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Human immunopathogenesis of severe acute respiratory syndrome (SARS)

Identifieur interne : 001588 ( Pmc/Curation ); précédent : 001587; suivant : 001589

Human immunopathogenesis of severe acute respiratory syndrome (SARS)

Auteurs : Mark J. Cameron [Canada] ; Jesus F. Bermejo-Martin [Espagne] ; Ali Danesh [Canada] ; Matthew P. Muller [Canada] ; David J. Kelvin [Canada]

Source :

RBID : PMC:7114310

Abstract

Progressive immune-associated injury is a hallmark of severe acute respiratory syndrome (SARS). Viral evasion of innate immunity, hypercytokinemia and systemic immunopathology in the SARS coronavirus (SARS CoV) infected host have been suggested as possible mechanisms for the cause of severe pathology and morbidity in SARS patients. The molecular and cellular basis for how SARS CoV impacts the host immune system resulting in severe SARS, however, has not been elucidated. The variable clinical course of SARS may be the result of complex programs of host responses against the infectious agent. Therefore, the systematic analysis of innate and adaptive immune responses to SARS CoV is imperative in building as complete an immunological model as possible of host immunity and inflammatory responses during illness. Here we review recent advances in SARS immunopathogenesis research and present a summary of our findings regarding host responses in SARS patients. We contend that dysregulated type I and II interferon (IFN) responses during SARS may culminate in a failure of the switch from hyper-innate immunity to protective adaptive immune responses in the human host.


Url:
DOI: 10.1016/j.virusres.2007.02.014
PubMed: 17374415
PubMed Central: 7114310

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PMC:7114310

Le document en format XML

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<p>Progressive immune-associated injury is a hallmark of severe acute respiratory syndrome (SARS). Viral evasion of innate immunity, hypercytokinemia and systemic immunopathology in the SARS coronavirus (SARS CoV) infected host have been suggested as possible mechanisms for the cause of severe pathology and morbidity in SARS patients. The molecular and cellular basis for how SARS CoV impacts the host immune system resulting in severe SARS, however, has not been elucidated. The variable clinical course of SARS may be the result of complex programs of host responses against the infectious agent. Therefore, the systematic analysis of innate and adaptive immune responses to SARS CoV is imperative in building as complete an immunological model as possible of host immunity and inflammatory responses during illness. Here we review recent advances in SARS immunopathogenesis research and present a summary of our findings regarding host responses in SARS patients. We contend that dysregulated type I and II interferon (IFN) responses during SARS may culminate in a failure of the switch from hyper-innate immunity to protective adaptive immune responses in the human host.</p>
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</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">17374415</article-id>
<article-id pub-id-type="pmc">7114310</article-id>
<article-id pub-id-type="publisher-id">S0168-1702(07)00054-8</article-id>
<article-id pub-id-type="doi">10.1016/j.virusres.2007.02.014</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Human immunopathogenesis of severe acute respiratory syndrome (SARS)</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Cameron</surname>
<given-names>Mark J.</given-names>
</name>
<email>mcameron@uhnres.utoronto.ca</email>
<xref rid="aff1" ref-type="aff">a</xref>
<xref rid="aff2" ref-type="aff">b</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Bermejo-Martin</surname>
<given-names>Jesus F.</given-names>
</name>
<email>bermejo@ped.uva.es</email>
<xref rid="aff3" ref-type="aff">c</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Danesh</surname>
<given-names>Ali</given-names>
</name>
<email>adanesh@uhnres.utoronto.ca</email>
<xref rid="aff1" ref-type="aff">a</xref>
<xref rid="aff2" ref-type="aff">b</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Muller</surname>
<given-names>Matthew P.</given-names>
</name>
<email>mmuller@mtsinai.on.ca</email>
<xref rid="aff2" ref-type="aff">b</xref>
<xref rid="aff4" ref-type="aff">d</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Kelvin</surname>
<given-names>David J.</given-names>
</name>
<email>dkelvin@uhnres.utoronto.ca</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>
University Health Network, MaRS Centre, 101 College Street, Toronto, Ontario M5G 1L7, Canada</aff>
<aff id="aff2">
<label>b</label>
University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada</aff>
<aff id="aff3">
<label>c</label>
University of Valladolid, Ramón y Cajal 7, Valladolid 47005, Spain</aff>
<aff id="aff4">
<label>d</label>
Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada</aff>
<author-notes>
<corresp id="cor1">
<label></label>
Corresponding author at: The University Health Network, MaRS Centre, TMDT 3-916, 101 College Street, Toronto, Ontario M5G 1L7, Canada. Tel.: +1 416 581 7605; fax: +1 416 581 7606.
<email>dkelvin@uhnres.utoronto.ca</email>
</corresp>
</author-notes>
<pub-date pub-type="pmc-release">
<day>19</day>
<month>3</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>19</day>
<month>3</month>
<year>2007</year>
</pub-date>
<volume>133</volume>
<issue>1</issue>
<fpage>13</fpage>
<lpage>19</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>Progressive immune-associated injury is a hallmark of severe acute respiratory syndrome (SARS). Viral evasion of innate immunity, hypercytokinemia and systemic immunopathology in the SARS coronavirus (SARS CoV) infected host have been suggested as possible mechanisms for the cause of severe pathology and morbidity in SARS patients. The molecular and cellular basis for how SARS CoV impacts the host immune system resulting in severe SARS, however, has not been elucidated. The variable clinical course of SARS may be the result of complex programs of host responses against the infectious agent. Therefore, the systematic analysis of innate and adaptive immune responses to SARS CoV is imperative in building as complete an immunological model as possible of host immunity and inflammatory responses during illness. Here we review recent advances in SARS immunopathogenesis research and present a summary of our findings regarding host responses in SARS patients. We contend that dysregulated type I and II interferon (IFN) responses during SARS may culminate in a failure of the switch from hyper-innate immunity to protective adaptive immune responses in the human host.</p>
</abstract>
<kwd-group>
<title>Keywords</title>
<kwd>SARS</kwd>
<kwd>Cytokine</kwd>
<kwd>Chemokine</kwd>
<kwd>Microarray</kwd>
<kwd>Host response</kwd>
<kwd>Interferon</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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