The Molecular Basis for Antigenic Drift of Human A/H2N2 Influenza Viruses
Identifieur interne : 000709 ( Pmc/Corpus ); précédent : 000708; suivant : 000710The Molecular Basis for Antigenic Drift of Human A/H2N2 Influenza Viruses
Auteurs : M. Linster ; E. J. A. Schrauwen ; S. Van Der Vliet ; D. F. Burke ; P. Lexmond ; T. M. Bestebroer ; D. J. Smith ; S. Herfst ; B. F. Koel ; R. A. M. FouchierSource :
- Journal of Virology [ 0022-538X ] ; 2019.
Abstract
While influenza A viruses of subtype H2N2 were at the origin of the Asian influenza pandemic, little is known about the antigenic changes that occurred during the twelve years of circulation in humans, the role of preexisting immunity, and the evolutionary rates of the virus. In this study, the antigenic map derived from hemagglutination inhibition (HI) titers of cell-cultured virus isolates and ferret postinfection sera displayed a directional evolution of viruses away from earlier isolates. Furthermore, individual mutations in close proximity to the receptor-binding site of the HA molecule determined the antigenic reactivity, confirming that individual amino acid substitutions in A/H2N2 viruses can confer major antigenic changes. This study adds to our understanding of virus evolution with respect to antigenic variability, rates of virus evolution, and potential escape mutants of A/H2N2.
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DOI: 10.1128/JVI.01907-18
PubMed: 30700609
PubMed Central: 6450109
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The Molecular Basis for Antigenic Drift of Human A/H2N2 Influenza Viruses</title><author><name sortKey="Linster, M" sort="Linster, M" uniqKey="Linster M" first="M." last="Linster">M. Linster</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation><affiliation><nlm:aff id="aff2"><addr-line>Programme in Emerging Infectious Diseases, Duke-NUS Medical School, Singapore</addr-line></nlm:aff></affiliation></author><author><name sortKey="Schrauwen, E J A" sort="Schrauwen, E J A" uniqKey="Schrauwen E" first="E. J. A." last="Schrauwen">E. J. A. Schrauwen</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation><affiliation><nlm:aff id="aff3"><addr-line>Avans University of Applied Science, Breda, The Netherlands</addr-line></nlm:aff></affiliation></author><author><name sortKey="Van Der Vliet, S" sort="Van Der Vliet, S" uniqKey="Van Der Vliet S" first="S." last="Van Der Vliet">S. Van Der Vliet</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation></author><author><name sortKey="Burke, D F" sort="Burke, D F" uniqKey="Burke D" first="D. F." last="Burke">D. F. Burke</name><affiliation><nlm:aff id="aff4"><addr-line>Center for Pathogen Evolution, Department of Zoology, University of Cambridge, Cambridge, United Kingdom</addr-line></nlm:aff></affiliation></author><author><name sortKey="Lexmond, P" sort="Lexmond, P" uniqKey="Lexmond P" first="P." last="Lexmond">P. Lexmond</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation></author><author><name sortKey="Bestebroer, T M" sort="Bestebroer, T M" uniqKey="Bestebroer T" first="T. M." last="Bestebroer">T. M. Bestebroer</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation></author><author><name sortKey="Smith, D J" sort="Smith, D J" uniqKey="Smith D" first="D. J." last="Smith">D. J. Smith</name><affiliation><nlm:aff id="aff4"><addr-line>Center for Pathogen Evolution, Department of Zoology, University of Cambridge, Cambridge, United Kingdom</addr-line></nlm:aff></affiliation></author><author><name sortKey="Herfst, S" sort="Herfst, S" uniqKey="Herfst S" first="S." last="Herfst">S. Herfst</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation></author><author><name sortKey="Koel, B F" sort="Koel, B F" uniqKey="Koel B" first="B. F." last="Koel">B. F. Koel</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation><affiliation><nlm:aff id="aff5"><addr-line>Department of Medical Microbiology, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands</addr-line></nlm:aff></affiliation></author><author><name sortKey="Fouchier, R A M" sort="Fouchier, R A M" uniqKey="Fouchier R" first="R. A. M." last="Fouchier">R. A. M. Fouchier</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">30700609</idno><idno type="pmc">6450109</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6450109</idno><idno