string>test medium</json:string><json:string>human umbilical venous</json:string><json:string>ulcerative colitis</json:string><json:string>systemic vasculitis</json:string><json:string>antibody</json:string></teeft></keywords><author><json:item><name>Yao‐Hsu Yang</name><affiliations><json:string>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>Yu‐Hui Huang</name><affiliations><json:string>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>Ya‐Hui Chuang</name><affiliations><json:string>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>Chung‐Min Peng</name><affiliations><json:string>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>Li‐Chieh Wang</name><affiliations><json:string>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>Yu‐Tsan Lin</name><affiliations><json:string>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>Bor‐Luen Chiang</name><affiliations><json:string>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</json:string><json:string>E-mail: gicmbor@ha.mc.ntu.edu.tw</json:string><json:string>Correspondence address: Department of Pediatrics, National Taiwan University Hospital, No. 7 Chung‐Shan South Road, Taipei, Taiwan.===</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>SARS</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>autoantibodies</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>epithelial cell</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>endothelial cell</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cytotoxicity</value></json:item></subject><articleId><json:string>JMV20407</json:string></articleId><arkIstex>ark:/67375/WNG-1Z85M5SJ-J</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>The severe acute respiratory syndrome (SARS) is caused by infection with the SARS‐associated coronavirus (SARS‐CoV) and characterized by severe pulmonary inflammation and fibrosis. In this study, the development of autoantibodies against human epithelial cells and endothelial cells in patients with SARS at different time periods (the first week: phase I, 1 month after the disease onset: phase II/phase III) were investigated. Antibodies in sera of patients and healthy controls against: (1) A549 human pulmonary epithelial cell‐line, (2) human umbilical venous endothelial cells (HUVEC), (3) primary human pulmonary endothelial cells (HPEC) were detected by cell‐based ELISA and indirect immunofluorescence staining. The results revealed that serum levels of IgG anti‐A549 cells antibodies, IgG anti‐HUVEC antibodies, and IgM anti‐HPEC antibodies were significantly higher in SARS patients at phase II/phase III than those in healthy controls. Sera from SARS patients at phase II/phase III could mediate complement dependent cytotoxicity against some A549 cells and HPEC. It is concluded that some autoantibodies against human epithelial cells and endothelial cells would be developed after SARS‐CoV infection and this phenomenon may indicate post‐infectious cellular injury and also induce SARS‐induced immunopathology. J. Med. Virol. 77:1–7, 2005. © 2005 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>8.681</score><pdfWordCount>4377</pdfWordCount><pdfCharCount>27375</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>594 x 792 pts</pdfPageSize><pdfWordsPerPage>625</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>192</abstractWordCount><abstractCharCount>1376</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection</title><pmid><json:string>16032747</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>77</volume><issue>1</issue><pages><first>1</first><last>7</last><total>7</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>2005</json:string><json:string>2003</json:string></date><geogName></geogName><orgName><json:string>HKU/UCH SARS Study Group</json:string><json:string>Department of Internal Medicine, National Taiwan University Hospital</json:string><json:string>SARS study group</json:string><json:string>Life Technologies</json:string><json:string>GIBCO BRL Life Technologies</json:string><json:string>Cambrex Bio Science Walkersville, Inc</json:string><json:string>Wiley-Liss, Inc</json:string><json:string>Beijing Group of National Research Project for SARS</json:string><json:string>Toronto SARS Critical Care Group</json:string><json:string>Celardane Laboratories Ltd.</json:string><json:string>LISS, INC.