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Interferon and cytokine responses to SARS-coronavirus infection

Identifieur interne : 001739 ( Pmc/Curation ); précédent : 001738; suivant : 001740

Interferon and cytokine responses to SARS-coronavirus infection

Auteurs : Volker Thiel [Suisse] ; Friedemann Weber [Allemagne]

Source :

RBID : PMC:7108449

Abstract

The sudden emergence of severe acute respiratory syndrome (SARS) has boosted research on innate immune responses to coronaviruses. It is now well established that the causative agent, a newly identified coronavirus termed SARS-CoV, employs multiple passive and active mechanisms to avoid induction of the antiviral type I interferons in tissue cells. By contrast, chemokines such as IP-10 or IL-8 are strongly upregulated. The imbalance in the IFN response is thought to contribute to the establishment of viremia early in infection, whereas the production of chemokines by infected organs may be responsible for (i) massive immune cell infiltrations found in the lungs of SARS victims, and (ii) the dysregulation of adaptive immunity. Here, we will review the most recent findings on the interaction of SARS-CoV and related Coronaviridae members with the type I interferon and cytokine responses and discuss implications for pathogenesis and therapy.


Url:
DOI: 10.1016/j.cytogfr.2008.01.001
PubMed: 18321765
PubMed Central: 7108449

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PMC:7108449

Le document en format XML

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<p>The sudden emergence of severe acute respiratory syndrome (SARS) has boosted research on innate immune responses to coronaviruses. It is now well established that the causative agent, a newly identified coronavirus termed SARS-CoV, employs multiple passive and active mechanisms to avoid induction of the antiviral type I interferons in tissue cells. By contrast, chemokines such as IP-10 or IL-8 are strongly upregulated. The imbalance in the IFN response is thought to contribute to the establishment of viremia early in infection, whereas the production of chemokines by infected organs may be responsible for (i) massive immune cell infiltrations found in the lungs of SARS victims, and (ii) the dysregulation of adaptive immunity. Here, we will review the most recent findings on the interaction of SARS-CoV and related Coronaviridae members with the type I interferon and cytokine responses and discuss implications for pathogenesis and therapy.</p>
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</TEI>
<pmc article-type="review-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">Cytokine Growth Factor Rev</journal-id>
<journal-id journal-id-type="iso-abbrev">Cytokine Growth Factor Rev</journal-id>
<journal-title-group>
<journal-title>Cytokine & Growth Factor Reviews</journal-title>
</journal-title-group>
<issn pub-type="ppub">1359-6101</issn>
<issn pub-type="epub">1879-0305</issn>
<publisher>
<publisher-name>Elsevier Ltd.</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">18321765</article-id>
<article-id pub-id-type="pmc">7108449</article-id>
<article-id pub-id-type="publisher-id">S1359-6101(08)00002-6</article-id>
<article-id pub-id-type="doi">10.1016/j.cytogfr.2008.01.001</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Interferon and cytokine responses to SARS-coronavirus infection</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Thiel</surname>
<given-names>Volker</given-names>
</name>
<xref rid="aff1" ref-type="aff">a</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Weber</surname>
<given-names>Friedemann</given-names>
</name>
<email>friedemann.weber@uniklinik-freiburg.de</email>
<xref rid="aff2" ref-type="aff">b</xref>
<xref rid="cor1" ref-type="corresp"></xref>
</contrib>
</contrib-group>
<aff id="aff1">
<label>a</label>
Research Department, Kantonal Hospital St. Gallen, Switzerland</aff>
<aff id="aff2">
<label>b</label>
Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, D-79008 Freiburg, Germany</aff>
<author-notes>
<corresp id="cor1">
<label></label>
Corresponding author. Tel.: +49 761 203 6614; fax: +49 761 203 6634.
<email>friedemann.weber@uniklinik-freiburg.de</email>
</corresp>
</author-notes>
<pub-date pub-type="pmc-release">
<day>5</day>
<month>3</month>
<year>2008</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>5</day>
<month>3</month>
<year>2008</year>
</pub-date>
<volume>19</volume>
<issue>2</issue>
<fpage>121</fpage>
<lpage>132</lpage>
<permissions>
<copyright-statement>Copyright © 2008 Elsevier Ltd. All rights reserved.</copyright-statement>
<copyright-year>2008</copyright-year>
<copyright-holder>Elsevier Ltd</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 sudden emergence of severe acute respiratory syndrome (SARS) has boosted research on innate immune responses to coronaviruses. It is now well established that the causative agent, a newly identified coronavirus termed SARS-CoV, employs multiple passive and active mechanisms to avoid induction of the antiviral type I interferons in tissue cells. By contrast, chemokines such as IP-10 or IL-8 are strongly upregulated. The imbalance in the IFN response is thought to contribute to the establishment of viremia early in infection, whereas the production of chemokines by infected organs may be responsible for (i) massive immune cell infiltrations found in the lungs of SARS victims, and (ii) the dysregulation of adaptive immunity. Here, we will review the most recent findings on the interaction of SARS-CoV and related Coronaviridae members with the type I interferon and cytokine responses and discuss implications for pathogenesis and therapy.</p>
</abstract>
<kwd-group>
<title>Keywords</title>
<kwd>SARS</kwd>
<kwd>Coronaviruses</kwd>
<kwd>Interferon</kwd>
<kwd>Chemokines</kwd>
<kwd>Viral countermeasures</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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