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<title xml:lang="en">Unraveling the complexities of the interferon response during SARS-CoV infection</title>
<author>
<name sortKey="De Lang, Anna" sort="De Lang, Anna" uniqKey="De Lang A" first="Anna" last="De Lang">Anna De Lang</name>
</author>
<author>
<name sortKey="Baas, Tracey" sort="Baas, Tracey" uniqKey="Baas T" first="Tracey" last="Baas">Tracey Baas</name>
</author>
<author>
<name sortKey="Smits, Saskia L" sort="Smits, Saskia L" uniqKey="Smits S" first="Saskia L" last="Smits">Saskia L. Smits</name>
</author>
<author>
<name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G" last="Katze">Michael G. Katze</name>
</author>
<author>
<name sortKey="Osterhaus, Albert Dme" sort="Osterhaus, Albert Dme" uniqKey="Osterhaus A" first="Albert Dme" last="Osterhaus">Albert Dme Osterhaus</name>
</author>
<author>
<name sortKey="Haagmans, Bart L" sort="Haagmans, Bart L" uniqKey="Haagmans B" first="Bart L" last="Haagmans">Bart L. Haagmans</name>
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<idno type="pmid">19885368</idno>
<idno type="pmc">2680287</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680287</idno>
<idno type="RBID">PMC:2680287</idno>
<idno type="doi">10.2217/17460794.4.1.71</idno>
<date when="2009">2009</date>
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<title xml:lang="en" level="a" type="main">Unraveling the complexities of the interferon response during SARS-CoV infection</title>
<author>
<name sortKey="De Lang, Anna" sort="De Lang, Anna" uniqKey="De Lang A" first="Anna" last="De Lang">Anna De Lang</name>
</author>
<author>
<name sortKey="Baas, Tracey" sort="Baas, Tracey" uniqKey="Baas T" first="Tracey" last="Baas">Tracey Baas</name>
</author>
<author>
<name sortKey="Smits, Saskia L" sort="Smits, Saskia L" uniqKey="Smits S" first="Saskia L" last="Smits">Saskia L. Smits</name>
</author>
<author>
<name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G" last="Katze">Michael G. Katze</name>
</author>
<author>
<name sortKey="Osterhaus, Albert Dme" sort="Osterhaus, Albert Dme" uniqKey="Osterhaus A" first="Albert Dme" last="Osterhaus">Albert Dme Osterhaus</name>
</author>
<author>
<name sortKey="Haagmans, Bart L" sort="Haagmans, Bart L" uniqKey="Haagmans B" first="Bart L" last="Haagmans">Bart L. Haagmans</name>
</author>
</analytic>
<series>
<title level="j">Future virology</title>
<idno type="ISSN">1746-0794</idno>
<idno type="eISSN">1746-0808</idno>
<imprint>
<date when="2009">2009</date>
</imprint>
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<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>
<journal-id journal-id-type="pubmed-jr-id">34879</journal-id>
<journal-id journal-id-type="nlm-ta">Future Virol</journal-id>
<journal-title>Future virology</journal-title>
<issn pub-type="ppub">1746-0794</issn>
<issn pub-type="epub">1746-0808</issn>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">19885368</article-id>
<article-id pub-id-type="pmc">2680287</article-id>
<article-id pub-id-type="manuscript">NIHMS88172</article-id>
<article-id pub-id-type="doi">10.2217/17460794.4.1.71</article-id>
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<subj-group subj-group-type="heading">
<subject>Article</subject>
</subj-group>
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<title-group>
<article-title>Unraveling the complexities of the interferon response during SARS-CoV infection</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>de Lang</surname>
<given-names>Anna</given-names>
</name>
<aff id="A1">Department of Virology, Erasmus Medical Center, Rotterdam, The Netherlands</aff>
</contrib>
<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>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Katze</surname>
<given-names>Michael G</given-names>
</name>
<aff id="A4">Department of Microbiology, School of Medicine, University of Washington, Seattle, WA, USA</aff>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Osterhaus</surname>
<given-names>Albert DME</given-names>
</name>
<aff id="A5">Department of Virology, Erasmus Medical Center, Rotterdam, The Netherlands</aff>
</contrib>
<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>
</contrib>
</contrib-group>
<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>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted">
<day>23</day>
<month>1</month>
<year>2009</year>
</pub-date>
<pub-date pub-type="ppub">
<day>1</day>
<month>1</month>
<year>2009</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>1</day>
<month>11</month>
<year>2009</year>
</pub-date>
<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>
</article-meta>
</front>
</pmc>
</record>

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