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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The interferon gamma gene polymorphism +874 A/T is associated with severe acute respiratory syndrome</title><author><name sortKey="Chong, Wai Po" sort="Chong, Wai Po" uniqKey="Chong W" first="Wai Po" last="Chong">Wai Po Chong</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author><author><name sortKey="Ip, Wk Eddie" sort="Ip, Wk Eddie" uniqKey="Ip W" first="Wk Eddie" last="Ip">Wk Eddie Ip</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author><author><name sortKey="Tso, Gloria Hoi Wan" sort="Tso, Gloria Hoi Wan" uniqKey="Tso G" first="Gloria Hoi Wan" last="Tso">Gloria Hoi Wan Tso</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author><author><name sortKey="Ng, Man Wai" sort="Ng, Man Wai" uniqKey="Ng M" first="Man Wai" last="Ng">Man Wai Ng</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author><author><name sortKey="Wong, Wilfred Hing Sang" sort="Wong, Wilfred Hing Sang" uniqKey="Wong W" first="Wilfred Hing Sang" last="Wong">Wilfred Hing Sang Wong</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author><author><name sortKey="Law, Helen Ka Wai" sort="Law, Helen Ka Wai" uniqKey="Law H" first="Helen Ka Wai" last="Law">Helen Ka Wai Law</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author><author><name sortKey="Yung, Raymond Wh" sort="Yung, Raymond Wh" uniqKey="Yung R" first="Raymond Wh" last="Yung">Raymond Wh Yung</name><affiliation><nlm:aff id="Aff2">Department of Pathology, Pamela Nethersole Youde Hospital, Hong Kong SAR, China</nlm:aff></affiliation></author><author><name sortKey="Chow, Eudora Y" sort="Chow, Eudora Y" uniqKey="Chow E" first="Eudora Y" last="Chow">Eudora Y. Chow</name><affiliation><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="GRID">grid.417037.6</institution-id><institution-id institution-id-type="ISNI">0000 0004 1771 3082</institution-id><institution>Department of Pathology,</institution><institution>United Christian Hospital,</institution></institution-wrap>Hong Kong SAR, China</nlm:aff></affiliation></author><author><name sortKey="Au, Kl" sort="Au, Kl" uniqKey="Au K" first="Kl" last="Au">Kl Au</name><affiliation><nlm:aff id="Aff4"><institution-wrap><institution-id institution-id-type="GRID">grid.415229.9</institution-id><institution-id institution-id-type="ISNI">0000 0004 1799 7070</institution-id><institution>Princess Margaret Hospital,</institution></institution-wrap>Hong Kong SAR, China</nlm:aff></affiliation></author><author><name sortKey="Chan, Eric Yt" sort="Chan, Eric Yt" uniqKey="Chan E" first="Eric Yt" last="Chan">Eric Yt Chan</name><affiliation><nlm:aff id="Aff5"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Queen Mary Hospital,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Hong Kong SAR, China</nlm:aff></affiliation></author><author><name sortKey="Lim, Wilina" sort="Lim, Wilina" uniqKey="Lim W" first="Wilina" last="Lim">Wilina Lim</name><affiliation><nlm:aff id="Aff6"><institution-wrap><institution-id institution-id-type="GRID">grid.461944.a</institution-id><institution-id institution-id-type="ISNI">000000041790898X</institution-id><institution>Government Virus Unit, Department of Health,</institution></institution-wrap>Hong Kong SAR, China</nlm:aff></affiliation></author><author><name sortKey="Peiris, Js Malik" sort="Peiris, Js Malik" uniqKey="Peiris J" first="Js Malik" last="Peiris">Js Malik Peiris</name><affiliation><nlm:aff id="Aff7"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Microbiology,</institution><institution>The Hong Kong Jockey Club Research Centre, Pokfulam, The University of Hong Kong,</institution></institution-wrap>Hong Kong SAR, China</nlm:aff></affiliation></author><author><name sortKey="Lau, Yu Lung" sort="Lau, Yu Lung" uniqKey="Lau Y" first="Yu Lung" last="Lau">Yu Lung Lau</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">16672072</idno><idno type="pmc">1468415</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1468415</idno><idno type="RBID">PMC:1468415</idno><idno type="doi">10.1186/1471-2334-6-82</idno><date when="2006">2006</date><idno type="wicri:Area/Pmc/Corpus">000292</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000292</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The interferon gamma gene polymorphism +874 A/T is associated with severe acute respiratory syndrome</title><author><name sortKey="Chong, Wai