SARS coronavirus and innate immunity
Identifieur interne : 000F04 ( Pmc/Checkpoint ); précédent : 000F03; suivant : 000F05SARS coronavirus and innate immunity
Auteurs : Matthew Frieman [États-Unis] ; Mark Heise [États-Unis] ; Ralph Baric [États-Unis]Source :
- Virus Research [ 0168-1702 ] ; 2007.
Abstract
The emergence of the highly pathogenic SARS coronavirus (SARS-CoV) has reignited interest in coronavirus biology and pathogenesis. An emerging theme in coronavirus pathogenesis is that the interaction between specific viral genes and the host immune system, specifically the innate immune system, functions as a key determinant in regulating virulence and disease outcomes. Using SARS-CoV as a model, we will review the current knowledge of the interplay between coronavirus infection and the host innate immune system in vivo, and then discuss the mechanisms by which specific gene products antagonize the host innate immune response in cell culture models. Our data suggests that the SARS-CoV uses specific strategies to evade and antagonize the sensing and signaling arms of the interferon pathway. We summarize by identifying future points of consideration that will contribute greatly to our understanding of the molecular mechanisms governing coronavirus pathogenesis and virulence, and the development of severe disease in humans and animals.
Url:
DOI: 10.1016/j.virusres.2007.03.015
PubMed: 17451827
PubMed Central: 2292640
Affiliations:
- États-Unis
- Caroline du Nord
- Chapel Hill (Caroline du Nord)
- Université de Caroline du Nord à Chapel Hill
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PMC:2292640Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>The emergence of the highly pathogenic SARS coronavirus (SARS-CoV) has reignited interest in coronavirus biology and pathogenesis. An emerging theme in coronavirus pathogenesis is that the interaction between specific viral genes and the host immune system, specifically the innate immune system, functions as a key determinant in regulating virulence and disease outcomes. Using SARS-CoV as a model, we will review the current knowledge of the interplay between coronavirus infection and the host innate immune system in vivo, and then discuss the mechanisms by which specific gene products antagonize the host innate immune response in cell culture models. Our data suggests that the SARS-CoV uses specific strategies to evade and antagonize the sensing and signaling arms of the interferon pathway. We summarize by identifying future points of consideration that will contribute greatly to our understanding of the molecular mechanisms governing coronavirus pathogenesis and virulence, and the development of severe disease in humans and animals.</p>
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<author><name sortKey="Beutler, B" uniqKey="Beutler B">B. Beutler</name>
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</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Ziegler, T" uniqKey="Ziegler T">T. Ziegler</name>
</author>
<author><name sortKey="Matikainen, S" uniqKey="Matikainen S">S. Matikainen</name>
</author>
<author><name sortKey="Ronkko, E" uniqKey="Ronkko E">E. Ronkko</name>
</author>
<author><name sortKey="Osterlund, P" uniqKey="Osterlund P">P. Osterlund</name>
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</author>
</analytic>
</biblStruct>
</listBibl>
</div1>
</back>
</TEI>
<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Virus Res</journal-id>
<journal-id journal-id-type="iso-abbrev">Virus Res</journal-id>
<journal-title-group><journal-title>Virus Research</journal-title>
</journal-title-group>
<issn pub-type="ppub">0168-1702</issn>
<issn pub-type="epub">1872-7492</issn>
<publisher><publisher-name>Elsevier B.V.</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">17451827</article-id>
<article-id pub-id-type="pmc">2292640</article-id>
<article-id pub-id-type="publisher-id">S0168-1702(07)00102-5</article-id>
<article-id pub-id-type="doi">10.1016/j.virusres.2007.03.015</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>SARS coronavirus and innate immunity</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Frieman</surname>
