Functional Balance of the Hemagglutinin and Neuraminidase Activities Accompanies the Emergence of the 2009 H1N1 Influenza Pandemic
Identifieur interne : 000739 ( Pmc/Corpus ); précédent : 000738; suivant : 000740Functional Balance of the Hemagglutinin and Neuraminidase Activities Accompanies the Emergence of the 2009 H1N1 Influenza Pandemic
Auteurs : Rui Xu ; Xueyong Zhu ; Ryan Mcbride ; Corwin M. Nycholat ; Wenli Yu ; James C. Paulson ; Ian A. WilsonSource :
- Journal of Virology [ 0022-538X ] ; 2012.
Abstract
The 2009 H1N1 influenza pandemic is the first human pandemic in decades and was of swine origin. Although swine are believed to be an intermediate host in the emergence of new human influenza viruses, there is still little known about the host barriers that keep swine influenza viruses from entering the human population. We surveyed swine progenitors and human viruses from the 2009 pandemic and measured the activities of the hemagglutinin (HA) and neuraminidase (NA), which are the two viral surface proteins that interact with host glycan receptors. A functional balance of these two activities (HA binding and NA cleavage) is found in human viruses but not in the swine progenitors. The human 2009 H1N1 pandemic virus exhibited both low HA avidity for glycan receptors as a result of mutations near the receptor binding site and weak NA enzymatic activity. Thus, a functional match between the hemagglutinin and neuraminidase appears to be necessary for efficient transmission between humans and may be an indicator of the pandemic potential of zoonotic viruses.
Url:
DOI: 10.1128/JVI.00697-12
PubMed: 22718832
PubMed Central: 3416152
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PMC:3416152Le document en format XML
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Nycholat</name><affiliation><nlm:aff id="aff2">Department of Chemical Physiology</nlm:aff></affiliation></author><author><name sortKey="Yu, Wenli" sort="Yu, Wenli" uniqKey="Yu W" first="Wenli" last="Yu">Wenli Yu</name><affiliation><nlm:aff id="aff1">Department of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Paulson, James C" sort="Paulson, James C" uniqKey="Paulson J" first="James C." last="Paulson">James C. Paulson</name><affiliation><nlm:aff id="aff1">Department of Molecular Biology</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Department of Chemical Physiology</nlm:aff></affiliation></author><author><name sortKey="Wilson, Ian A" sort="Wilson, Ian A" uniqKey="Wilson I" first="Ian A." last="Wilson">Ian A. Wilson</name><affiliation><nlm:aff id="aff1">Department of Molecular Biology</nlm:aff></affiliation><affiliation><nlm:aff id="aff3">Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, California, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22718832</idno><idno type="pmc">3416152</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3416152</idno><idno type="RBID">PMC:3416152</idno><idno type="doi">10.1128/JVI.00697-12</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">000739</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000739</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Functional Balance of the Hemagglutinin and Neuraminidase Activities Accompanies the Emergence of the 2009 H1N1 Influenza Pandemic</title><author><name sortKey="Xu, Rui" sort="Xu, Rui" uniqKey="Xu R" first="Rui" last="Xu">Rui Xu</name><affiliation><nlm:aff id="aff1">Department of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Zhu, Xueyong" sort="Zhu, Xueyong" uniqKey="Zhu X" first="Xueyong" last="Zhu">Xueyong Zhu</name><affiliation><nlm:aff id="aff1">Department of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Mcbride, Ryan" sort="Mcbride, Ryan" uniqKey="Mcbride R" first="Ryan" last="Mcbride">Ryan Mcbride</name><affiliation><nlm:aff id="aff2">Department of Chemical Physiology</nlm:aff></affiliation></author><author><name sortKey="Nycholat, Corwin M" sort="Nycholat, Corwin M" uniqKey="Nycholat C" first="Corwin M." last="Nycholat">Corwin M. Nycholat</name><affiliation><nlm:aff id="aff2">Department of Chemical Physiology</nlm:aff></affiliation></author><author><name sortKey="Yu, Wenli" sort="Yu, Wenli" uniqKey="Yu W" first="Wenli" last="Yu">Wenli Yu</name><affiliation><nlm:aff id="aff1">Department of Molecular Biology</nlm:aff></affiliation></author><author><name sortKey="Paulson, James C" sort="Paulson, James C" uniqKey="Paulson J" first="James C." last="Paulson">James C. Paulson</name><affiliation><nlm:aff id="aff1">Department of Molecular Biology</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Department of Chemical Physiology</nlm:aff></affiliation></author><author><name sortKey="Wilson, Ian A" sort="Wilson, Ian A" uniqKey="Wilson I" first="Ian A." last="Wilson">Ian A. Wilson</name><affiliation><nlm:aff id="aff1">Department of Molecular Biology</nlm:aff></affiliation><affiliation><nlm:aff id="aff3">Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, California, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Virology</title><idno type="ISSN">0022-538X</idno><idno type="eISSN">1098-5514</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The 2009 H1N1 