Po" sort="Chong, Wai Po" uniqKey="Chong W" first="Wai Po" last="Chong">Wai Po Chong</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author><author><name sortKey="Ip, Wk Eddie" sort="Ip, Wk Eddie" uniqKey="Ip W" first="Wk Eddie" last="Ip">Wk Eddie Ip</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author><author><name sortKey="Tso, Gloria Hoi Wan" sort="Tso, Gloria Hoi Wan" uniqKey="Tso G" first="Gloria Hoi Wan" last="Tso">Gloria Hoi Wan Tso</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author><author><name sortKey="Ng, Man Wai" sort="Ng, Man Wai" uniqKey="Ng M" first="Man Wai" last="Ng">Man Wai Ng</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author><author><name sortKey="Wong, Wilfred Hing Sang" sort="Wong, Wilfred Hing Sang" uniqKey="Wong W" first="Wilfred Hing Sang" last="Wong">Wilfred Hing Sang Wong</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author><author><name sortKey="Law, Helen Ka Wai" sort="Law, Helen Ka Wai" uniqKey="Law H" first="Helen Ka Wai" last="Law">Helen Ka Wai Law</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author><author><name sortKey="Yung, Raymond Wh" sort="Yung, Raymond Wh" uniqKey="Yung R" first="Raymond Wh" last="Yung">Raymond Wh Yung</name><affiliation><nlm:aff id="Aff2">Department of Pathology, Pamela Nethersole Youde Hospital, Hong Kong SAR, China</nlm:aff></affiliation></author><author><name sortKey="Chow, Eudora Y" sort="Chow, Eudora Y" uniqKey="Chow E" first="Eudora Y" last="Chow">Eudora Y. Chow</name><affiliation><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="GRID">grid.417037.6</institution-id><institution-id institution-id-type="ISNI">0000 0004 1771 3082</institution-id><institution>Department of Pathology,</institution><institution>United Christian Hospital,</institution></institution-wrap>Hong Kong SAR, China</nlm:aff></affiliation></author><author><name sortKey="Au, Kl" sort="Au, Kl" uniqKey="Au K" first="Kl" last="Au">Kl Au</name><affiliation><nlm:aff id="Aff4"><institution-wrap><institution-id institution-id-type="GRID">grid.415229.9</institution-id><institution-id institution-id-type="ISNI">0000 0004 1799 7070</institution-id><institution>Princess Margaret Hospital,</institution></institution-wrap>Hong Kong SAR, China</nlm:aff></affiliation></author><author><name sortKey="Chan, Eric Yt" sort="Chan, Eric Yt" uniqKey="Chan E" first="Eric Yt" last="Chan">Eric Yt Chan</name><affiliation><nlm:aff id="Aff5"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Queen Mary Hospital,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Hong Kong SAR, China</nlm:aff></affiliation></author><author><name sortKey="Lim, Wilina" sort="Lim, Wilina" uniqKey="Lim W" first="Wilina" last="Lim">Wilina Lim</name><affiliation><nlm:aff id="Aff6"><institution-wrap><institution-id institution-id-type="GRID">grid.461944.a</institution-id><institution-id institution-id-type="ISNI">000000041790898X</institution-id><institution>Government Virus Unit, Department of Health,</institution></institution-wrap>Hong Kong SAR, China</nlm:aff></affiliation></author><author><name sortKey="Peiris, Js Malik" sort="Peiris, Js Malik" uniqKey="Peiris J" first="Js Malik" last="Peiris">Js Malik Peiris</name><affiliation><nlm:aff id="Aff7"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Microbiology,</institution><institution>The Hong Kong Jockey Club Research Centre, Pokfulam, The University of Hong Kong,</institution></institution-wrap>Hong Kong SAR, China</nlm:aff></affiliation></author><author><name sortKey="Lau, Yu Lung" sort="Lau, Yu Lung" uniqKey="Lau Y" first="Yu Lung" last="Lau">Yu Lung Lau</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</nlm:aff></affiliation></author></analytic><series><title level="j">BMC Infectious Diseases</title><idno type="eISSN">1471-2334</idno><imprint><date when="2006">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>Cytokines play important roles in antiviral action. We examined whether polymorphisms of <italic>IFN-γ</italic>,<italic>TNF-α</italic> and <italic>IL-10</italic> affect the susceptibility to and outcome of severe acute respiratory syndrome (SARS).</p></sec><sec><title>Methods</title><p>A case-control study was carried out in 476 Chinese SARS patients and 449 healthy controls. We tested the polymorphisms of <italic>IFN-γ</italic>,<italic>TNF-α</italic> and <italic>IL-10</italic> for their associations with SARS.