type="RBID">PMC:6450109</idno><idno type="doi">10.1128/JVI.01907-18</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000709</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000709</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The Molecular Basis for Antigenic Drift of Human A/H2N2 Influenza Viruses</title><author><name sortKey="Linster, M" sort="Linster, M" uniqKey="Linster M" first="M." last="Linster">M. Linster</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation><affiliation><nlm:aff id="aff2"><addr-line>Programme in Emerging Infectious Diseases, Duke-NUS Medical School, Singapore</addr-line></nlm:aff></affiliation></author><author><name sortKey="Schrauwen, E J A" sort="Schrauwen, E J A" uniqKey="Schrauwen E" first="E. J. A." last="Schrauwen">E. J. A. Schrauwen</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation><affiliation><nlm:aff id="aff3"><addr-line>Avans University of Applied Science, Breda, The Netherlands</addr-line></nlm:aff></affiliation></author><author><name sortKey="Van Der Vliet, S" sort="Van Der Vliet, S" uniqKey="Van Der Vliet S" first="S." last="Van Der Vliet">S. Van Der Vliet</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation></author><author><name sortKey="Burke, D F" sort="Burke, D F" uniqKey="Burke D" first="D. F." last="Burke">D. F. Burke</name><affiliation><nlm:aff id="aff4"><addr-line>Center for Pathogen Evolution, Department of Zoology, University of Cambridge, Cambridge, United Kingdom</addr-line></nlm:aff></affiliation></author><author><name sortKey="Lexmond, P" sort="Lexmond, P" uniqKey="Lexmond P" first="P." last="Lexmond">P. Lexmond</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation></author><author><name sortKey="Bestebroer, T M" sort="Bestebroer, T M" uniqKey="Bestebroer T" first="T. M." last="Bestebroer">T. M. Bestebroer</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation></author><author><name sortKey="Smith, D J" sort="Smith, D J" uniqKey="Smith D" first="D. J." last="Smith">D. J. Smith</name><affiliation><nlm:aff id="aff4"><addr-line>Center for Pathogen Evolution, Department of Zoology, University of Cambridge, Cambridge, United Kingdom</addr-line></nlm:aff></affiliation></author><author><name sortKey="Herfst, S" sort="Herfst, S" uniqKey="Herfst S" first="S." last="Herfst">S. Herfst</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation></author><author><name sortKey="Koel, B F" sort="Koel, B F" uniqKey="Koel B" first="B. F." last="Koel">B. F. Koel</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></nlm:aff></affiliation><affiliation><nlm:aff id="aff5"><addr-line>Department of Medical Microbiology, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands</addr-line></nlm:aff></affiliation></author><author><name sortKey="Fouchier, R A M" sort="Fouchier, R A M" uniqKey="Fouchier R" first="R. A. M." last="Fouchier">R. A. M. Fouchier</name><affiliation><nlm:aff id="aff1"><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></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="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>While influenza A viruses of subtype H2N2 were at the origin of the Asian influenza pandemic, little is known about the antigenic changes that occurred during the twelve years of circulation in humans, the role of preexisting immunity, and the evolutionary rates of the virus. In this study, the antigenic map derived from hemagglutination inhibition (HI) titers of cell-cultured virus isolates and ferret postinfection sera displayed a directional evolution of viruses away from earlier isolates. Furthermore, individual mutations in close proximity to the receptor-binding site of the HA molecule determined the antigenic reactivity, confirming that individual amino acid substitutions in A/H2N2 viruses can confer major antigenic changes. This study adds to our understanding of virus evolution with respect to antigenic variability, rates of virus evolution, and potential escape mutants of A/H2N2.</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">30700609</article-id><article-id pub-id-type="pmc">6450109</article-id><article-id pub-id-type="publisher-id">01907-18</article-id><article-id pub-id-type="doi">10.1128/JVI.01907-18</article-id><article-categories><subj-group subj-group-type="heading"><subject>Genetic Diversity and Evolution</subject></subj-group></article-categories><title-group><article-title>The Molecular Basis for Antigenic Drift of Human A/H2N2 Influenza Viruses</article-title><alt-title alt-title-type="running-head">Antigenic Evolution of IAV H2N2</alt-title><alt-title alt-title-type="short-authors">Linster et al.