</json:string><json:string>Department of Pediatrics, National Taiwan University Hospital</json:string><json:string>The National Science Council</json:string></orgName><orgName_funder><json:string>The National Science Council</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Chang</json:string><json:string>Serum</json:string><json:string>Ya-Hui Chuang</json:string><json:string>Beijing Group</json:string><json:string>Bor-Luen Chiang</json:string><json:string>Sera</json:string><json:string>J. Med</json:string><json:string>ELISA Figure</json:string><json:string>Min Peng</json:string></persName><placeName><json:string>Cytotoxicity</json:string><json:string>Germany</json:string><json:string>Australia</json:string><json:string>Mannheim</json:string><json:string>Taiwan</json:string><json:string>Canada</json:string><json:string>Kawasaki</json:string><json:string>Denmark</json:string><json:string>Republic of China</json:string><json:string>Taipei</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Ho et al., 2003</json:string><json:string>Poon et al., 2004</json:string><json:string>Franks et al., 2003</json:string><json:string>Grunebaum et al., 2002</json:string><json:string>Carvalho et al., 1999</json:string><json:string>Chiang et al., 2003</json:string><json:string>Bordron et al., 2001</json:string><json:string>Drosten et al., 2003</json:string><json:string>Tsang et al., 2003</json:string><json:string>Praprotnik et al., 2001</json:string><json:string>Lang et al., 2003</json:string><json:string>Ng et al., 2004</json:string><json:string>Twu et al., 2003</json:string><json:string>Sun et al., 2000</json:string><json:string>Cacoub et al., 1999</json:string><json:string>Peiris et al., 2003b</json:string><json:string>Yang et al.</json:string><json:string>Jaffe et al., 1973</json:string><json:string>Yang et al., 2002</json:string><json:string>Peiris et al. 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type="first">Yao‐Hsu</forename><surname>Yang</surname></persName><affiliation><orgName type="division">Department of Pediatrics</orgName><orgName type="institution">National Taiwan University Hospital</orgName><orgName type="institution">College of Medicine</orgName><orgName type="institution">National Taiwan University</orgName><address><addrLine>Taipei</addrLine><addrLine>Taiwan</addrLine><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Yu‐Hui</forename><surname>Huang</surname></persName><affiliation><orgName type="division">Department of Pediatrics</orgName><orgName type="institution">National Taiwan University Hospital</orgName><orgName type="institution">College of Medicine</orgName><orgName type="institution">National Taiwan University</orgName><address><addrLine>Taipei</addrLine><addrLine>Taiwan</addrLine><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Ya‐Hui</forename><surname>Chuang</surname></persName><affiliation><orgName type="division">Department of Pediatrics</orgName><orgName type="institution">National Taiwan University Hospital</orgName><orgName type="institution">College of Medicine</orgName><orgName type="institution">National Taiwan University</orgName><address><addrLine>Taipei</addrLine><addrLine>Taiwan</addrLine><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Chung‐Min</forename><surname>Peng</surname></persName><affiliation><orgName type="division">Department of Pediatrics</orgName><orgName type="institution">National Taiwan University Hospital</orgName><orgName type="institution">College of Medicine</orgName><orgName type="institution">National Taiwan University</orgName><address><addrLine>Taipei</addrLine><addrLine>Taiwan</addrLine><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Li‐Chieh</forename><surname>Wang</surname></persName><affiliation><orgName type="division">Department of Pediatrics</orgName><orgName type="institution">National Taiwan University Hospital</orgName><orgName type="institution">College of Medicine</orgName><orgName type="institution">National Taiwan University</orgName><address><addrLine>Taipei</addrLine><addrLine>Taiwan</addrLine><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Yu‐Tsan</forename><surname>Lin</surname></persName><affiliation><orgName type="division">Department of Pediatrics</orgName><orgName type="institution">National Taiwan University Hospital</orgName><orgName type="institution">College of Medicine</orgName><orgName type="institution">National Taiwan University</orgName><address><addrLine>Taipei</addrLine><addrLine>Taiwan</addrLine><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><author xml:id="author-0006" role="corresp"><persName><forename type="first">Bor‐Luen</forename><surname>Chiang</surname></persName><email>gicmbor@ha.mc.ntu.edu.tw</email><affiliation><orgName type="division">Department of Pediatrics</orgName><orgName type="institution">National Taiwan University Hospital</orgName><orgName type="institution">College of Medicine</orgName><orgName type="institution">National Taiwan University</orgName><address><addrLine>Taipei</addrLine><addrLine>Taiwan</addrLine><country