</p></sec><sec><title>Results</title><p><italic>IFN-γ</italic> +874A allele was associated with susceptibility to SARS in a dose-dependent manner (<italic>P</italic> < 0.001). Individuals with <italic>IFN-γ</italic> +874 AA and AT genotype had a 5.19-fold (95% Confidence Interval [CI], 2.78-9.68) and 2.57-fold (95% CI, 1.35-4.88) increased risk of developing SARS respectively. The polymorphisms of <italic>IL-10</italic> and <italic>TNF-α</italic> were not associated with SARS susceptibility.</p></sec><sec><title>Conclusion</title><p><italic>IFN-γ</italic> +874A allele was shown to be a risk factor in SARS susceptibility.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Peiris, Js" uniqKey="Peiris J">JS Peiris</name></author><author><name sortKey="Lai, St" uniqKey="Lai S">ST Lai</name></author><author><name sortKey="Poon, Ll" uniqKey="Poon L">LL Poon</name></author><author><name sortKey="Guan, Y" uniqKey="Guan Y">Y Guan</name></author><author><name sortKey="Yam, Ly" uniqKey="Yam L">LY Yam</name></author><author><name sortKey="Lim, W" uniqKey="Lim W">W Lim</name></author><author><name sortKey="Nicholls, J" uniqKey="Nicholls J">J Nicholls</name></author><author><name sortKey="Yee, Wk" uniqKey="Yee W">WK Yee</name></author><author><name sortKey="Yan, Ww" uniqKey="Yan W">WW 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<front><journal-meta><journal-id journal-id-type="nlm-ta">BMC Infect Dis</journal-id><journal-id journal-id-type="iso-abbrev">BMC Infect. Dis</journal-id><journal-title-group><journal-title>BMC Infectious Diseases</journal-title></journal-title-group><issn pub-type="epub">1471-2334</issn><publisher><publisher-name>BioMed Central</publisher-name><publisher-loc>London</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">16672072</article-id><article-id pub-id-type="pmc">1468415</article-id><article-id pub-id-type="publisher-id">346</article-id><article-id pub-id-type="doi">10.1186/1471-2334-6-82</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>The interferon gamma gene polymorphism +874 A/T is associated with severe acute respiratory syndrome</article-title></title-group><contrib-group><contrib contrib-type="author" equal-contrib="yes"><name><surname>Chong</surname><given-names>Wai Po</given-names></name><address><email>h9820905@graduate.hku.hk</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author" equal-contrib="yes"><name><surname>Ip</surname><given-names>WK Eddie</given-names></name><address><email>WIP@partners.org</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Tso</surname><given-names>Gloria Hoi Wan</given-names></name><address><email>h98083405@hkusua.hku.hk</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Ng</surname><given-names>Man Wai</given-names></name><address><email>ivy_natsu@yahoo.com.hk</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Wong</surname><given-names>Wilfred Hing Sang</given-names></name><address><email>whswong@hkucc.hku.hk</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Law</surname><given-names>Helen Ka Wai</given-names></name><address><email>hkwlaw@hkucc.hku.hk</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Yung</surname><given-names>Raymond WH</given-names></name><address><email>rwhyung@ha.org.hk</email></address><xref ref-type="aff" rid="Aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Chow</surname><given-names>Eudora Y</given-names></name><address><email>chowe@ha.org.hk</email></address><xref ref-type="aff" rid="Aff3">3</xref></contrib><contrib contrib-type="author"><name><surname>Au</surname><given-names>KL</given-names></name><address><email>klau@ha.org.hk</email></address><xref ref-type="aff" rid="Aff4">4</xref></contrib><contrib contrib-type="author"><name><surname>Chan</surname><given-names>Eric YT</given-names></name><address><email>eytchan@ha.org.hk</email></address><xref ref-type="aff" rid="Aff5">5</xref></contrib><contrib contrib-type="author"><name><surname>Lim</surname><given-names>Wilina</given-names></name><address><email>wllim@pacific.net.hk</email></address><xref ref-type="aff" rid="Aff6">6</xref></contrib><contrib contrib-type="author"><name><surname>Peiris</surname><given-names>JS Malik</given-names></name><address><email>malik@hkucc.hku.hk</email></address><xref ref-type="aff" rid="Aff7">7</xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Lau</surname><given-names>Yu Lung</given-names></name><address><email>lauylung@hkucc.hku.hk</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><aff