Haemagglutinin mutations and glycosylation changes shaped the 2012/13 influenza A(H3N2) epidemic, Houston, Texas
Identifieur interne : 000822 ( Pmc/Curation ); précédent : 000821; suivant : 000823Haemagglutinin mutations and glycosylation changes shaped the 2012/13 influenza A(H3N2) epidemic, Houston, Texas
Auteurs : K M Stucker [États-Unis] ; S A Schobel [États-Unis] ; R J Olsen [États-Unis] ; H L Hodges [États-Unis] ; X. Lin [États-Unis] ; R A Halpin [États-Unis] ; N. Fedorova [États-Unis] ; T B Stockwell [États-Unis] ; A. Tovchigrechko [États-Unis] ; S R Das [États-Unis] ; D E Wentworth [États-Unis] ; J M Musser [États-Unis]Source :
- Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin [ 1025-496X ] ; 2015.
Abstract
While the early start and higher intensity of the 2012/13 influenza A virus (IAV) epidemic was not unprecedented, it was the first IAV epidemic season since the 2009 H1N1 influenza pandemic where the H3N2 subtype predominated. We directly sequenced the genomes of 154 H3N2 clinical specimens collected throughout the epidemic to better understand the evolution of H3N2 strains and to inform the H3N2 vaccine selection process. Phylogenetic analyses indicated that multiple co-circulating clades and continual antigenic drift in the haemagglutinin (HA) of clades 5, 3A, and 3C, with the evolution of a new 3C subgroup (3C-2012/13), were the driving causes of the epidemic. Drift variants contained HA substitutions and alterations in the potential N-linked glycosylation sites of HA. Antigenic analysis demonstrated that viruses in the emerging subclade 3C.3 and subgroup 3C-2012/13 were not well inhibited by antisera generated against the 3C.1 vaccine strains used for the 2012/13 (A/Victoria/361/2011) or 2013/14 (A/Texas/50/2012) seasons. Our data support updating the H3N2 vaccine strain to a clade 3C.2 or 3C.3-like strain or a subclade that has drifted further. They also underscore the challenges in vaccine strain selection, particularly regarding HA and neuraminidase substitutions derived during laboratory passage that may alter antigenic testing accuracy.
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PubMed: 25990233
PubMed Central: 5477787
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Craig Venter Institute, Rockville, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Wentworth, D E" sort="Wentworth, D E" uniqKey="Wentworth D" first="D E" last="Wentworth">D E Wentworth</name><affiliation wicri:level="1"><nlm:aff id="A1">Virology Group, J. Craig Venter Institute, Rockville, Maryland, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Virology Group, J. Craig Venter Institute, Rockville, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Musser, J M" sort="Musser, J M" uniqKey="Musser J" first="J M" last="Musser">J M Musser</name><affiliation wicri:level="1"><nlm:aff id="A4">Department of Pathology and Genomic Medicine, Houston Methodist Hospital, and Center for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, Houston, Texas, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Genomic Medicine, Houston Methodist Hospital, and Center for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, Houston, Texas</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">25990233</idno><idno type="pmc">5477787</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5477787</idno><idno type="RBID">PMC:5477787</idno><date when="2015">2015</date><idno type="wicri:Area/Pmc/Corpus">000822</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000822</idno><idno type="wicri:Area/Pmc/Curation">000822</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000822</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Haemagglutinin mutations and glycosylation changes shaped the 2012/13
influenza A(H3N2) epidemic, Houston, Texas</title><author><name sortKey="Stucker, K M" sort="Stucker, K M" uniqKey="Stucker K" first="K M" last="Stucker">K M Stucker</name><affiliation wicri:level="1"><nlm:aff id="A1">Virology Group, J. Craig Venter Institute, Rockville, Maryland, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Virology Group, J. Craig Venter Institute, Rockville, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Schobel, S A" sort="Schobel, S A" uniqKey="Schobel S" first="S A" last="Schobel">S A Schobel</name><affiliation wicri:level="1"><nlm:aff id="A2">Bioinformatics Group, J. Craig Venter Institute, Rockville, Maryland, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Bioinformatics Group, J. Craig Venter Institute, Rockville, Maryland</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="A3">Center for Bioinformatics and Computational Biology, University of Maryland, College Park, Maryland, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Bioinformatics and Computational Biology, University of Maryland, College Park, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Olsen, R J" sort="Olsen, R J" uniqKey="Olsen R" first="R J" last="Olsen">R J Olsen</name><affiliation wicri:level="1"><nlm:aff id="A4">Department of Pathology and Genomic Medicine, Houston Methodist Hospital, and Center for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, Houston, Texas, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Genomic Medicine, Houston Methodist Hospital, and Center for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, Houston, Texas</wicri:regionArea></affiliation></author><author><name