The PB2-E627K Mutation Attenuates Viruses Containing the 2009 H1N1 Influenza Pandemic Polymerase
Identifieur interne : 000E52 ( Pmc/Curation ); précédent : 000E51; suivant : 000E53The PB2-E627K Mutation Attenuates Viruses Containing the 2009 H1N1 Influenza Pandemic Polymerase
Auteurs : Brett W. Jagger ; Matthew J. Memoli ; Zong-Mei Sheng ; Li Qi ; Rachel J. Hrabal ; Genevieve L. Allen ; Vivien G. Dugan ; Ruixue Wang ; Paul Digard ; John C. Kash ; Jeffery K. TaubenbergerSource :
- mBio [ 2150-7511 ] ; 2010.
Abstract
The swine-origin H1N1 influenza A virus emerged in early 2009 and caused the first influenza pandemic in 41 years. The virus has spread efficiently to both the Northern and the Southern Hemispheres and has been associated with over 16,000 deaths. Given the virus’s recent zoonotic origin, there is concern that the virus could acquire signature mutations associated with the enhanced pathogenicity of previous pandemic viruses or H5N1 viruses with pandemic potential. We tested the hypothesis that mutations in the polymerase PB2 gene at residues 627 and 701 would enhance virulence but found that influenza viruses containing these mutations in the context of the pandemic virus polymerase complex are attenuated in cell culture and mice.
Url:
DOI: 10.1128/mBio.00067-10
PubMed: 20689744
PubMed Central: 2912665
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PMC:2912665Le document en format XML
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<front><div type="abstract" xml:lang="en"><title>ABSTRACT</title>
<p>The swine-origin H1N1 influenza A virus emerged in early 2009 and caused the first influenza pandemic in 41 years. The virus has spread efficiently to both the Northern and the Southern Hemispheres and has been associated with over 16,000 deaths. Given the virus’s recent zoonotic origin, there is concern that the virus could acquire signature mutations associated with the enhanced pathogenicity of previous pandemic viruses or H5N1 viruses with pandemic potential. We tested the hypothesis that mutations in the polymerase PB2 gene at residues 627 and 701 would enhance virulence but found that influenza viruses containing these mutations in the context of the pandemic virus polymerase complex are attenuated in cell culture and mice.</p>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">mBio</journal-id>
<journal-id journal-id-type="iso-abbrev">MBio</journal-id>
<journal-id journal-id-type="hwp">mbio</journal-id>
<journal-id journal-id-type="pmc">mbio</journal-id>
<journal-id journal-id-type="publisher-id">mBio</journal-id>
<journal-title-group><journal-title>mBio</journal-title>
</journal-title-group>
<issn pub-type="epub">2150-7511</issn>
<publisher><publisher-name>American Society of Microbiology</publisher-name>
<publisher-loc>1752 N St., N.W., Washington, DC</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">20689744</article-id>
<article-id pub-id-type="pmc">2912665</article-id>
<article-id pub-id-type="publisher-id">mBio00067-10</article-id>
<article-id pub-id-type="doi">10.1128/mBio.00067-10</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>The PB2-E627K Mutation Attenuates Viruses Containing the 2009 H1N1 Influenza Pandemic Polymerase</article-title>
<alt-title>PB2-E627K and the 2009 H1N1 Pandemic Virus Polymerase</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Jagger</surname>
<given-names>Brett W.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
<xref ref-type="author-notes" rid="fn1">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Memoli</surname>
<given-names>Matthew J.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Sheng</surname>
<given-names>Zong-Mei</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Qi</surname>
<given-names>Li</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Hrabal</surname>
<given-names>Rachel J.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Allen</surname>
<given-names>Genevieve L.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Dugan</surname>
<given-names>Vivien G.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Wang</surname>
<given-names>Ruixue</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Digard</surname>
<given-names>Paul</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>b</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kash</surname>
<given-names>John C.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Taubenberger</surname>
<given-names>Jeffery K.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<aff id="aff1">Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA,<label><sup>a</sup>
</label>
and</aff>
<aff id="aff2">Division of Virology, Department of Pathology, Cambridge University, Cambridge, United Kingdom<label><sup>b</sup>
</label>
</aff>
</contrib-group>
<author-notes><fn id="fn1" fn-type="present-address"><label>*</label>
<p>Present address: Division of Virology, Department of Pathology, Cambridge University, Cambridge, United Kingdom.</p>
</fn>
<corresp id="cor1">Address correspondence to Jeffery K. Taubenberger, <email>taubenbergerj@niaid.nih.gov</email>
.</corresp>
<fn fn-type="edited-by"><p><bold>Editor</bold>
W. Ian Lipkin, Columbia University</p>
</fn>
</author-notes>
<pub-date pub-type="epub"><day>18</day>
<month>5</month>
<year>2010</year>
</pub-date>
<pub-date pub-type="collection"><month>4</month>
<year>2010</year>
</pub-date>
<volume>1</volume>
<issue>1</issue>
<elocation-id>e00067-10</elocation-id>
<history><date date-type="received"><day>3</day>
<month>3</month>
<year>2010</year>
</date>
<date date-type="accepted"><day>8</day>
<month>3</month>
<year>2010</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2010 Jagger et al.</copyright-statement>
<copyright-year>2010</copyright-year>
<copyright-holder>Jagger et al.</copyright-holder>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc-sa/3.0/"><license-p>This is an open-access article distributed under the terms of the <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc-sa/3.0/">Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License</ext-link>
, which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the author and source are credited.</license-p>
</license>
</permissions>
<abstract><title>ABSTRACT</title>
<p>The swine-origin H1N1 influenza A virus emerged in early 2009 and caused the first influenza pandemic in 41 years. The virus has spread efficiently to both the Northern and the Southern Hemispheres and has been associated with over 16,000 deaths. Given the virus’s recent zoonotic origin, there is concern that the virus could acquire signature mutations associated with the enhanced pathogenicity of previous pandemic viruses or H5N1 viruses with pandemic potential. We tested the hypothesis that mutations in the polymerase PB2 gene at residues 627 and 701 would enhance virulence but found that influenza viruses containing these mutations in the context of the pandemic virus polymerase complex are attenuated in cell culture and mice.</p>
</abstract>
<abstract abstract-type="executive-summary"><title>IMPORTANCE</title>
<p> Influenza A virus (IAV) evolution is characterized by host-specific lineages, and IAVs derived in whole or in part from animal reservoirs have caused pandemics in humans. Because IAVs are known to acquire host-adaptive genome mutations, and since the PB2 gene of the 2009 H1N1 virus is of recent avian derivation, there exists concern that the pathogenicity of the 2009 H1N1 influenza A pandemic virus could be potentiated by acquisition of the host-adaptive PB2-E627K or -D701N mutations, which have been shown to enhance the virulence of other influenza viruses. We present data from a mouse model of influenza infection showing that such mutations do not increase the virulence of viruses containing the 2009 H1N1 viral polymerase.</p>
</abstract>
</article-meta>
</front>
</pmc>
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