</alt-title></title-group><contrib-group><contrib contrib-type="author" equal-contrib="yes"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0003-2636-2512</contrib-id><name><surname>Linster</surname><given-names>M.</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" equal-contrib="yes"><name><surname>Schrauwen</surname><given-names>E. J. 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><contrib contrib-type="author" equal-contrib="no"><name><surname>van der Vliet</surname><given-names>S.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author" equal-contrib="no"><name><surname>Burke</surname><given-names>D. F.</given-names></name><xref ref-type="aff" rid="aff4"><sup>d</sup></xref></contrib><contrib contrib-type="author" equal-contrib="no"><name><surname>Lexmond</surname><given-names>P.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author" equal-contrib="no"><name><surname>Bestebroer</surname><given-names>T. M.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author" equal-contrib="no"><name><surname>Smith</surname><given-names>D. J.</given-names></name><xref ref-type="aff" rid="aff4"><sup>d</sup></xref></contrib><contrib contrib-type="author" equal-contrib="no"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0001-9866-8903</contrib-id><name><surname>Herfst</surname><given-names>S.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author" equal-contrib="no"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0003-4692-3989</contrib-id><name><surname>Koel</surname><given-names>B. F.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="aff" rid="aff5"><sup>e</sup></xref></contrib><contrib contrib-type="author" corresp="yes" equal-contrib="no"><name><surname>Fouchier</surname><given-names>R. A. M.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><aff id="aff1"><label>a</label><addr-line>Department of Viroscience, Erasmus Medical Center, Rotterdam, The Netherlands</addr-line></aff><aff id="aff2"><label>b</label><addr-line>Programme in Emerging Infectious Diseases, Duke-NUS Medical School, Singapore</addr-line></aff><aff id="aff3"><label>c</label><addr-line>Avans University of Applied Science, Breda, The Netherlands</addr-line></aff><aff id="aff4"><label>d</label><addr-line>Center for Pathogen Evolution, Department of Zoology, University of Cambridge, Cambridge, United Kingdom</addr-line></aff><aff id="aff5"><label>e</label><addr-line>Department of Medical Microbiology, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands</addr-line></aff></contrib-group><contrib-group><contrib contrib-type="editor"><name><surname>García-Sastre</surname><given-names>Adolfo</given-names></name><role>Editor</role><aff>Icahn School of Medicine at Mount Sinai</aff></contrib></contrib-group><author-notes><corresp id="cor1">Address correspondence to R. A. M. Fouchier, <email>r.fouchier@erasmusmc.nl</email>.</corresp><fn fn-type="equal"><p>M.L. and E.J.A.S. contributed equally to this work.</p></fn><fn fn-type="other"><p><bold>Citation</bold> Linster M, Schrauwen EJA, van der Vliet S, Burke DF, Lexmond P, Bestebroer TM, Smith DJ, Herfst S, Koel BF, Fouchier RAM. 2019. The molecular basis for antigenic drift of human A/H2N2 influenza viruses. J Virol 93:e01907-18. <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.1128/JVI.01907-18">https://doi.org/10.1128/JVI.01907-18</ext-link>.</p></fn></author-notes><pub-date pub-type="epreprint"><day>30</day><month>1</month><year>2019</year></pub-date><pub-date pub-type="epub"><day>3</day><month>4</month><year>2019</year></pub-date><pub-date pub-type="collection"><day>15</day><month>4</month><year>2019</year></pub-date><volume>93</volume><issue>8</issue><elocation-id>e01907-18</elocation-id><history><date date-type="received"><day>30</day><month>10</month><year>2018</year></date><date date-type="accepted"><day>21</day><month>1</month><year>2019</year></date></history><permissions><copyright-statement>Copyright © 2019 American Society for Microbiology.