Unraveling the complexities of the interferon response during SARS-CoV infection
Identifieur interne : 000C12 ( Pmc/Corpus ); précédent : 000C11; suivant : 000C13Unraveling the complexities of the interferon response during SARS-CoV infection
Auteurs : Anna De Lang ; Tracey Baas ; Saskia L. Smits ; Michael G. Katze ; Albert Dme Osterhaus ; Bart L. HaagmansSource :
- Future virology [ 1746-0794 ] ; 2009.
Abstract
Viruses employ different strategies to circumvent the antiviral actions of the innate immune response. SARS coronavirus (SARS-CoV), a virus that causes severe lung damage, encodes an array of proteins able to inhibit induction and signaling of type-I interferons. However, recent studies have demonstrated that interferons are produced during SARS-CoV infection in humans and macaques. Furthermore, nuclear translocation of activated STAT1 and a range of interferon-stimulated genes could be demonstrated in the lungs of SARS-CoV-infected macaques. In line with these observations, plasmacytoid dendritic cells have been shown to produce interferons upon SARS-CoV infection
Url:
DOI: 10.2217/17460794.4.1.71
PubMed: 19885368
PubMed Central: 2680287
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PMC:2680287Le document en format XML
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<front><div type="abstract" xml:lang="en"><p id="P1">Viruses employ different strategies to circumvent the antiviral actions of the innate immune response. SARS coronavirus (SARS-CoV), a virus that causes severe lung damage, encodes an array of proteins able to inhibit induction and signaling of type-I interferons. However, recent studies have demonstrated that interferons are produced during SARS-CoV infection in humans and macaques. Furthermore, nuclear translocation of activated STAT1 and a range of interferon-stimulated genes could be demonstrated in the lungs of SARS-CoV-infected macaques. In line with these observations, plasmacytoid dendritic cells have been shown to produce interferons upon SARS-CoV infection <italic>in vitro</italic>
. Given the pivotal role of interferons during viral infections, (differential) induction of interferons may affect the outcome of the infection. Therefore, the functional implication of interferon production during SARS-CoV infection remains to be re-investigated.</p>
</div>
</front>
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<front><journal-meta><journal-id journal-id-type="nlm-journal-id">101278124</journal-id>
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<journal-id journal-id-type="nlm-ta">Future Virol</journal-id>
<journal-title>Future virology</journal-title>
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<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
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<title-group><article-title>Unraveling the complexities of the interferon response during SARS-CoV infection</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>de Lang</surname>
<given-names>Anna</given-names>
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<aff id="A1">Department of Virology, Erasmus Medical Center, Rotterdam, The Netherlands</aff>
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<contrib contrib-type="author"><name><surname>Baas</surname>
<given-names>Tracey</given-names>
</name>
<aff id="A2">Department of Microbiology, School of Medicine, University of Washington, Seattle, WA, USA</aff>
</contrib>
<contrib contrib-type="author"><name><surname>Smits</surname>
<given-names>Saskia L</given-names>
</name>
<aff id="A3">Department of Virology, Erasmus Medical Center, Rotterdam, The Netherlands</aff>
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<contrib contrib-type="author"><name><surname>Katze</surname>
<given-names>Michael G</given-names>
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<aff id="A4">Department of Microbiology, School of Medicine, University of Washington, Seattle, WA, USA</aff>
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<contrib contrib-type="author"><name><surname>Osterhaus</surname>
<given-names>Albert DME</given-names>
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<aff id="A5">Department of Virology, Erasmus Medical Center, Rotterdam, The Netherlands</aff>
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<contrib contrib-type="author"><name><surname>Haagmans</surname>
<given-names>Bart L</given-names>
</name>
<xref ref-type="corresp" rid="cor1">†</xref>
<aff id="A6">Department of Virology, Erasmus MC, PO box 2040, 3000 CA Rotterdam, The Netherlands, Tel.: +31 107 044 004;, Fax: +31 107 044 760;<email>b.haagmans@erasmusmc.nl</email>
</aff>
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<author-notes><corresp id="cor1"><label>†</label>
Author for correspondence: Department of Virology, Erasmus MC, PO box 2040, 3000 CA Rotterdam,, The Netherlands, Tel.: +31 107 044 004, Fax: +31 107 044 760, <email>b.haagmans@erasmusmc.nl</email>
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<month>1</month>
<year>2009</year>
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<month>1</month>
<year>2009</year>
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<month>11</month>
<year>2009</year>
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<volume>4</volume>
<issue>1</issue>
<fpage>71</fpage>
<lpage>78</lpage>
<permissions><copyright-statement>© 2009 Future Medicine</copyright-statement>
<copyright-year>2009</copyright-year>
</permissions>
<abstract><p id="P1">Viruses employ different strategies to circumvent the antiviral actions of the innate immune response. SARS coronavirus (SARS-CoV), a virus that causes severe lung damage, encodes an array of proteins able to inhibit induction and signaling of type-I interferons. However, recent studies have demonstrated that interferons are produced during SARS-CoV infection in humans and macaques. Furthermore, nuclear translocation of activated STAT1 and a range of interferon-stimulated genes could be demonstrated in the lungs of SARS-CoV-infected macaques. In line with these observations, plasmacytoid dendritic cells have been shown to produce interferons upon SARS-CoV infection <italic>in vitro</italic>
. Given the pivotal role of interferons during viral infections, (differential) induction of interferons may affect the outcome of the infection. Therefore, the functional implication of interferon production during SARS-CoV infection remains to be re-investigated.</p>
</abstract>
<kwd-group><kwd>innate immunity</kwd>
<kwd>interferon</kwd>
<kwd>plasmacytoid dendritic cell</kwd>
<kwd>SARS coronavirus</kwd>
</kwd-group>
<contract-num rid="HL1">R01 HL080621-01A1
||HL</contract-num>
<contract-sponsor id="HL1">National Heart, Lung, and Blood Institute : NHLBI</contract-sponsor>
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