id="Aff1"><label>1</label><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Paediatrics and Adolescent Medicine, The Hong Kong Jockey Club Research Centre,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Pokfulam, Hong Kong SAR China</aff><aff id="Aff2"><label>2</label>Department of Pathology, Pamela Nethersole Youde Hospital, Hong Kong SAR, China</aff><aff id="Aff3"><label>3</label><institution-wrap><institution-id institution-id-type="GRID">grid.417037.6</institution-id><institution-id institution-id-type="ISNI">0000 0004 1771 3082</institution-id><institution>Department of Pathology,</institution><institution>United Christian Hospital,</institution></institution-wrap>Hong Kong SAR, China</aff><aff id="Aff4"><label>4</label><institution-wrap><institution-id institution-id-type="GRID">grid.415229.9</institution-id><institution-id institution-id-type="ISNI">0000 0004 1799 7070</institution-id><institution>Princess Margaret Hospital,</institution></institution-wrap>Hong Kong SAR, China</aff><aff id="Aff5"><label>5</label><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Queen Mary Hospital,</institution><institution>The University of Hong Kong,</institution></institution-wrap>Hong Kong SAR, China</aff><aff id="Aff6"><label>6</label><institution-wrap><institution-id institution-id-type="GRID">grid.461944.a</institution-id><institution-id institution-id-type="ISNI">000000041790898X</institution-id><institution>Government Virus Unit, Department of Health,</institution></institution-wrap>Hong Kong SAR, China</aff><aff id="Aff7"><label>7</label><institution-wrap><institution-id institution-id-type="GRID">grid.194645.b</institution-id><institution-id institution-id-type="ISNI">0000000121742757</institution-id><institution>Department of Microbiology,</institution><institution>The Hong Kong Jockey Club Research Centre, Pokfulam, The University of Hong Kong,</institution></institution-wrap>Hong Kong SAR, China</aff></contrib-group><pub-date pub-type="epub"><day>04</day><month>5</month><year>2006</year></pub-date><pub-date pub-type="pmc-release"><day>04</day><month>5</month><year>2006</year></pub-date><pub-date pub-type="collection"><year>2006</year></pub-date><volume>6</volume><elocation-id>82</elocation-id><history><date date-type="received"><day>07</day><month>2</month><year>2006</year></date><date date-type="accepted"><day>04</day><month>5</month><year>2006</year></date></history><permissions><copyright-statement>© Po Chong et al; licensee BioMed Central Ltd. 2006</copyright-statement><license><license-p>This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.</license-p></license></permissions><abstract id="Abs1"><sec><title>Background</title><p>Cytokines play important roles in antiviral action. We examined whether polymorphisms of <italic>IFN-γ</italic>,<italic>TNF-α</italic> and <italic>IL-10</italic> affect the susceptibility to and outcome of severe acute respiratory syndrome (SARS).</p></sec><sec><title>Methods</title><p>A case-control study was carried out in 476 Chinese SARS patients and 449 healthy controls. We tested the polymorphisms of <italic>IFN-γ</italic>,<italic>TNF-α</italic> and <italic>IL-10</italic> for their associations with SARS.</p></sec><sec><title>Results</title><p><italic>IFN-γ</italic> +874A allele was associated with susceptibility to SARS in a dose-dependent manner (<italic>P</italic> < 0.001). Individuals with <italic>IFN-γ</italic> +874 AA and AT genotype had a 5.19-fold (95% Confidence Interval [CI], 2.78-9.68) and 2.57-fold (95% CI, 1.35-4.88) increased risk of developing SARS respectively. The polymorphisms of <italic>IL-10</italic> and <italic>TNF-α</italic> were not associated with SARS susceptibility.</p></sec><sec><title>Conclusion</title><p><italic>IFN-γ</italic> +874A allele was shown to be a risk factor in SARS susceptibility.