Evolutionary Trends of A(H1N1) Influenza Virus Hemagglutinin Since 1918
Identifieur interne : 000A57 ( Pmc/Checkpoint ); précédent : 000A56; suivant : 000A58Evolutionary Trends of A(H1N1) Influenza Virus Hemagglutinin Since 1918
Auteurs : Jun Shen [États-Unis] ; Jianpeng Ma [États-Unis] ; Qinghua Wang [États-Unis]Source :
- PLoS ONE [ 1932-6203 ] ; 2009.
Abstract
The Pandemic (H1N1) 2009 is spreading to numerous countries and causing many human deaths. Although the symptoms in humans are mild at present, fears are that further mutations in the virus could lead to a potentially more dangerous outbreak in subsequent months. As the primary immunity-eliciting antigen, hemagglutinin (HA) is the major agent for host-driven antigenic drift in A(H3N2) virus. However, whether and how the evolution of HA is influenced by existing immunity is poorly understood for A(H1N1). Here, by analyzing hundreds of A(H1N1) HA sequences since 1918, we show the first evidence that host selections are indeed present in A(H1N1) HAs. Among a subgroup of human A(H1N1) HAs between 1918∼2008, we found strong diversifying (positive) selection at HA1 156 and 190. We also analyzed the evolutionary trends at HA1 190 and 225 that are critical determinants for receptor-binding specificity of A(H1N1) HA. Different A(H1N1) viruses appeared to favor one of these two sites in host-driven antigenic drift: epidemic A(H1N1) HAs favor HA1 190 while the 1918 pandemic and swine HAs favor HA1 225. Thus, our results highlight the urgency to understand the interplay between antigenic drift and receptor binding in HA evolution, and provide molecular signatures for monitoring future antigenically drifted 2009 pandemic and seasonal A(H1N1) influenza viruses.
Url:
DOI: 10.1371/journal.pone.0007789
PubMed: 19924230
PubMed Central: 2773012
Affiliations:
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of Bioengineering, Rice University, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation><affiliation wicri:level="2"><nlm:aff id="aff2"><addr-line>Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Wang, Qinghua" sort="Wang, Qinghua" uniqKey="Wang Q" first="Qinghua" last="Wang">Qinghua Wang</name><affiliation wicri:level="2"><nlm:aff id="aff2"><addr-line>Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of 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type="main">Evolutionary Trends of A(H1N1) Influenza Virus Hemagglutinin Since 1918</title><author><name sortKey="Shen, Jun" sort="Shen, Jun" uniqKey="Shen J" first="Jun" last="Shen">Jun Shen</name><affiliation wicri:level="2"><nlm:aff id="aff1"><addr-line>Department of Bioengineering, Rice University, Houston, Texas, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Bioengineering, Rice University, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Ma, Jianpeng" sort="Ma, Jianpeng" uniqKey="Ma J" first="Jianpeng" last="Ma">Jianpeng Ma</name><affiliation wicri:level="2"><nlm:aff id="aff1"><addr-line>Department of Bioengineering, Rice University, Houston, Texas, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Bioengineering, Rice University, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation><affiliation wicri:level="2"><nlm:aff id="aff2"><addr-line>Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Wang, Qinghua" sort="Wang, Qinghua" uniqKey="Wang Q" first="Qinghua" last="Wang">Qinghua Wang</name><affiliation wicri:level="2"><nlm:aff id="aff2"><addr-line>Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The Pandemic (H1N1) 2009 is spreading to numerous countries and causing many human deaths. Although the symptoms in humans are mild at present, fears are that further mutations in the virus could lead to a potentially more dangerous outbreak in subsequent months. As the primary immunity-eliciting antigen, hemagglutinin (HA) is the major agent for host-driven antigenic drift in A(H3N2) virus. However, whether and how the evolution of HA is influenced by existing immunity is poorly understood for A(H1N1). Here, by analyzing hundreds of A(H1N1) HA sequences since 1918, we show the first evidence that host selections are indeed present in A(H1N1) HAs. Among a subgroup of human A(H1N1) HAs between 1918∼2008, we found strong diversifying (positive) selection at HA<sub>1</sub> 156 and 190. We also analyzed the evolutionary trends at HA<sub>1</sub> 190 and 225 that are critical determinants for receptor-binding specificity of A(H1N1) HA. Different A(H1N1) viruses appeared to favor one of these two sites in host-driven antigenic drift: epidemic A(H1N1) HAs favor HA<sub>1</sub> 190 while the 1918 pandemic and swine HAs favor HA<sub>1</sub> 225. Thus, our results highlight the urgency to understand the interplay between antigenic drift and receptor binding in HA evolution, and provide molecular signatures for monitoring future antigenically drifted 2009 pandemic and seasonal A(H1N1) influenza viruses.