H3N2 influenza viruses in humans: Viral mechanisms, evolution, and evaluation
Identifieur interne : 000D65 ( Pmc/Curation ); précédent : 000D64; suivant : 000D66H3N2 influenza viruses in humans: Viral mechanisms, evolution, and evaluation
Auteurs : James D. Allen [États-Unis] ; Ted M. Ross [États-Unis]Source :
- Human Vaccines & Immunotherapeutics [ 2164-5515 ] ; 2018.
Abstract
Annual seasonal influenza vaccines are composed of two influenza A strains representing the H1N1 and H3N2 subtypes, and two influenza B strains representing the Victoria and Yamagata lineages. Strains from these Influenza A and Influenza B viruses currently co-circulate in humans. Of these, strains associated with the H3N2 subtype are affiliated with severe influenza seasons. H3N2 influenza viruses pre-dominated during 3 of the last 5 quite severe influenza seasons. During the 2016/2017 flu season, the H3N2 component of the influenza vaccine exhibited a poor protective efficacy (∼28–42%) against preventing infection of co-circulating strains. Since their introduction to the human population in 1968, H3N2 Influenza viruses have rapidly evolved both genetically and antigenically in an attempt to escape host immune pressures. As a result, these viruses have added numerous N-linked glycans to the viral hemagglutinin (HA), increased the overall net charge of the HA molecule, changed their preferences in receptor binding, and altered the ability of neuraminidase (NA) to agglutinate red blood cells prior to host entry. Over time, these adaptations have made characterizing these viruses increasingly difficult. This review investigates these recent changes in modern H3N2 influenza viruses and explores the methods that researchers are currently developing in order to study these viruses.
Url:
DOI: 10.1080/21645515.2018.1462639
PubMed: 29641358
PubMed Central: 6149781
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<front><div type="abstract" xml:lang="en"><title>ABSTRACT</title>
<p>Annual seasonal influenza vaccines are composed of two influenza A strains representing the H1N1 and H3N2 subtypes, and two influenza B strains representing the Victoria and Yamagata lineages. Strains from these Influenza A and Influenza B viruses currently co-circulate in humans. Of these, strains associated with the H3N2 subtype are affiliated with severe influenza seasons. H3N2 influenza viruses pre-dominated during 3 of the last 5 quite severe influenza seasons. During the 2016/2017 flu season, the H3N2 component of the influenza vaccine exhibited a poor protective efficacy (∼28–42%) against preventing infection of co-circulating strains. Since their introduction to the human population in 1968, H3N2 Influenza viruses have rapidly evolved both genetically and antigenically in an attempt to escape host immune pressures. As a result, these viruses have added numerous N-linked glycans to the viral hemagglutinin (HA), increased the overall net charge of the HA molecule, changed their preferences in receptor binding, and altered the ability of neuraminidase (NA) to agglutinate red blood cells prior to host entry. Over time, these adaptations have made characterizing these viruses increasingly difficult. This review investigates these recent changes in modern H3N2 influenza viruses and explores the methods that researchers are currently developing in order to study these viruses.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Hum Vaccin Immunother</journal-id>
<journal-id journal-id-type="iso-abbrev">Hum Vaccin Immunother</journal-id>
<journal-id journal-id-type="publisher-id">KHVI</journal-id>
<journal-id journal-id-type="publisher-id">khvi20</journal-id>
<journal-title-group><journal-title>Human Vaccines & Immunotherapeutics</journal-title>
</journal-title-group>
<issn pub-type="ppub">2164-5515</issn>
<issn pub-type="epub">2164-554X</issn>
<publisher><publisher-name>Taylor & Francis</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">29641358</article-id>
<article-id pub-id-type="pmc">6149781</article-id>
<article-id pub-id-type="publisher-id">1462639</article-id>
<article-id pub-id-type="doi">10.1080/21645515.2018.1462639</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Reviews</subject>
</subj-group>
</article-categories>
<title-group><article-title>H3N2 influenza viruses in humans: Viral mechanisms, evolution, and evaluation</article-title>
<alt-title alt-title-type="running-authors">J. D. ALLEN AND T. M. ROSS</alt-title>
<alt-title alt-title-type="running-title">HUMAN VACCINES & IMMUNOTHERAPEUTICS</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Allen</surname>
<given-names>James D.</given-names>
</name>