key="TW" xml:lang="en">TAIWAN, PROVINCE OF CHINA</country></address></affiliation></author><idno type="istex">6D8019B1F040C7D2802514A11B2E72485323ACE2</idno><idno type="ark">ark:/67375/WNG-1Z85M5SJ-J</idno><idno 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The results revealed that serum levels of IgG anti‐A549 cells antibodies, IgG anti‐HUVEC antibodies, and IgM anti‐HPEC antibodies were significantly higher in SARS patients at phase II/phase III than those in healthy controls. Sera from SARS patients at phase II/phase III could mediate complement dependent cytotoxicity against some A549 cells and HPEC. It is concluded that some autoantibodies against human epithelial cells and endothelial cells would be developed after SARS‐CoV infection and this phenomenon may indicate post‐infectious cellular injury and also induce SARS‐induced immunopathology. J. Med. Virol. 77:1–7, 2005. © 2005 Wiley‐Liss, Inc.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="kwd1">SARS</term><term xml:id="kwd2">autoantibodies</term><term xml:id="kwd3">epithelial cell</term><term xml:id="kwd4">endothelial cell</term><term xml:id="kwd5">cytotoxicity</term></keywords><keywords rend="articleCategory"><term>Research Article</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-1Z85M5SJ-J/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1096-9071</doi><issn type="print">0146-6615</issn><issn type="electronic">1096-9071</issn><idGroup><id type="product" value="JMV"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF MEDICAL VIROLOGY">Journal of Medical Virology</title><title type="short">J. 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Virol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="10"><doi origin="wiley" registered="yes">10.1002/jmv.v77:1</doi><numberingGroup><numbering type="journalVolume" number="77">77</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2005-09">September 2005</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="1" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jmv.20407</doi><idGroup><id type="unit" value="JMV20407"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title></titleGroup><copyright ownership="publisher">Copyright © 2005 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptAccepted" date="2005-05-24"></event><event type="firstOnline" date="2005-07-19"></event><event type="publishedOnlineFinalForm" date="2005-07-19"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-15"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-20"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-30"></event></eventGroup><numberingGroup><numbering type="pageFirst">1</numbering><numbering type="pageLast">7</numbering></numberingGroup><correspondenceTo>Department of Pediatrics, National Taiwan University Hospital, No. 7 Chung‐Shan South Road, Taipei, Taiwan.===</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JMV.JMV20407.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="34"></count><count type="wordTotal" number="1194"></count></countGroup><titleGroup><title type="main" xml:lang="en">Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection</title><title type="short" xml:lang="en">Autoantibodies After SARS‐CoV Infection</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Yao‐Hsu</givenNames><familyName>Yang</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Yu‐Hui</givenNames><familyName>Huang</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Ya‐Hui</givenNames><familyName>Chuang</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Chung‐Min</givenNames><familyName>Peng</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Li‐Chieh</givenNames><familyName>Wang</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Yu‐Tsan</givenNames><familyName>Lin</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Bor‐Luen</givenNames><familyName>Chiang</familyName></personName><contactDetails><email>gicmbor@ha.mc.ntu.edu.tw</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="TW" type="organization"><unparsedAffiliation>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">SARS</keyword><keyword xml:id="kwd2">autoantibodies</keyword><keyword xml:id="kwd3">epithelial cell</keyword><keyword xml:id="kwd4">endothelial cell</keyword><keyword xml:id="kwd5">cytotoxicity</keyword></keywordGroup><fundingInfo><fundingAgency>The National Science Council, Republic of China</fundingAgency><fundingNumber>NSC‐92‐2751‐B‐002‐001‐Y</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The severe acute respiratory syndrome (SARS) is caused by infection with the SARS‐associated coronavirus (SARS‐CoV) and characterized by severe pulmonary inflammation