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Wang, Tt" uniqKey="Wang T">TT Wang</name></author><author><name sortKey="Palese, P" uniqKey="Palese P">P Palese</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Neumann, G" uniqKey="Neumann G">G Neumann</name></author><author><name sortKey="Noda, T" uniqKey="Noda T">T Noda</name></author><author><name sortKey="Kawaoka, Y" uniqKey="Kawaoka Y">Y Kawaoka</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Peiris, Js" uniqKey="Peiris J">JS Peiris</name></author><author><name sortKey="Poon, Ll" uniqKey="Poon L">LL Poon</name></author><author><name sortKey="Guan, Y" 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<front><journal-meta><journal-id journal-id-type="nlm-ta">PLoS One</journal-id><journal-id journal-id-type="iso-abbrev">PLoS ONE</journal-id><journal-id journal-id-type="publisher-id">plos</journal-id><journal-id journal-id-type="pmc">plosone</journal-id><journal-title-group><journal-title>PLoS ONE</journal-title></journal-title-group><issn pub-type="epub">1932-6203</issn><publisher><publisher-name>Public Library of Science</publisher-name><publisher-loc>San Francisco, USA</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">19924230</article-id><article-id pub-id-type="pmc">2773012</article-id><article-id pub-id-type="publisher-id">09-PONE-RA-12140R1</article-id><article-id pub-id-type="doi">10.1371/journal.pone.0007789</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="Discipline"><subject>Virology</subject><subject>Virology/Emerging Viral Diseases</subject><subject>Virology/Virus Evolution and Symbiosis</subject></subj-group></article-categories><title-group><article-title>Evolutionary Trends of A(H1N1) Influenza Virus Hemagglutinin Since 1918</article-title><alt-title alt-title-type="running-head">Evolution of A(H1N1) HA</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Shen</surname><given-names>Jun</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ma</surname><given-names>Jianpeng</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Qinghua</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib></contrib-group><aff id="aff1"><label>1</label><addr-line>Department of Bioengineering, Rice University, Houston, Texas, United States of America</addr-line></aff><aff id="aff2"><label>2</label><addr-line>Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas, United States of America</addr-line></aff><contrib-group><contrib contrib-type="editor"><name><surname>Martin</surname><given-names>Darren P.</given-names></name><role>Editor</role><xref ref-type="aff" rid="edit1"></xref></contrib></contrib-group><aff id="edit1">Institute of Infectious Disease and Molecular Medicine, South Africa</aff><author-notes><corresp id="cor1">* E-mail: <email>E-mail: qinghuaw@bcm.tmc.edu</email> (QW); <email>jpma@bcm.tmc.edu</email> (JM)</corresp><fn fn-type="con"><p>Conceived and designed the experiments: JM QW. Performed the experiments: JS QW. Analyzed the data: JM QW. Contributed reagents/materials/analysis tools: JM QW. Wrote the paper: JS JM QW.</p></fn></author-notes><pub-date pub-type="collection"><year>2009</year></pub-date><pub-date pub-type="epub"><day>17</day><month>11</month><year>2009</year></pub-date><volume>4</volume><issue>11</issue><elocation-id>e7789</elocation-id><history><date date-type="received"><day>7</day><month>8</month><year>2009</year></date><date date-type="accepted"><day>15</day><month>10</month><year>2009</year></date></history><permissions><copyright-statement>Shen et al.</copyright-statement><copyright-year>2009</copyright-year><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.</license-p></license></permissions><abstract><p>The Pandemic (H1N1) 2009 is spreading to numerous countries and causing many human deaths. Although the symptoms in humans are mild at present, fears are that further mutations in the virus could lead to a potentially more dangerous outbreak in subsequent months. As the primary immunity-eliciting antigen, hemagglutinin (HA) is the major agent for host-driven antigenic drift in A(H3N2) virus. However, whether and how the evolution of HA is influenced by existing immunity is poorly understood for A(H1N1). Here, by analyzing hundreds of A(H1N1) HA sequences since 1918, we show the first evidence that host selections are indeed present in A(H1N1) HAs. Among a subgroup of human A(H1N1) HAs between 1918∼2008, we found strong diversifying (positive) selection at HA<sub>1</sub> 156 and 190. We also analyzed the evolutionary trends at HA<sub>1</sub> 190 and 225 that are critical determinants for receptor-binding specificity of A(H1N1) HA. Different A(H1N1) viruses appeared to favor one of these two sites in host-driven antigenic drift: epidemic A(H1N1) HAs favor HA<sub>1</sub> 190 while the 1918 pandemic and swine HAs favor HA<sub>1</sub> 225. Thus, our results highlight the urgency to understand the interplay between antigenic drift and receptor binding in HA evolution, and provide molecular signatures for monitoring future antigenically drifted 2009 pandemic and seasonal A(H1N1) influenza viruses.</p></abstract><counts><page-count count="10"></page-count></counts></article-meta></front></pmc><affiliations><list><country><li>États-Unis</li></country><region><li>Texas</li></region></list><tree><country name="États-Unis"><region name="Texas"><name sortKey="Shen, Jun" sort="Shen, Jun" uniqKey="Shen J" first="Jun" last="Shen">Jun Shen</name></region><name sortKey="Ma, Jianpeng" sort="Ma, Jianpeng" uniqKey="Ma J" first="Jianpeng" last="Ma">Jianpeng Ma</name><name sortKey="Ma, Jianpeng" sort="Ma, Jianpeng" uniqKey="Ma J" first="Jianpeng" last="Ma">Jianpeng Ma</name><name sortKey="Wang, Qinghua" sort="Wang, Qinghua" uniqKey="Wang Q" first="Qinghua" last="Wang">Qinghua Wang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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