<xref ref-type="aff" rid="af0001"><sup>a</sup>
</xref>
<xref ref-type="corresp" rid="an0001"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ross</surname>
<given-names>Ted M.</given-names>
</name>
<xref ref-type="aff" rid="af0001"><sup>a</sup>
</xref>
<xref ref-type="aff" rid="af0002"><sup>b</sup>
</xref>
</contrib>
<aff id="af0001"><label>a</label>
<institution>Center for Vaccines and Immunology, University of Georgia</institution>
, Athens, GA,<country>USA</country>
</aff>
<aff id="af0002"><label>b</label>
<institution>Department of Infectious Diseases, University of Georgia</institution>
, Athens, GA,<country>USA</country>
</aff>
</contrib-group>
<author-notes><corresp id="an0001"><bold>CONTACT</bold>
James D. Allen <email xlink:href="jdallen@uga.edu">jdallen@uga.edu</email>
<institution>Center for Vaccines and Immunology, University of Georgia</institution>
, <addr-line>501 D.W. Brooks Drive, CVI Room 1503</addr-line>
, Athens, GA 30602, USA</corresp>
<fn id="afn0001"><p>Color versions of one or more of the figures in the article can be found online at <ext-link ext-link-type="uri" xlink:href="http://www.tandfonline.com/khvi">www.tandfonline.com/khvi</ext-link>
.</p>
</fn>
</author-notes>
<pub-date pub-type="collection"><year>2018</year>
</pub-date>
<pub-date pub-type="epub"><day>14</day>
<month>5</month>
<year>2018</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>14</day>
<month>5</month>
<year>2018</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on the . </pmc-comment>
<volume>14</volume>
<issue>8</issue>
<fpage seq="4">1840</fpage>
<lpage>1847</lpage>
<history><date date-type="received"><day>14</day>
<month>2</month>
<year>2018</year>
</date>
<date date-type="accepted"><day>26</day>
<month>3</month>
<year>2018</year>
</date>
</history>
<permissions><pmc-comment> © James D. Allen and Ted M. Ross </pmc-comment>
<copyright-statement>© 2018 The Author(s). Published with license by Taylor & Francis</copyright-statement>
<copyright-year>2018</copyright-year>
<copyright-holder>The Author(s)</copyright-holder>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc-nd/4.0/"><license-p>This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc-nd/4.0/">http://creativecommons.org/licenses/by-nc-nd/4.0/</ext-link>
), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.</license-p>
</license>
</permissions>
<self-uri content-type="pdf" xlink:href="khvi-14-08-1462639.pdf"></self-uri>
<abstract><title>ABSTRACT</title>
<p>Annual seasonal influenza vaccines are composed of two influenza A strains representing the H1N1 and H3N2 subtypes, and two influenza B strains representing the Victoria and Yamagata lineages. Strains from these Influenza A and Influenza B viruses currently co-circulate in humans. Of these, strains associated with the H3N2 subtype are affiliated with severe influenza seasons. H3N2 influenza viruses pre-dominated during 3 of the last 5 quite severe influenza seasons. During the 2016/2017 flu season, the H3N2 component of the influenza vaccine exhibited a poor protective efficacy (∼28–42%) against preventing infection of co-circulating strains. Since their introduction to the human population in 1968, H3N2 Influenza viruses have rapidly evolved both genetically and antigenically in an attempt to escape host immune pressures. As a result, these viruses have added numerous N-linked glycans to the viral hemagglutinin (HA), increased the overall net charge of the HA molecule, changed their preferences in receptor binding, and altered the ability of neuraminidase (NA) to agglutinate red blood cells prior to host entry. Over time, these adaptations have made characterizing these viruses increasingly difficult. This review investigates these recent changes in modern H3N2 influenza viruses and explores the methods that researchers are currently developing in order to study these viruses.</p>
</abstract>
<kwd-group kwd-group-type="author"><title>KEYWORDS</title>
<kwd>focal reduction assay</kwd>
<kwd>glycosylation</kwd>
<kwd>H3N2</kwd>
<kwd>hemagglutination inhibition assay</kwd>
<kwd>Influenza</kwd>
<kwd>molecular virology</kwd>
<kwd>oseltamivir carboxylate</kwd>
<kwd>micro-neutralization assay</kwd>
</kwd-group>
<funding-group><award-group><funding-source><named-content content-type="funder-name">University of Georgia</named-content>
</funding-source>
<award-id>#001</award-id>
</award-group>
</funding-group>
<counts><fig-count count="1"></fig-count>
<table-count count="0"></table-count>
<equation-count count="0"></equation-count>
<ref-count count="45"></ref-count>
<page-count count="8"></page-count>
</counts>
</article-meta>
</front>
</pmc>
</record>
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