Recent Human Influenza A/H3N2 Virus Evolution Driven by Novel Selection Factors in Addition to Antigenic Drift
Identifieur interne : 000535 ( Pmc/Corpus ); précédent : 000534; suivant : 000536Recent Human Influenza A/H3N2 Virus Evolution Driven by Novel Selection Factors in Addition to Antigenic Drift
Auteurs : Matthew J. Memoli ; Brett W. Jagger ; Vivien G. Dugan ; Li Qi ; Jadon P. Jackson ; Jeffery K. TaubenbergerSource :
- The Journal of infectious diseases [ 0022-1899 ] ; 2009.
Abstract
Examination of the evolutionary dynamics of complete influenza viral genomes reveals that other processes, in conjunction with antigenic drift, play important roles in viral evolution and selection, but there is little biological evidence to support these genomic data. Previous work demonstrated that after the A/Fujian/411/2002-like H3N2 influenza A epidemic during 2003–2004, a preexisting nondominant Fujian-like viral clade gained a small number of changes in genes encoding the viral polymerase complex, along with several changes in the antigenic regions of hemagglutinin, and in a genome-wide selective sweep, it replaced other co-circulating H3N2 clades.
Representative strains of these virus clades were evaluated in vitro and in vivo.
The newly dominant 2004–2005 A/California/7/2004-like H3N2 clade, which featured 2 key amino acid changes in the polymerase PA segment, grew to higher titers in MDCK cells and ferret tissues and caused more-severe disease in ferrets. The polymerase complex of this virus demonstrated enhanced activity in vitro, correlating directly to the enhanced replicative fitness and virulence in vivo.
These data suggest that influenza strains can be selected in humans through mutations that increase replicative fitness and virulence, in addition to the well-characterized antigenic changes in the surface glycoproteins.
Url:
DOI: 10.1086/605893
PubMed: 19743921
PubMed Central: 2778484
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PMC:2778484Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Recent Human Influenza A/H3N2 Virus Evolution Driven by Novel Selection Factors in Addition to Antigenic Drift</title>
<author><name sortKey="Memoli, Matthew J" sort="Memoli, Matthew J" uniqKey="Memoli M" first="Matthew J." last="Memoli">Matthew J. Memoli</name>
</author>
<author><name sortKey="Jagger, Brett W" sort="Jagger, Brett W" uniqKey="Jagger B" first="Brett W." last="Jagger">Brett W. Jagger</name>
</author>
<author><name sortKey="Dugan, Vivien G" sort="Dugan, Vivien G" uniqKey="Dugan V" first="Vivien G." last="Dugan">Vivien G. Dugan</name>
</author>
<author><name sortKey="Qi, Li" sort="Qi, Li" uniqKey="Qi L" first="Li" last="Qi">Li Qi</name>
</author>
<author><name sortKey="Jackson, Jadon P" sort="Jackson, Jadon P" uniqKey="Jackson J" first="Jadon P." last="Jackson">Jadon P. Jackson</name>
</author>
<author><name sortKey="Taubenberger, Jeffery K" sort="Taubenberger, Jeffery K" uniqKey="Taubenberger J" first="Jeffery K." last="Taubenberger">Jeffery K. Taubenberger</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Recent Human Influenza A/H3N2 Virus Evolution Driven by Novel Selection Factors in Addition to Antigenic Drift</title>
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</author>
<author><name sortKey="Jagger, Brett W" sort="Jagger, Brett W" uniqKey="Jagger B" first="Brett W." last="Jagger">Brett W. Jagger</name>
</author>
<author><name sortKey="Dugan, Vivien G" sort="Dugan, Vivien G" uniqKey="Dugan V" first="Vivien G." last="Dugan">Vivien G. Dugan</name>
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<author><name sortKey="Qi, Li" sort="Qi, Li" uniqKey="Qi L" first="Li" last="Qi">Li Qi</name>
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<author><name sortKey="Jackson, Jadon P" sort="Jackson, Jadon P" uniqKey="Jackson J" first="Jadon P." last="Jackson">Jadon P. Jackson</name>
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<author><name sortKey="Taubenberger, Jeffery K" sort="Taubenberger, Jeffery K" uniqKey="Taubenberger J" first="Jeffery K." last="Taubenberger">Jeffery K. Taubenberger</name>
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<series><title level="j">The Journal of infectious diseases</title>
<idno type="ISSN">0022-1899</idno>
<idno type="eISSN">1537-6613</idno>
<imprint><date when="2009">2009</date>
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title>
<p id="P1">Examination of the evolutionary dynamics of complete influenza viral genomes reveals that other processes, in conjunction with antigenic drift, play important roles in viral evolution and selection, but there is little biological evidence to support these genomic data. Previous work demonstrated that after the A/Fujian/411/2002-like H3N2 influenza A epidemic during 2003–2004, a preexisting nondominant Fujian-like viral clade gained a small number of changes in genes encoding the viral polymerase complex, along with several changes in the antigenic regions of hemagglutinin, and in a genome-wide selective sweep, it replaced other co-circulating H3N2 clades.</p>
