Canalization of the evolutionary trajectory of the human influenza virus
Identifieur interne : 000904 ( Pmc/Curation ); précédent : 000903; suivant : 000905Canalization of the evolutionary trajectory of the human influenza virus
Auteurs : Trevor Bedford [États-Unis, Royaume-Uni] ; Andrew Rambaut [Royaume-Uni, États-Unis] ; Mercedes Pascual [États-Unis]Source :
- BMC Biology [ 1741-7007 ] ; 2012.
Abstract
Since its emergence in 1968, influenza A (H3N2) has evolved extensively in genotype and antigenic phenotype. However, despite strong pressure to evolve away from human immunity and to diversify in antigenic phenotype, H3N2 influenza shows paradoxically limited genetic and antigenic diversity present at any one time. Here, we propose a simple model of antigenic evolution in the influenza virus that accounts for this apparent discrepancy.
In this model, antigenic phenotype is represented by a
Selective dynamics induce a canalized evolutionary trajectory, in which the evolutionary fate of the influenza population is surprisingly repeatable. In the model, the influenza population shows a 1- to 2-year timescale of repeatability, suggesting a window in which evolutionary dynamics could be, in theory, predictable.
Url:
DOI: 10.1186/1741-7007-10-38
PubMed: 22546494
PubMed Central: 3373370
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Biology, University of Edinburgh, Edinburgh, EH9 3JT, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, EH9 3JT</wicri:regionArea></affiliation></author><author><name sortKey="Rambaut, Andrew" sort="Rambaut, Andrew" uniqKey="Rambaut A" first="Andrew" last="Rambaut">Andrew Rambaut</name><affiliation wicri:level="1"><nlm:aff id="I3">Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, EH9 3JT, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, EH9 3JT</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I4">Fogarty International Center, National Institutes of Health, Bethesda, MD, 20892, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Fogarty International Center, National Institutes of Health, Bethesda, MD, 20892</wicri:regionArea></affiliation></author><author><name sortKey="Pascual, Mercedes" sort="Pascual, Mercedes" uniqKey="Pascual M" first="Mercedes" last="Pascual">Mercedes Pascual</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, MI, 48109, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, MI, 48109</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I2">Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI, 48109, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI, 48109</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22546494</idno><idno type="pmc">3373370</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3373370</idno><idno type="RBID">PMC:3373370</idno><idno type="doi">10.1186/1741-7007-10-38</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">000904</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000904</idno><idno type="wicri:Area/Pmc/Curation">000904</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000904</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Canalization of the evolutionary trajectory of the human influenza virus</title><author><name sortKey="Bedford, Trevor" sort="Bedford, Trevor" uniqKey="Bedford T" first="Trevor" last="Bedford">Trevor Bedford</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, MI, 48109, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, MI, 48109</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I2">Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI, 48109, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI, 48109</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I3">Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, EH9 3JT, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, EH9 3JT</wicri:regionArea></affiliation></author><author><name sortKey="Rambaut, Andrew" sort="Rambaut, Andrew" uniqKey="Rambaut A" first="Andrew" last="Rambaut">Andrew Rambaut</name><affiliation wicri:level="1"><nlm:aff id="I3">Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, EH9 3JT, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, EH9 3JT</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I4">Fogarty International Center, National Institutes of Health, Bethesda, MD, 20892, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Fogarty International Center, National Institutes of Health, Bethesda, MD, 20892</wicri:regionArea></affiliation></author><author><name sortKey="Pascual, Mercedes" sort="Pascual, Mercedes" uniqKey="Pascual M" first="Mercedes" last="Pascual">Mercedes Pascual</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, MI, 48109, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, MI, 48109</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I2">Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI, 48109, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI, 48109</wicri:regionArea></affiliation></author></analytic><series><title level="j">BMC Biology</title><idno type="eISSN">1741-7007</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>Since its emergence in 1968, influenza A (H3N2) has evolved extensively in genotype and antigenic phenotype. However, despite strong pressure to evolve away from human immunity and to diversify in antigenic phenotype, H3N2 influenza shows paradoxically limited genetic and antigenic diversity present at any one time. Here, we propose a simple model of antigenic evolution in the influenza virus that accounts for this apparent discrepancy.</p></sec><sec><title>Results</title><p>In this model, antigenic phenotype is represented by a <italic>N</italic>-dimensional vector, and virus mutations perturb phenotype within this continuous Euclidean space. We implement this model in a large-scale individual-based simulation, and in doing so, we find a remarkable correspondence between model behavior and observed influenza dynamics. This model displays rapid evolution but low standing diversity and simultaneously accounts for the epidemiological, genetic, antigenic, and geographical patterns displayed by the virus. We find that evolution away from existing human immunity results in rapid population turnover in the influenza virus and that this population turnover occurs primarily along a single antigenic axis.