NS1 Proteins of Avian Influenza A Viruses Can Act as Antagonists of the Human Alpha/Beta Interferon Response▿
Identifieur interne : 000384 ( Pmc/Corpus ); précédent : 000383; suivant : 000385NS1 Proteins of Avian Influenza A Viruses Can Act as Antagonists of the Human Alpha/Beta Interferon Response▿
Auteurs : A. Hayman ; S. Comely ; A. Lackenby ; L. C. S. Hartgroves ; S. Goodbourn ; J. W. Mccauley ; W. S. BarclaySource :
- Journal of Virology [ 0022-538X ] ; 2006.
Abstract
Many viruses, including human influenza A virus, have developed strategies for counteracting the host type I interferon (IFN) response. We have explored whether avian influenza viruses were less capable of combating the type I IFN response in mammalian cells, as this might be a determinant of host range restriction. A panel of avian influenza viruses isolated between 1927 and 1997 was assembled. The selected viruses showed variation in their ability to activate the expression of a reporter gene under the control of the IFN-β promoter and in the levels of IFN induced in mammalian cells. Surprisingly, the avian NS1 proteins expressed alone or in the genetic background of a human influenza virus controlled IFN-β induction in a manner similar to the NS1 protein of human strains. There was no direct correlation between the IFN-β induction and replication of avian influenza viruses in human A549 cells. Nevertheless, human cells deficient in the type I IFN system showed enhanced replication of the avian viruses studied, implying that the human type I IFN response limits avian influenza viruses and can contribute to host range restriction.
Url:
DOI: 10.1128/JVI.01856-06
PubMed: 17182679
PubMed Central: 1865923
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PMC:1865923Le document en format XML
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<series><title level="j">Journal of Virology</title>
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<front><div type="abstract" xml:lang="en"><p>Many viruses, including human influenza A virus, have developed strategies for counteracting the host type I interferon (IFN) response. We have explored whether avian influenza viruses were less capable of combating the type I IFN response in mammalian cells, as this might be a determinant of host range restriction. A panel of avian influenza viruses isolated between 1927 and 1997 was assembled. The selected viruses showed variation in their ability to activate the expression of a reporter gene under the control of the IFN-β promoter and in the levels of IFN induced in mammalian cells. Surprisingly, the avian NS1 proteins expressed alone or in the genetic background of a human influenza virus controlled IFN-β induction in a manner similar to the NS1 protein of human strains. There was no direct correlation between the IFN-β induction and replication of avian influenza viruses in human A549 cells. Nevertheless, human cells deficient in the type I IFN system showed enhanced replication of the avian viruses studied, implying that the human type I IFN response limits avian influenza viruses and can contribute to host range restriction.</p>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Virol</journal-id>
<journal-id journal-id-type="publisher-id">jvi</journal-id>
<journal-title>Journal of Virology</journal-title>
<issn pub-type="ppub">0022-538X</issn>
<issn pub-type="epub">1098-5514</issn>
<publisher><publisher-name>American Society for Microbiology</publisher-name>
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<article-meta><article-id pub-id-type="pmid">17182679</article-id>
<article-id pub-id-type="pmc">1865923</article-id>
<article-id pub-id-type="publisher-id">1856-06</article-id>
<article-id pub-id-type="doi">10.1128/JVI.01856-06</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Cellular Response to Infection</subject>
</subj-group>
</article-categories>
<title-group><article-title>NS1 Proteins of Avian Influenza A Viruses Can Act as Antagonists of the Human Alpha/Beta Interferon Response<xref ref-type="fn" rid="fn4">▿</xref>
</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Hayman</surname>
<given-names>A.</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="fn" rid="fn1">†</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Comely</surname>
<given-names>S.</given-names>
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<xref ref-type="aff" rid="aff1">2</xref>
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<contrib contrib-type="author"><name><surname>Lackenby</surname>
<given-names>A.</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="aff" rid="aff1">2</xref>
<xref ref-type="fn" rid="fn2">‡</xref>
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<contrib contrib-type="author"><name><surname>Hartgroves</surname>
<given-names>L. C. S.</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
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<contrib contrib-type="author"><name><surname>Goodbourn</surname>
<given-names>S.</given-names>
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<xref ref-type="aff" rid="aff1">3</xref>
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<contrib contrib-type="author"><name><surname>McCauley</surname>
<given-names>J. W.</given-names>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
<xref ref-type="fn" rid="fn3">§</xref>
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<contrib contrib-type="author"><name><surname>Barclay</surname>
<given-names>W. S.</given-names>
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<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
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<aff id="aff1">School of Biological Sciences, University of Reading, Whiteknights, Reading RG6 6AJ, United Kingdom,<label>1</label>
Division of Microbiology, Institute for Animal Health, Compton Laboratory, Berkshire RG20 7NN, United Kingdom,<label>2</label>
Division of Basic Medical Sciences, St. George's, University of London, London SW17 0RE, United Kingdom<label>3</label>
</aff>
<author-notes><fn id="cor1"><label>*</label>
<p>Corresponding author. Mailing address: School of Biological Sciences, University of Reading, Whiteknights, Reading RG6 6AJ, United Kingdom. Phone: 44-1189-316671. Fax: 44-1189-316671. E-mail: <email>w.s.barclay@reading.ac.uk</email>
.</p>
</fn>
<fn id="fn1"><label>†</label>
<p>Present address: Institute of Immunology, University of Oslo, Rikshospitalet-Radiumhospitalet Medical Centre, 0027 Oslo, Norway.</p>
</fn>
<fn id="fn2"><label>‡</label>
<p>Present address: Respiratory Virus Unit, Virus Reference Division, Centre for Infection, Health Protection Agency, 61 Colindale Avenue, London NW9 5EQ, United Kingdom.</p>
</fn>
<fn id="fn3"><label>§</label>
<p>Present address: Division of Virology, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, United Kingdom.</p>
</fn>
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<pub-date pub-type="ppub"><month>3</month>
<year>2007</year>
</pub-date>
<pub-date pub-type="epub"><day>20</day>
<month>12</month>
<year>2006</year>
</pub-date>
<volume>81</volume>
<issue>5</issue>
<fpage>2318</fpage>
<lpage>2327</lpage>
<history><date date-type="received"><day>25</day>
<month>8</month>
<year>2006</year>
</date>
<date date-type="accepted"><day>1</day>
<month>12</month>
<year>2006</year>
</date>
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<copyright-statement>Copyright © 2007, American Society for Microbiology</copyright-statement>
<copyright-year>2007</copyright-year>
<self-uri xlink:title="pdf" xlink:href="zjv00507002318.pdf"></self-uri>
<abstract><p>Many viruses, including human influenza A virus, have developed strategies for counteracting the host type I interferon (IFN) response. We have explored whether avian influenza viruses were less capable of combating the type I IFN response in mammalian cells, as this might be a determinant of host range restriction. A panel of avian influenza viruses isolated between 1927 and 1997 was assembled. The selected viruses showed variation in their ability to activate the expression of a reporter gene under the control of the IFN-β promoter and in the levels of IFN induced in mammalian cells. Surprisingly, the avian NS1 proteins expressed alone or in the genetic background of a human influenza virus controlled IFN-β induction in a manner similar to the NS1 protein of human strains. There was no direct correlation between the IFN-β induction and replication of avian influenza viruses in human A549 cells. Nevertheless, human cells deficient in the type I IFN system showed enhanced replication of the avian viruses studied, implying that the human type I IFN response limits avian influenza viruses and can contribute to host range restriction.</p>
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