</sec>
<sec sec-type="methods" id="S2"><title>Methods</title>
<p id="P2">Representative strains of these virus clades were evaluated in vitro and in vivo.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">The newly dominant 2004–2005 A/California/7/2004-like H3N2 clade, which featured 2 key amino acid changes in the polymerase PA segment, grew to higher titers in MDCK cells and ferret tissues and caused more-severe disease in ferrets. The polymerase complex of this virus demonstrated enhanced activity in vitro, correlating directly to the enhanced replicative fitness and virulence in vivo.</p>
</sec>
<sec id="S4"><title>Conclusion</title>
<p id="P4">These data suggest that influenza strains can be selected in humans through mutations that increase replicative fitness and virulence, in addition to the well-characterized antigenic changes in the surface glycoproteins.</p>
</sec>
</div>
</front>
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<pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">0413675</journal-id>
<journal-id journal-id-type="pubmed-jr-id">4830</journal-id>
<journal-id journal-id-type="nlm-ta">J Infect Dis</journal-id>
<journal-title>The Journal of infectious diseases</journal-title>
<issn pub-type="ppub">0022-1899</issn>
<issn pub-type="epub">1537-6613</issn>
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<article-id pub-id-type="doi">10.1086/605893</article-id>
<article-id pub-id-type="manuscript">NIHMS156515</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
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<title-group><article-title>Recent Human Influenza A/H3N2 Virus Evolution Driven by Novel Selection Factors in Addition to Antigenic Drift</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Memoli</surname>
<given-names>Matthew J.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Jagger</surname>
<given-names>Brett W.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Dugan</surname>
<given-names>Vivien G.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Qi</surname>
<given-names>Li</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Jackson</surname>
<given-names>Jadon P.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Taubenberger</surname>
<given-names>Jeffery K.</given-names>
</name>
</contrib>
<aff id="A1">Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland</aff>
</contrib-group>
<author-notes><corresp id="FN1">Reprints or correspondence: Dr. Jeffery K. Taubenberger, Viral Pathogenesis and Evolution Section Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 33 North Dr., Rm. 3E19A.2 Bethesda, MD 20892 (<email>taubenbergerj@niaid.nih.gov</email>
)</corresp>
<fn id="FN2" fn-type="conflict"><p>Potential conflicts of interest: none reported.</p>
</fn>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>2</day>
<month>11</month>
<year>2009</year>
</pub-date>
<pub-date pub-type="ppub"><day>15</day>
<month>10</month>
<year>2009</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>15</day>
<month>10</month>
<year>2010</year>
</pub-date>
<volume>200</volume>
<issue>8</issue>
<fpage>1232</fpage>
<lpage>1241</lpage>
<abstract><sec id="S1"><title>Background</title>
<p id="P1">Examination of the evolutionary dynamics of complete influenza viral genomes reveals that other processes, in conjunction with antigenic drift, play important roles in viral evolution and selection, but there is little biological evidence to support these genomic data. Previous work demonstrated that after the A/Fujian/411/2002-like H3N2 influenza A epidemic during 2003–2004, a preexisting nondominant Fujian-like viral clade gained a small number of changes in genes encoding the viral polymerase complex, along with several changes in the antigenic regions of hemagglutinin, and in a genome-wide selective sweep, it replaced other co-circulating H3N2 clades.</p>
</sec>
<sec sec-type="methods" id="S2"><title>Methods</title>
<p id="P2">Representative strains of these virus clades were evaluated in vitro and in vivo.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">The newly dominant 2004–2005 A/California/7/2004-like H3N2 clade, which featured 2 key amino acid changes in the polymerase PA segment, grew to higher titers in MDCK cells and ferret tissues and caused more-severe disease in ferrets. The polymerase complex of this virus demonstrated enhanced activity in vitro, correlating directly to the enhanced replicative fitness and virulence in vivo.</p>
</sec>
<sec id="S4"><title>Conclusion</title>
<p id="P4">These data suggest that influenza strains can be selected in humans through mutations that increase replicative fitness and virulence, in addition to the well-characterized antigenic changes in the surface glycoproteins.</p>
</sec>
</abstract>
<contract-num rid="AI1">ZIA AI000986-03
||AI</contract-num>
<contract-sponsor id="AI1">National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID</contract-sponsor>
</article-meta>
</front>
</pmc>
</record>
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