</p></sec></abstract><kwd-group xml:lang="en"><title>Keywords</title><kwd>Severe Acute Respiratory Syndrome</kwd><kwd>Antiviral Response</kwd><kwd>Severe Acute Respiratory Syndrome</kwd><kwd>Severe Acute Respiratory Syndrome Patient</kwd><kwd>Severe Acute Respiratory Syndrome Coronavirus</kwd></kwd-group><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© The Author(s) 2006</meta-value></custom-meta></custom-meta-group></article-meta></front><body><sec id="Sec1"><title>Background</title><p>Severe acute respiratory syndrome (SARS) is an infectious disease caused by SARS coronavirus [<xref ref-type="bibr" rid="CR1">1</xref>] with >8000 cases and 774 deaths reported in 2003 [<xref ref-type="bibr" rid="CR2">2</xref>]. Much progress has been made in understanding SARS coronavirus but the pathogenesis is still unclear [<xref ref-type="bibr" rid="CR3">3</xref>]. It was reported that old age, diabetes mellitus and heart disease were risk factors for adverse prognosis of SARS [<xref ref-type="bibr" rid="CR4">4</xref>–<xref ref-type="bibr" rid="CR6">6</xref>], however, little is known about the contribution of genetic factors. We have demonstrated that genetic haplotypes associated with low serum mannose-binding lectin (MBL) were associated with SARS [<xref ref-type="bibr" rid="CR7">7</xref>] and our findings were recently replicated [<xref ref-type="bibr" rid="CR8">8</xref>]. Recently, homozygotes for <italic>CLEC4M</italic> tandem repeats were reported to be less susceptible to SARS in Hong Kong Chinese [<xref ref-type="bibr" rid="CR9">9</xref>].</p><p>Cytokines are known to be important in antiviral action. Interferon (IFN)-γ from T and natural killer (NK) cells is important in driving the T helper cell type 1 (Th1) responses. It also activates monocytes and macrophages, which in turn take part in antiviral responses by producing free radicals and pro-inflammatory cytokines like tumor necrosis factor (TNF)-α. [<xref ref-type="bibr" rid="CR10">10</xref>]. TNF-α then regulates expression of neutrophil-endothelial cell adhesion molecules and chemokines, which recruit leukocytes to the site of infection [<xref ref-type="bibr" rid="CR11">11</xref>–<xref ref-type="bibr" rid="CR13">13</xref>]. Thus, IFN-γand TNF-α play important role in antiviral response and inflammation.</p><p>Interleukin 10 (IL-10) is an antiinflammatory cytokine that inhibits the activation and effector function of Th1 cells, monocytes, and macrophages [<xref ref-type="bibr" rid="CR14">14</xref>]. IL-10 appears to limit and ultimately terminate inflammatory responses by blocking the expression of a number of pro-inflammatory cytokines and chemokines [<xref ref-type="bibr" rid="CR15">15</xref>]. In animal model, IL10 counteracts the inflammatory response by inhibiting TNF-α production and neutrophil activation, and leads to a reduction of the lung tissue injury [<xref ref-type="bibr" rid="CR16">16</xref>]. Thus, IL-10 plays an important role in regulating many immune and inflammatory processes. Various studies showed that a high IL-10 level would result in suppression of innate host defense and lead to increasing susceptibility of the host to various microbes and death [<xref ref-type="bibr" rid="CR17">17</xref>–<xref ref-type="bibr" rid="CR19">19</xref>].</p><p>In this study, we hypothesized that the polymorphisms of the cytokine genes, i.e. <italic>IFN-γ</italic> +874A/T, <italic>TNF-α</italic> -308G/A, <italic>IL-10</italic> -1082G/A and -592A/C, might be associated with SARS. These genes were chosen based on their functions in antiviral response and inflammation regulation that may be involved in SARS pathogenesis and their polymorphisms based on their potential regulation on gene expression (Table <xref rid="Tab1" ref-type="table">1</xref>). We tested our hypotheses in 476 SARS patients and 449 healthy controls and found that polymorphism of <italic>IFN-γ</italic> +874A allele was associated with susceptibility to SARS in a dose-dependent manner.<table-wrap id="Tab1"><label>Table 1</label><caption><p>Polymorphisms of the genes genotyped</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left">Genes</th><th align="left">SNPs</th><th align="left">rs number</th><th align="left">References</th></tr></thead><tbody><tr><td align="left"><italic>IFN-γ</italic></td><td align="left"><italic>IFN-γ</italic> +874 A/T</td><td align="left">rs2430561</td><td align="left">[23]</td></tr><tr><td align="left"><italic>IL-10</italic></td><td align="left"><italic>IL-10</italic> -1082 A/G</td><td align="left">rs1800896</td><td align="left">[23,26-27]</td></tr><tr><td></td><td align="left"><italic>IL-10</italic> -592 A/C</td><td align="left">rs1800872</td><td></td></tr><tr><td align="left"><italic>TNF-α</italic></td><td align="left"><italic>TNF-α</italic> -308G/A</td><td align="left">rs1800629</td><td align="left">[28]</td></tr></tbody></table></table-wrap></p></sec><sec id="Sec2"><title>Methods</title><sec id="Sec3"><title>Patient populations</title><p>The study was approved by the Clinical Research Ethics Committee of the Institutional Review Board of the University of Hong Kong/Hospital Authority Hong Kong West Cluster and included 476 Chinese patients with SARS (201 male, mean age = 39.8 ± 15.2) and 449 ethnically matched healthy controls from Red Cross (273 male, mean age = 29.1 ± 10.4). At least 95% of the patients were documented with SARS-CoV antibody seroconversion and/or detectable SARS-CoV RNA in respiratory secretions by RT-PCR.