sortKey="Hodges, H L" sort="Hodges, H L" uniqKey="Hodges H" first="H L" last="Hodges">H L Hodges</name><affiliation wicri:level="1"><nlm:aff id="A1">Virology Group, J. Craig Venter Institute, Rockville, Maryland, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Virology Group, J. Craig Venter Institute, Rockville, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Lin, X" sort="Lin, X" uniqKey="Lin X" first="X" last="Lin">X. Lin</name><affiliation wicri:level="1"><nlm:aff id="A1">Virology Group, J. Craig Venter Institute, Rockville, Maryland, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Virology Group, J. Craig Venter Institute, Rockville, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Halpin, R A" sort="Halpin, R A" uniqKey="Halpin R" first="R A" last="Halpin">R A Halpin</name><affiliation wicri:level="1"><nlm:aff id="A1">Virology Group, J. Craig Venter Institute, Rockville, Maryland, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Virology Group, J. Craig Venter Institute, Rockville, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Fedorova, N" sort="Fedorova, N" uniqKey="Fedorova N" first="N" last="Fedorova">N. Fedorova</name><affiliation wicri:level="1"><nlm:aff id="A1">Virology Group, J. Craig Venter Institute, Rockville, Maryland, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Virology Group, J. Craig Venter Institute, Rockville, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Stockwell, T B" sort="Stockwell, T B" uniqKey="Stockwell T" first="T B" last="Stockwell">T B Stockwell</name><affiliation wicri:level="1"><nlm:aff id="A2">Bioinformatics Group, J. Craig Venter Institute, Rockville, Maryland, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Bioinformatics Group, J. Craig Venter Institute, Rockville, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Tovchigrechko, A" sort="Tovchigrechko, A" uniqKey="Tovchigrechko A" first="A" last="Tovchigrechko">A. Tovchigrechko</name><affiliation wicri:level="1"><nlm:aff id="A5">Genomic Medicine Group, J. Craig Venter Institute, Rockville, Maryland, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Genomic Medicine Group, J. Craig Venter Institute, Rockville, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Das, S R" sort="Das, S R" uniqKey="Das S" first="S R" last="Das">S R Das</name><affiliation wicri:level="1"><nlm:aff id="A1">Virology Group, J. Craig Venter Institute, Rockville, Maryland, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Virology Group, J. Craig Venter Institute, Rockville, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Wentworth, D E" sort="Wentworth, D E" uniqKey="Wentworth D" first="D E" last="Wentworth">D E Wentworth</name><affiliation wicri:level="1"><nlm:aff id="A1">Virology Group, J. Craig Venter Institute, Rockville, Maryland, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Virology Group, J. Craig Venter Institute, Rockville, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Musser, J M" sort="Musser, J M" uniqKey="Musser J" first="J M" last="Musser">J M Musser</name><affiliation wicri:level="1"><nlm:aff id="A4">Department of Pathology and Genomic Medicine, Houston Methodist Hospital, and Center for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, Houston, Texas, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Genomic Medicine, Houston Methodist Hospital, and Center for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, Houston, Texas</wicri:regionArea></affiliation></author></analytic><series><title level="j">Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin</title><idno type="ISSN">1025-496X</idno><idno type="eISSN">1560-7917</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">While the early start and higher intensity of the 2012/13 influenza A
virus (IAV) epidemic was not unprecedented, it was the first IAV epidemic season
since the 2009 H1N1 influenza pandemic where the H3N2 subtype predominated. We
directly sequenced the genomes of 154 H3N2 clinical specimens collected
throughout the epidemic to better understand the evolution of H3N2 strains and
to inform the H3N2 vaccine selection process. Phylogenetic analyses indicated
that multiple co-circulating clades and continual antigenic drift in the
haemagglutinin (HA) of clades 5, 3A, and 3C, with the evolution of a new 3C
subgroup (3C-2012/13), were the driving causes of the epidemic. Drift variants
contained HA substitutions and alterations in the potential N-linked
glycosylation sites of HA. Antigenic analysis demonstrated that viruses in the
emerging subclade 3C.3 and subgroup 3C-2012/13 were not well inhibited by
antisera generated against the 3C.1 vaccine strains used for the 2012/13
(A/Victoria/361/2011) or 2013/14 (A/Texas/50/2012) seasons. Our data support
updating the H3N2 vaccine strain to a clade 3C.2 or 3C.3-like strain or a
subclade that has drifted further. They also underscore the challenges in
vaccine strain selection, particularly regarding HA and neuraminidase
substitutions derived during laboratory passage that may alter antigenic testing