</copyright-statement><copyright-year>2019</copyright-year><copyright-holder>American Society for Microbiology</copyright-holder><license license-type="asm" xlink:href="https://doi.org/10.1128/ASMCopyrightv2"><license-p><ext-link ext-link-type="uri" xlink:href="https://doi.org/10.1128/ASMCopyrightv2">All Rights Reserved</ext-link>.</license-p></license></permissions><self-uri content-type="pdf" xlink:href="JVI.01907-18.pdf"></self-uri><abstract abstract-type="precis"><p>While influenza A viruses of subtype H2N2 were at the origin of the Asian influenza pandemic, little is known about the antigenic changes that occurred during the twelve years of circulation in humans, the role of preexisting immunity, and the evolutionary rates of the virus. In this study, the antigenic map derived from hemagglutination inhibition (HI) titers of cell-cultured virus isolates and ferret postinfection sera displayed a directional evolution of viruses away from earlier isolates. Furthermore, individual mutations in close proximity to the receptor-binding site of the HA molecule determined the antigenic reactivity, confirming that individual amino acid substitutions in A/H2N2 viruses can confer major antigenic changes. This study adds to our understanding of virus evolution with respect to antigenic variability, rates of virus evolution, and potential escape mutants of A/H2N2.</p></abstract><abstract><title>ABSTRACT</title><p>Influenza A/H2N2 viruses caused a pandemic in 1957 and continued to circulate in humans until 1968. The antigenic evolution of A/H2N2 viruses over time and the amino acid substitutions responsible for this antigenic evolution are not known. Here, the antigenic diversity of a representative set of human A/H2N2 viruses isolated between 1957 and 1968 was characterized. The antigenic change of influenza A/H2N2 viruses during the 12 years that this virus circulated was modest. Two amino acid substitutions, T128D and N139K, located in the head domain of the H2 hemagglutinin (HA) molecule, were identified as important determinants of antigenic change during A/H2N2 virus evolution. The rate of A/H2N2 virus antigenic evolution during the 12-year period after introduction in humans was half that of A/H3N2 viruses, despite similar rates of genetic change.</p><p><bold>IMPORTANCE</bold> While influenza A viruses of subtype H2N2 were at the origin of the Asian influenza pandemic, little is known about the antigenic changes that occurred during the twelve years of circulation in humans, the role of preexisting immunity, and the evolutionary rates of the virus. In this study, the antigenic map derived from hemagglutination inhibition (HI) titers of cell-cultured virus isolates and ferret postinfection sera displayed a directional evolution of viruses away from earlier isolates. Furthermore, individual mutations in close proximity to the receptor-binding site of the HA molecule determined the antigenic reactivity, confirming that individual amino acid substitutions in A/H2N2 viruses can confer major antigenic changes. This study adds to our understanding of virus evolution with respect to antigenic variability, rates of virus evolution, and potential escape mutants of A/H2N2.</p></abstract><kwd-group><title>KEYWORDS</title><kwd>antigenic evolution</kwd><kwd>influenza virus A/H2N2</kwd><kwd>molecular drift</kwd><kwd>pandemic</kwd></kwd-group><funding-group><award-group id="award1"><funding-source><institution-wrap><institution>HHS | National Institutes of Health (NIH)</institution><institution-id>https://doi.org/10.13039/100000002</institution-id></institution-wrap></funding-source><award-id>HHSN272201400008C</award-id><award-id>DP1-OD000490-01</award-id><award-id>HHSN226200700010C</award-id><principal-award-recipient><string-name>Ron A. M. Fouchier</string-name></principal-award-recipient><principal-award-recipient><name><surname>Smith</surname><given-names>Derek J.</given-names></name></principal-award-recipient></award-group></funding-group><counts><fig-count count="4"></fig-count><table-count count="2"></table-count><equation-count count="0"></equation-count><ref-count count="44"></ref-count><page-count count="11"></page-count><word-count count="6616"></word-count></counts><custom-meta-group><custom-meta><meta-name>cover-date</meta-name><meta-value>April 2019</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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