</p></sec><sec id="Sec4"><title>Genotyping</title><p><italic>IFN-γ</italic> +874A/T, <italic>IL-10</italic> -1082G/A and -592A/C were genotyped by TaqMan system (Applied Biosystems, Foster City, CA, USA) as described previously [<xref ref-type="bibr" rid="CR20">20</xref>]. <italic>TNF-α</italic> -308 G/A was also genotyped by TaqMan system with same condition. The sequences of the primers were 5'-CCT GGT CCC CAA AAG AAA TG-3' and 5'-TCT TCT GGG CCA CTG ACT GA-3' and the probes were 6-FAM-TTG AGG GGC ATG <bold>G</bold>GG ACG G-TAMRA and VIC-TTG AGG GGC ATG <bold>A</bold>GG ACG GG-TAMRA.</p></sec><sec id="Sec5"><title>Statistical analysis</title><p>The frequencies of genotypes and alleles of the 4 single nucleotide polymorphisms (SNPs) were compared between the SARS patients and healthy controls by 3 × 2 and 2 × 2 chi square test respectively. In case of significance, logistic regression was used for calculating OR with 95% CI and corresponding <italic>P-</italic>values between groups by controlling age and sex as covariables. The genotypes of all SNPs were tested for Hardy-Weinberg equilibrium (HWE) by chi square test.</p></sec></sec><sec id="Sec6"><title>Results and discussion</title><p>Our case-control study genotyped the 4 SNPs <italic>IFN-γ</italic> +874A/T, <italic>TNF-α</italic> -308G/A, <italic>IL-10</italic> -1082G/A and -592A/C in 476 Chinese patients with SARS and 449 healthy controls. The genotype distributions and allele frequencies of these 4 SNPs were shown in Table <xref rid="Tab2" ref-type="table">2</xref>. The <italic>IFN-γ</italic> +874A allele was overrepresented in SARS patients (83.1%) when compared with the controls (66.3%) (<italic>P</italic> < 0.001). It was also significantly associated with susceptibility to SARS in a dose-dependent manner (<italic>P</italic> < 0.001), i.e. individuals with <italic>IFN-γ</italic> +874 AA and AT genotype had an odds ratio (OR) of 5.19 (95% CI, 2.78-9.68) and 2.57 (95% CI, 1.35-4.88) in developing SARS respectively. However, no significant correlation was observed in SNPs of <italic>IL-10</italic> and <italic>TNF-α</italic>. All SNPs were in Hardy-Weinberg equilibrium (HWE) (<italic>P</italic> > 0.05) in SARS patients and controls by chi square test, except <italic>IL-10</italic>-592A/C.<table-wrap id="Tab2"><label>Table 2</label><caption><p>Allele frequencies and genotype frequencies in SARS patients and controls*</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="center">SNP</th><th align="center">SARS (n = 476)</th><th align="center">Control (n = 449)</th><th align="center">OR (95% CI)</th><th align="center"><italic>P</italic></th></tr><tr><th></th><th align="center" colspan="2">Number (%)</th><th></th><th></th></tr></thead><tbody><tr><td align="center"><bold>Genotype</bold></td><td></td><td></td><td></td><td></td></tr><tr><td align="center"><italic>IFN-γ</italic> +874</td><td></td><td></td><td></td><td align="center"><0.001</td></tr><tr><td align="center">A/A</td><td align="center">332 (69.8)</td><td align="center">203 (45.2)</td><td align="center">5.19 (2.78 – 9.68)</td><td></td></tr><tr><td align="center">A/T</td><td align="center">127 (26.7)</td><td align="center">189 (42.1)</td><td align="center">2.57 (1.35 – 4.88)</td><td></td></tr><tr><td align="center">T/T</td><td align="center">17 (3.6)</td><td align="center">57 (12.7)</td><td align="center">Reference</td><td></td></tr><tr><td align="center"><italic>IL-10</italic> -1082</td><td></td><td></td><td></td><td align="center">NS</td></tr><tr><td align="center">A/A</td><td align="center">439 (92.2)</td><td align="center">411 (91.5)</td><td align="center">..</td><td></td></tr><tr><td align="center">A/G</td><td align="center">35 (7.4)</td><td align="center">38 (8.5)</td><td align="center">..</td><td></td></tr><tr><td align="center">G/G</td><td align="center">2 (0.4)</td><td align="center">0 (0)</td><td align="center">..