</p></sec><sec><title>Conclusions</title><p>Selective dynamics induce a canalized evolutionary trajectory, in which the evolutionary fate of the influenza population is surprisingly repeatable. In the model, the influenza population shows a 1- to 2-year timescale of repeatability, suggesting a window in which evolutionary dynamics could be, in theory, predictable.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Nelson, Mi" uniqKey="Nelson M">MI Nelson</name></author><author><name sortKey="Holmes, Ec" uniqKey="Holmes E">EC Holmes</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fitch, Wm" uniqKey="Fitch W">WM Fitch</name></author><author><name sortKey="Bush, Rm" uniqKey="Bush R">RM Bush</name></author><author><name sortKey="Bender, Ca" uniqKey="Bender C">CA Bender</name></author><author><name sortKey="Cox, Nj" uniqKey="Cox N">NJ Cox</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ferguson, Nm" uniqKey="Ferguson N">NM Ferguson</name></author><author><name sortKey="Galvani, Ap" uniqKey="Galvani A">AP 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<front><journal-meta><journal-id journal-id-type="nlm-ta">BMC Biol</journal-id><journal-id journal-id-type="iso-abbrev">BMC Biol</journal-id><journal-title-group><journal-title>BMC Biology</journal-title></journal-title-group><issn pub-type="epub">1741-7007</issn><publisher><publisher-name>BioMed Central</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">22546494</article-id><article-id pub-id-type="pmc">3373370</article-id><article-id pub-id-type="publisher-id">1741-7007-10-38</article-id><article-id pub-id-type="doi">10.1186/1741-7007-10-38</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Canalization of the evolutionary trajectory of the human influenza virus</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes" id="A1"><name><surname>Bedford</surname><given-names>Trevor</given-names></name><xref ref-type="aff" rid="I1">1</xref><xref ref-type="aff" rid="I2">2</xref><xref ref-type="aff" rid="I3">3</xref><email>t.bedford@ed.ac.uk</email></contrib><contrib contrib-type="author" id="A2"><name><surname>Rambaut</surname><given-names>Andrew</given-names></name><xref ref-type="aff" rid="I3">3</xref><xref ref-type="aff" rid="I4">4</xref><email>a.rambaut@ed.ac.uk</email></contrib><contrib contrib-type="author" id="A3"><name><surname>Pascual</surname><given-names>Mercedes</given-names></name><xref ref-type="aff" rid="I1">1</xref><xref ref-type="aff" rid="I2">2</xref><email>pascual@umich.edu</email></contrib></contrib-group><aff id="I1"><label>1</label>Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, MI, 48109, USA</aff><aff id="I2"><label>2</label>Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI, 48109, USA</aff><aff id="I3"><label>3</label>Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, EH9 3JT, UK</aff><aff id="I4"><label>4</label>Fogarty International Center, National Institutes of Health, Bethesda, MD, 20892, USA</aff><pub-date pub-type="collection"><year>2012</year></pub-date><pub-date pub-type="epub"><day>30</day><month>4</month><year>2012</year></pub-date><volume>10</volume><fpage>38</fpage><lpage>38</lpage><history><date date-type="received"><day>13</day><month>1</month><year>2012</year></date><date date-type="accepted"><day>30</day><month>4</month><year>2012</year></date></history><permissions><copyright-statement>Copyright ©2012 Bedford et al; licensee BioMed Central Ltd.</copyright-statement><copyright-year>2012</copyright-year><copyright-holder>Bedford et al; licensee BioMed Central Ltd.</copyright-holder><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/2.0"><license-p>This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/2.0">http://creativecommons.org/licenses/by/2.0</ext-link>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><self-uri xlink:href="http://www.biomedcentral.com/1741-7007/10/38"></self-uri><abstract><sec><title>Background</title><p>Since its emergence in 1968, influenza A (H3N2) has evolved extensively in genotype and antigenic phenotype. However, despite strong pressure to evolve away from human immunity and to diversify in antigenic phenotype, H3N2 influenza shows paradoxically limited genetic and antigenic diversity present at any one time. Here, we propose a simple model of antigenic evolution in the influenza virus that accounts for this apparent discrepancy.</p></sec><sec><title>Results</title><p>In this model, antigenic phenotype is represented by a <italic>N</italic>-dimensional vector, and virus mutations perturb phenotype within this continuous Euclidean space. We implement this model in a large-scale individual-based simulation, and in doing so, we find a remarkable correspondence between model behavior and observed influenza dynamics. This model displays rapid evolution but low standing diversity and simultaneously accounts for the epidemiological, genetic, antigenic, and geographical patterns displayed by the virus. We find that evolution away from existing human immunity results in rapid population turnover in the influenza virus and that this population turnover occurs primarily along a single antigenic axis.</p></sec><sec><title>Conclusions</title><p>Selective dynamics induce a canalized evolutionary trajectory, in which the evolutionary fate of the influenza population is surprisingly repeatable. In the model, the influenza population shows a 1- to 2-year timescale of repeatability, suggesting a window in which evolutionary dynamics could be, in theory, predictable.</p></sec></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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