and fibrosis. In this study, the development of autoantibodies against human epithelial cells and endothelial cells in patients with SARS at different time periods (the first week: phase I, 1 month after the disease onset: phase II/phase III) were investigated. Antibodies in sera of patients and healthy controls against: (1) A549 human pulmonary epithelial cell‐line, (2) human umbilical venous endothelial cells (HUVEC), (3) primary human pulmonary endothelial cells (HPEC) were detected by cell‐based ELISA and indirect immunofluorescence staining. The results revealed that serum levels of IgG anti‐A549 cells antibodies, IgG anti‐HUVEC antibodies, and IgM anti‐HPEC antibodies were significantly higher in SARS patients at phase II/phase III than those in healthy controls. Sera from SARS patients at phase II/phase III could mediate complement dependent cytotoxicity against some A549 cells and HPEC. It is concluded that some autoantibodies against human epithelial cells and endothelial cells would be developed after SARS‐CoV infection and this phenomenon may indicate post‐infectious cellular injury and also induce SARS‐induced immunopathology. J. Med. Virol. 77:1–7, 2005. © 2005 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Autoantibodies After SARS‐CoV Infection</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection</title></titleInfo><name type="personal"><namePart type="given">Yao‐Hsu</namePart><namePart type="family">Yang</namePart><affiliation>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yu‐Hui</namePart><namePart type="family">Huang</namePart><affiliation>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ya‐Hui</namePart><namePart type="family">Chuang</namePart><affiliation>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chung‐Min</namePart><namePart type="family">Peng</namePart><affiliation>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Li‐Chieh</namePart><namePart type="family">Wang</namePart><affiliation>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yu‐Tsan</namePart><namePart type="family">Lin</namePart><affiliation>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bor‐Luen</namePart><namePart type="family">Chiang</namePart><affiliation>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan</affiliation><affiliation>E-mail: gicmbor@ha.mc.ntu.edu.tw</affiliation><affiliation>Correspondence address: Department of Pediatrics, National Taiwan University Hospital, No. 7 Chung‐Shan South Road, Taipei, Taiwan.===</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">2005-09</dateIssued><dateValid encoding="w3cdtf">2005-05-24</dateValid><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">4</extent><extent unit="tables">0</extent><extent unit="references">34</extent><extent unit="words">1194</extent></physicalDescription><abstract lang="en">The severe acute respiratory syndrome (SARS) is caused by infection with the SARS‐associated coronavirus (SARS‐CoV) and characterized by severe pulmonary inflammation and fibrosis. In this study, the development of autoantibodies against human epithelial cells and endothelial cells in patients with SARS at different time periods (the first week: phase I, 1 month after the disease onset: phase II/phase III) were investigated. Antibodies in sera of patients and healthy controls against: (1) A549 human pulmonary epithelial cell‐line, (2) human umbilical venous endothelial cells (HUVEC), (3) primary human pulmonary endothelial cells (HPEC) were detected by cell‐based ELISA and indirect immunofluorescence staining. The results revealed that serum levels of IgG anti‐A549 cells antibodies, IgG anti‐HUVEC antibodies, and IgM anti‐HPEC antibodies were significantly higher in SARS patients at phase II/phase III than those in healthy controls. Sera from SARS patients at phase II/phase III could mediate complement dependent cytotoxicity against some A549 cells and HPEC. It is concluded that some autoantibodies against human epithelial cells and endothelial cells would be developed after SARS‐CoV infection and this phenomenon may indicate post‐infectious cellular injury and also induce SARS‐induced immunopathology. J. Med. Virol. 77:1–7, 2005. © 2005 Wiley‐Liss, Inc.</abstract><note type="funding">The National Science Council, Republic of China - No. NSC‐92‐2751‐B‐002‐001‐Y; </note><subject lang="en"><genre>keywords</genre><topic>SARS</topic><topic>autoantibodies</topic><topic>epithelial cell</topic><topic>endothelial cell</topic><topic>cytotoxicity</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Medical Virology</title></titleInfo><titleInfo type="abbreviated"><title>J. Med. 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