</td><td></td></tr><tr><td align="center"><italic>IL-10</italic> -592</td><td></td><td></td><td></td><td align="center">NS</td></tr><tr><td align="center">A/A</td><td align="center">244 (51.3)</td><td align="center">209 (46.6)</td><td align="center">..</td><td></td></tr><tr><td align="center">A/C</td><td align="center">188 (39.5)</td><td align="center">214 (47.7)</td><td align="center">..</td><td></td></tr><tr><td align="center">C/C</td><td align="center">44 (9.2)</td><td align="center">26 (5.8)</td><td align="center">..</td><td></td></tr><tr><td align="center"><italic>TNF-a</italic> -308</td><td></td><td></td><td></td><td align="center">NS</td></tr><tr><td align="center">GG</td><td align="center">403 (84.7)</td><td align="center">377 (83.9)</td><td align="center">..</td><td></td></tr><tr><td align="center">GA</td><td align="center">70 (14.7)</td><td align="center">70 (15.6)</td><td align="center">..</td><td></td></tr><tr><td align="center">AA</td><td align="center">3 (0.6)</td><td align="center">2 (0.5)</td><td align="center">..</td><td></td></tr><tr><td align="center"><bold>Allele</bold></td><td></td><td></td><td></td><td></td></tr><tr><td align="center"><italic>IFN-γ</italic> +874</td><td></td><td></td><td></td><td align="center"><0.001</td></tr><tr><td align="center">A</td><td align="center">791 (83.1)</td><td align="center">595 (66.3)</td><td align="center">2.23 (1.75 – 2.83)</td><td></td></tr><tr><td align="center">T</td><td align="center">161 (16.9)</td><td align="center">303 (33.7)</td><td></td><td></td></tr><tr><td align="center"><italic>IL-10</italic> -1082</td><td></td><td></td><td></td><td align="center">NS</td></tr><tr><td align="center">A</td><td align="center">913 (95.9)</td><td align="center">860 (95.8)</td><td align="center">..</td><td></td></tr><tr><td align="center">G</td><td align="center">39 (4.1)</td><td align="center">38 (4.2)</td><td align="center">..</td><td></td></tr><tr><td align="center"><italic>IL-10</italic> -592</td><td></td><td></td><td></td><td align="center">NS</td></tr><tr><td align="center">A</td><td align="center">676 (71.0)</td><td align="center">632 (70.4)</td><td align="center">..</td><td></td></tr><tr><td align="center">C</td><td align="center">276 (29.0)</td><td align="center">266 (29.6)</td><td align="center">..</td><td></td></tr><tr><td align="center"><italic>TNF-a</italic> -308</td><td></td><td></td><td></td><td align="center">NS</td></tr><tr><td align="center">G</td><td align="center">876 (92.0)</td><td align="center">824 (91.8)</td><td align="center">..</td><td></td></tr><tr><td align="center">A</td><td align="center">76 (8.0)</td><td align="center">74 (8.2)</td><td align="center">..</td><td></td></tr></tbody></table><table-wrap-foot><p>NS = not significant.</p><p>*<italic>P</italic>-value and OR (95% CI) were calculated with the use of logistic regression models, adjusted with sex and age.</p></table-wrap-foot></table-wrap></p><p><italic>IFN-γ</italic> +874A allele has been previously reported to be associated with infectious diseases such as tuberculosis, hepatitis B virus infection, and parvovirus infection [<xref ref-type="bibr" rid="CR20">20</xref>–<xref ref-type="bibr" rid="CR22">22</xref>], revealing its potential role of function in host defense against microbial infections. The mechanism by which the <italic>IFN-γ</italic> +874A/T allele influences the susceptibility to SARS may depend on its role in the regulation of IFN-γ production. The T allele of <italic>IFN-γ</italic> +874A/T provides a binding site for the transcription factor nuclear factor-κB (NF-κB), which is able to regulate <italic>IFN-γ</italic> expression [<xref ref-type="bibr" rid="CR23">23</xref>]. It is possible that low IFN-γ production may impair their anti-viral response against SARS-CoV, rendering these individuals more susceptible to this virus infection. Our observation that <italic>IFN-γ</italic> +874A allele was significantly associated with SARS-CoV infection suggests a genetic risk factor for SARS. The role of IFN-γ in antiviral response against SARS-CoV has also been supported by recent studies showing that IFN-γ can inhibit the replication of SARS-CoV in combination with IFN-β <italic>in vitro</italic> [<xref ref-type="bibr" rid="CR24">24</xref>, <xref ref-type="bibr" rid="CR25">25</xref>].