<given-names>Matthew</given-names>
</name>
<email>frieman@email.unc.edu</email>
<xref rid="aff1" ref-type="aff">a</xref>
<xref rid="cor1" ref-type="corresp">⁎</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Heise</surname>
<given-names>Mark</given-names>
</name>
<xref rid="aff2" ref-type="aff">b</xref>
<xref rid="aff3" ref-type="aff">c</xref>
<xref rid="aff4" ref-type="aff">d</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Baric</surname>
<given-names>Ralph</given-names>
</name>
<xref rid="aff1" ref-type="aff">a</xref>
<xref rid="aff2" ref-type="aff">b</xref>
<xref rid="aff4" ref-type="aff">d</xref>
</contrib>
</contrib-group>
<aff id="aff1"><label>a</label>
Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States</aff>
<aff id="aff2"><label>b</label>
Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States</aff>
<aff id="aff3"><label>c</label>
Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States</aff>
<aff id="aff4"><label>d</label>
Carolina Vaccine Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States</aff>
<author-notes><corresp id="cor1"><label>⁎</label>
Corresponding author. Tel.: +1 919 966 3890; fax: +1 919 955 0586. <email>frieman@email.unc.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="pmc-release"><day>23</day>
<month>4</month>
<year>2007</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>4</month>
<year>2008</year>
</pub-date>
<pub-date pub-type="epub"><day>23</day>
<month>4</month>
<year>2007</year>
</pub-date>
<volume>133</volume>
<issue>1</issue>
<fpage>101</fpage>
<lpage>112</lpage>
<permissions><copyright-statement>Copyright © 2007 Elsevier B.V. All rights reserved.</copyright-statement>
<copyright-year>2007</copyright-year>
<copyright-holder>Elsevier B.V.</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><p>The emergence of the highly pathogenic SARS coronavirus (SARS-CoV) has reignited interest in coronavirus biology and pathogenesis. An emerging theme in coronavirus pathogenesis is that the interaction between specific viral genes and the host immune system, specifically the innate immune system, functions as a key determinant in regulating virulence and disease outcomes. Using SARS-CoV as a model, we will review the current knowledge of the interplay between coronavirus infection and the host innate immune system in vivo, and then discuss the mechanisms by which specific gene products antagonize the host innate immune response in cell culture models. Our data suggests that the SARS-CoV uses specific strategies to evade and antagonize the sensing and signaling arms of the interferon pathway. We summarize by identifying future points of consideration that will contribute greatly to our understanding of the molecular mechanisms governing coronavirus pathogenesis and virulence, and the development of severe disease in humans and animals.</p>
</abstract>
<kwd-group><title>Keywords</title>
<kwd>SARS coronavirus</kwd>
<kwd>Innate immunity</kwd>
<kwd>Interferon</kwd>
<kwd>RNA virus</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Caroline du Nord</li>
</region>
<settlement><li>Chapel Hill (Caroline du Nord)</li>
</settlement>
<orgName><li>Université de Caroline du Nord à Chapel Hill</li>
</orgName>
</list>
<tree><country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Frieman, Matthew" sort="Frieman, Matthew" uniqKey="Frieman M" first="Matthew" last="Frieman">Matthew Frieman</name>
</region>
<name sortKey="Baric, Ralph" sort="Baric, Ralph" uniqKey="Baric R" first="Ralph" last="Baric">Ralph Baric</name>
<name sortKey="Baric, Ralph" sort="Baric, Ralph" uniqKey="Baric R" first="Ralph" last="Baric">Ralph Baric</name>
<name sortKey="Baric, Ralph" sort="Baric, Ralph" uniqKey="Baric R" first="Ralph" last="Baric">Ralph Baric</name>
<name sortKey="Heise, Mark" sort="Heise, Mark" uniqKey="Heise M" first="Mark" last="Heise">Mark Heise</name>
<name sortKey="Heise, Mark" sort="Heise, Mark" uniqKey="Heise M" first="Mark" last="Heise">Mark Heise</name>
<name sortKey="Heise, Mark" sort="Heise, Mark" uniqKey="Heise M" first="Mark" last="Heise">Mark Heise</name>
</country>
</tree>
</affiliations>
</record>
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