accuracy.</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>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">100887452</journal-id><journal-id journal-id-type="pubmed-jr-id">26737</journal-id><journal-id journal-id-type="nlm-ta">Euro Surveill</journal-id><journal-id journal-id-type="iso-abbrev">Euro Surveill.</journal-id><journal-title-group><journal-title>Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin</journal-title></journal-title-group><issn pub-type="ppub">1025-496X</issn><issn pub-type="epub">1560-7917</issn></journal-meta><article-meta><article-id pub-id-type="pmid">25990233</article-id><article-id pub-id-type="pmc">5477787</article-id><article-id pub-id-type="manuscript">NIHMS855467</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Haemagglutinin mutations and glycosylation changes shaped the 2012/13
influenza A(H3N2) epidemic, Houston, Texas</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Stucker</surname><given-names>K M</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Schobel</surname><given-names>S A</given-names></name><xref ref-type="aff" rid="A2">2</xref><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Olsen</surname><given-names>R J</given-names></name><xref ref-type="aff" rid="A4">4</xref></contrib><contrib contrib-type="author"><name><surname>Hodges</surname><given-names>H L</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref rid="FN1" ref-type="author-notes">5</xref></contrib><contrib contrib-type="author"><name><surname>Lin</surname><given-names>X</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Halpin</surname><given-names>R A</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Fedorova</surname><given-names>N</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Stockwell</surname><given-names>T B</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Tovchigrechko</surname><given-names>A</given-names></name><xref ref-type="aff" rid="A5">6</xref></contrib><contrib contrib-type="author"><name><surname>Das</surname><given-names>S R</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Wentworth</surname><given-names>D E</given-names></name><email>dwentworth@cdc.gov</email><xref ref-type="aff" rid="A1">1</xref><xref rid="FN2" ref-type="author-notes">7</xref></contrib><contrib contrib-type="author"><name><surname>Musser</surname><given-names>J M</given-names></name><email>jmmusser@houstonmethodist.org</email><xref ref-type="aff" rid="A4">4</xref></contrib></contrib-group><aff id="A1"><label>1</label>Virology Group, J. Craig Venter Institute, Rockville, Maryland, United States</aff><aff id="A2"><label>2</label>Bioinformatics Group, J. Craig Venter Institute, Rockville, Maryland, United States</aff><aff id="A3"><label>3</label>Center for Bioinformatics and Computational Biology, University of Maryland, College Park, Maryland, United States</aff><aff id="A4"><label>4</label>Department of Pathology and Genomic Medicine, Houston Methodist Hospital, and Center for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, Houston, Texas, United States</aff><aff id="A5"><label>6</label>Genomic Medicine Group, J. Craig Venter Institute, Rockville, Maryland, United States</aff><author-notes><fn id="FN1" fn-type="present-address"><label>5</label><p>Current address: Department of Chemistry, University of Wisconsin-Madison,
Madison, Wisconsin, United States</p></fn><fn id="FN2" fn-type="present-address"><label>7</label><p>Current address: Virology Surveillance and Diagnosis Branch, Influenza
Division, Centers for Disease Control and Prevention, Atlanta, Georgia,
United States</p></fn><fn fn-type="COI-statement" id="FN3"><p><bold>Conflict of interest</bold>: None declared.</p></fn></author-notes><pub-date pub-type="nihms-submitted"><day>23</day><month>3</month><year>2017</year></pub-date><pub-date pub-type="epub"><day>07</day><month>5</month><year>2015</year></pub-date><pub-date pub-type="collection"><day>07</day><month>5</month><year>2015</year></pub-date><pub-date pub-type="pmc-release"><day>20</day><month>6</month><year>2017</year></pub-date><volume>20</volume><issue>18</issue><elocation-id>21122</elocation-id><abstract><p id="P1">While the early start and higher intensity of the 2012/13 influenza A
virus (IAV) epidemic was not unprecedented, it was the first IAV epidemic season
since the 2009 H1N1 influenza pandemic where the H3N2 subtype predominated. We
directly sequenced the genomes of 154 H3N2 clinical specimens collected
throughout the epidemic to better understand the evolution of H3N2 strains and
to inform the H3N2 vaccine selection process. Phylogenetic analyses indicated
that multiple co-circulating clades and continual antigenic drift in the
haemagglutinin (HA) of clades 5, 3A, and 3C, with the evolution of a new 3C
subgroup (3C-2012/13), were the driving causes of the epidemic. Drift variants
contained HA substitutions and alterations in the potential N-linked
glycosylation sites of HA. Antigenic analysis demonstrated that viruses in the
emerging subclade 3C.3 and subgroup 3C-2012/13 were not well inhibited by
antisera generated against the 3C.1 vaccine strains used for the 2012/13
(A/Victoria/361/2011) or 2013/14 (A/Texas/50/2012) seasons. Our data support
updating the H3N2 vaccine strain to a clade 3C.2 or 3C.3-like strain or a
subclade that has drifted further. They also underscore the challenges in
vaccine strain selection, particularly regarding HA and neuraminidase
substitutions derived during laboratory passage that may alter antigenic testing
accuracy.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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