</p><p><italic>IL-10</italic> and <italic>TNF-α</italic> SNPs were also included in this study. They were chosen due to their potential regulation on protein expression level [<xref ref-type="bibr" rid="CR26">26</xref>–<xref ref-type="bibr" rid="CR28">28</xref>]. However, our present data did not show any significant association of these SNPs with SARS (Table <xref rid="Tab2" ref-type="table">2</xref>). Nevertheless, we cannot exclude the role of <italic>IL-10</italic> and <italic>TNF-α</italic> as the susceptibility genes for SARS, because other SNPs in these 2 genes may also be involved in gene expression regulation. Further association studies on other SNPs, which could alter the gene expression level are required to ascertain the relationship of <italic>IL-10</italic> and <italic>TNF-α</italic> in SARS.</p><p>We have also compared the genotype and allele frequencies of all the polymorphisms between the death group and survival group of the SARS patients (Table <xref rid="Tab3" ref-type="table">3</xref>). However, no significant association was established.<table-wrap id="Tab3"><label>Table 3</label><caption><p>Genotype frequencies among survival and death SARS cases</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="center">SNP</th><th align="center">Death (n = 57)</th><th align="center">Survival (n = 415)</th><th align="center"><italic>P</italic></th></tr><tr><th></th><th align="center" colspan="2">Number (%)</th><th></th></tr></thead><tbody><tr><td align="center"><bold>Genotype</bold></td><td></td><td></td><td></td></tr><tr><td align="center"><italic>IFN-γ</italic> +874</td><td></td><td></td><td align="center">NS</td></tr><tr><td align="center">A/A</td><td align="center">41 (71.9)</td><td align="center">289 (69.6)</td><td></td></tr><tr><td align="center">A/T</td><td align="center">13 (22.8)</td><td align="center">112 (27.0)</td><td></td></tr><tr><td align="center">T/T</td><td align="center">3 (5.3)</td><td align="center">14 (3.4)</td><td></td></tr><tr><td align="center"><italic>IL-10</italic>-1082</td><td></td><td></td><td align="center">NS</td></tr><tr><td align="center">A/A</td><td align="center">52 (91.2)</td><td align="center">383 (92.3)</td><td></td></tr><tr><td align="center">A/G</td><td align="center">4 (7.0)</td><td align="center">31 (7.5)</td><td></td></tr><tr><td align="center">G/G</td><td align="center">1 (1.8)</td><td align="center">1 (0.2)</td><td></td></tr><tr><td align="center"><italic>IL-10</italic>-592</td><td></td><td></td><td align="center">NS</td></tr><tr><td align="center">A/A</td><td align="center">28 (49.1)</td><td align="center">214 (51.6)</td><td></td></tr><tr><td align="center">A/C</td><td align="center">21 (36.8)</td><td align="center">165 (39.8)</td><td></td></tr><tr><td align="center">C/C</td><td align="center">8 (14.0)</td><td align="center">36 (8.7)</td><td></td></tr><tr><td align="center"><italic>TNF-a</italic>-308</td><td></td><td></td><td align="center">NS</td></tr><tr><td align="center">GG</td><td align="center">46 (80.7)</td><td align="center">353 (85.1)</td><td></td></tr><tr><td align="center">GA</td><td align="center">11 (19.3)</td><td align="center">59 (14.2)</td><td></td></tr><tr><td align="center">AA</td><td align="center">0 (0)</td><td align="center">3 (0.7)</td><td></td></tr></tbody></table><table-wrap-foot><p>NS = not significant.</p></table-wrap-foot></table-wrap></p></sec><sec id="Sec7"><title>Conclusion</title><p>We demonstrated that <italic>IFN-γ</italic> +874A allele was significantly associated with SARS susceptibility in a dose dependent manner. Due to its role in regulating IFN-γ expression [<xref ref-type="bibr" rid="CR15">15</xref>], this allele may be involved in the pathogenesis of SARS by altering the IFN-γ production.</p></sec></body><back><fn-group><fn><p>Wai Po Chong, WK Eddie Ip contributed equally to this work.</p></fn><fn><p><bold>Competing interests</bold></p><p>The author(s) declare that they have no competing interests.</p></fn><fn><p><bold>Authors' contributions</bold></p><p>WPC and WKEI: Genotyping, data analyses, drafting the manuscript</p><p>GHWT: Genotyping</p><p>MWN and WHSW: Data analyses, drafting the manuscript</p><p>HKWL, RWHY, EYC, KLA, EYTC: Sample collection, revising for medical content</p><p>WL and JSMP: Sample collection, providing virological data</p><p>YLL: Study design, conception and co-ordination, drafting the manuscript</p><p><italic>All authors contributed to writing of the final manuscript</italic></p><p><italic>All authors read and approved the final 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