influenza pandemic is the first human pandemic in decades and was of swine origin. Although swine are believed to be an intermediate host in the emergence of new human influenza viruses, there is still little known about the host barriers that keep swine influenza viruses from entering the human population. We surveyed swine progenitors and human viruses from the 2009 pandemic and measured the activities of the hemagglutinin (HA) and neuraminidase (NA), which are the two viral surface proteins that interact with host glycan receptors. A functional balance of these two activities (HA binding and NA cleavage) is found in human viruses but not in the swine progenitors. The human 2009 H1N1 pandemic virus exhibited both low HA avidity for glycan receptors as a result of mutations near the receptor binding site and weak NA enzymatic activity. Thus, a functional match between the hemagglutinin and neuraminidase appears to be necessary for efficient transmission between humans and may be an indicator of the pandemic potential of zoonotic viruses.</p></div></front></TEI><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="iso-abbrev">J. Virol</journal-id><journal-id journal-id-type="hwp">jvi</journal-id><journal-id journal-id-type="pmc">jvi</journal-id><journal-id journal-id-type="publisher-id">JVI</journal-id><journal-title-group><journal-title>Journal of Virology</journal-title></journal-title-group><issn pub-type="ppub">0022-538X</issn><issn pub-type="epub">1098-5514</issn><publisher><publisher-name>American Society for 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">22718832</article-id><article-id pub-id-type="pmc">3416152</article-id><article-id pub-id-type="publisher-id">00697-12</article-id><article-id pub-id-type="doi">10.1128/JVI.00697-12</article-id><article-categories><subj-group subj-group-type="heading"><subject>Virus-Cell Interactions</subject></subj-group></article-categories><title-group><article-title>Functional Balance of the Hemagglutinin and Neuraminidase Activities Accompanies the Emergence of the 2009 H1N1 Influenza Pandemic</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Xu</surname><given-names>Rui</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Zhu</surname><given-names>Xueyong</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>McBride</surname><given-names>Ryan</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Nycholat</surname><given-names>Corwin M.</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Yu</surname><given-names>Wenli</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Paulson</surname><given-names>James C.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Wilson</surname><given-names>Ian A.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="aff" rid="aff3"><sup>c</sup></xref></contrib><aff id="aff1"><label>a</label>Department of Molecular Biology</aff><aff id="aff2"><label>b</label>Department of Chemical Physiology</aff><aff id="aff3"><label>c</label>Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, California, USA</aff></contrib-group><author-notes><corresp>Address correspondence to Ian A. Wilson, <email>wilson@scripps.edu</email>, or James C. Paulson, <email>jpaulson@scripps.edu</email>.</corresp><fn fn-type="equal"><p>R.X. and X.Z. contributed equally to this article.</p></fn></author-notes><pub-date pub-type="ppub"><month>9</month><year>2012</year></pub-date><volume>86</volume><issue>17</issue><fpage>9221</fpage><lpage>9232</lpage><history><date date-type="received"><day>19</day><month>3</month><year>2012</year></date><date date-type="accepted"><day>6</day><month>6</month><year>2012</year></date></history><permissions><copyright-statement>Copyright © 2012, American Society for Microbiology. All Rights Reserved.</copyright-statement><copyright-year>2012</copyright-year><copyright-holder>American Society for Microbiology</copyright-holder></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zjv01712009221.pdf"></self-uri><abstract><p>The 2009 H1N1 influenza pandemic is the first human pandemic in decades and was of swine origin. Although swine are believed to be an intermediate host in the emergence of new human influenza viruses, there is still little known about the host barriers that keep swine influenza viruses from entering the human population. We surveyed swine progenitors and human viruses from the 2009 pandemic and measured the activities of the hemagglutinin (HA) and neuraminidase (NA), which are the two viral surface proteins that interact with host glycan receptors. A functional balance of these two activities (HA binding and NA cleavage) is found in human viruses but not in the swine progenitors. The human 2009 H1N1 pandemic virus exhibited both low HA avidity for glycan receptors as a result of mutations near the receptor binding site and weak NA enzymatic activity. Thus, a functional match between the hemagglutinin and neuraminidase appears to be necessary for efficient transmission between humans and may be an indicator of the pandemic potential of zoonotic viruses.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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