H2N2V1, Hal, Corpus, bibRecord, 000114

Genetic and antigenic characterization of influenza A(H3N2) in Cameroon during the 2014-2016 influenza seasons

Identifieur interne : 000114 ( Hal/Corpus ); précédent : 000113; suivant : 000115

Genetic and antigenic characterization of influenza A(H3N2) in Cameroon during the 2014-2016 influenza seasons

Auteurs : Gwladys Monamele ; Marie-Astrid Vernet ; Mohammed Njankouo ; Kathleen Victoir ; Jane Akoachere ; Damian Anong ; Richard Njouom

Source :

PLoS ONE [ 1932-6203 ] ; 2017-09-06.

RBID : Hal:pasteur-01659289

English descriptors

mix :
- Antimicrobial resistance, Cameroon, DNA sequence analysis, Influenza, Influenza A virus, Influenza viruses, Vaccines, Viral vaccines.

Abstract

The first outbreak of influenza A(H3N2) occurred in 1968 and caused the third flu pandemic of the 20th century. It has affected multiple countries over time. The best strategy to reduce the burden of influenza is through vaccination whose efficacy varies with respect to the circulating strains. This study was performed to better understand the molecular evolution of influenza A(H3N2) and assess vaccine efficacy in Cameroon. Complete sequences of three gene segments were obtained from 2014 to 2016 influenza seasons in Cameroon. Hemagglutinin (HA), Neuraminidase (NA) and matrix (M) genes of 35 A(H3N2) virus strains were amplified and sequenced. Predicted vaccine efficacy was measured using the Pepitope model. Phylogenetic analysis of the HA gene showed that all Cameroonian strains had evolved away from the 3C.1-A/Texas/50/2012-like clade. Globally, 2014 virus strains clustered with the 2015-2016 vaccine strain, 3C.3a-A/Switzerland/9715293/2013, whereas 2015 and 2016 virus strains clustered with the 2016-2017 vaccine strain, 3C.2a-A/HongKong/4801/2014. In order to determine the genotypic drug susceptibility to neuraminidase inhibitors and amantadine, the NA and M2 protein coding sequences were analyzed. There was no strain with characteristic mutation for resistance to neuraminidase inhibitors, per contra; all strains possessed the substitution S31N, peculiar of resistance to adamantanes. There was drift in influenza A(H3N2) dominant epitopes B (2014 and 2015) to epitopes A (2016) with a theoretical efficiency in vaccine ranging from low to moderate. The presence of several antigenic site mutations among H3N2 virus strains between 2014-2016 influenza seasons in Cameroon confirms the progressing evolution of circulating H3N2 strains.

Url:

https://hal-pasteur.archives-ouvertes.fr/pasteur-01659289

DOI: 10.1371/journal.pone.0184411

Links to Exploration step

Hal:pasteur-01659289

Le document en format XML

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<front><div type="abstract" xml:lang="en">              <p>The first outbreak of influenza A(H3N2) occurred in 1968 and caused the third flu pandemic of the 20th century. It has affected multiple countries over time. The best strategy to reduce the burden of influenza is through vaccination whose efficacy varies with respect to the circulating strains. This study was performed to better understand the molecular evolution of influenza A(H3N2) and assess vaccine efficacy in Cameroon. Complete sequences of three gene segments were obtained from 2014 to 2016 influenza seasons in Cameroon. Hemagglutinin (HA), Neuraminidase (NA) and matrix (M) genes of 35 A(H3N2) virus strains were amplified and sequenced. Predicted vaccine efficacy was measured using the Pepitope model. Phylogenetic analysis of the HA gene showed that all Cameroonian strains had evolved away from the 3C.1-A/Texas/50/2012-like clade. Globally, 2014 virus strains clustered with the 2015-2016 vaccine strain, 3C.3a-A/Switzerland/9715293/2013, whereas 2015 and 2016 virus strains clustered with the 2016-2017 vaccine strain, 3C.2a-A/HongKong/4801/2014. In order to determine the genotypic drug susceptibility to neuraminidase inhibitors and amantadine, the NA and M2 protein coding sequences were analyzed. There was no strain with characteristic mutation for resistance to neuraminidase inhibitors, per contra; all strains possessed the substitution S31N, peculiar of resistance to adamantanes. There was drift in influenza A(H3N2) dominant epitopes B (2014 and 2015) to epitopes A (2016) with a theoretical efficiency in vaccine ranging from low to moderate. The presence of several antigenic site mutations among H3N2 virus strains between 2014-2016 influenza seasons in Cameroon confirms the progressing evolution of circulating H3N2 strains.</p>
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            <availability status="restricted">              <licence target="http://creativecommons.org/licenses/by/">Attribution</licence>
            </availability>
          </publicationStmt>
          <seriesStmt>            <idno type="stamp" n="PASTEUR">Institut Pasteur</idno>
            <idno type="stamp" n="RIIP">Institut Pasteur RIIP (Réseau International)</idno>
            <idno type="stamp" n="RIIP_CAMEROUN" corresp="RIIP">Centre Pasteur du Cameroun</idno>
          </seriesStmt>
          <notesStmt>            <note type="audience" n="2">International</note>
            <note type="popular" n="0">No</note>
            <note type="peer" n="1">Yes</note>
          </notesStmt>
          <sourceDesc>            <biblStruct>              <analytic>                <title xml:lang="en">Genetic and antigenic characterization of influenza A(H3N2) in Cameroon during the 2014-2016 influenza seasons</title>
                <author role="aut">                  <persName>                    <forename type="first">Gwladys</forename>
                    <forename type="middle">C</forename>
                    <surname>Monamele</surname>
                  </persName>
                  <idno type="halauthorid">1695429</idno>
                  <affiliation ref="#struct-55917"></affiliation>
                  <affiliation ref="#struct-302471"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Marie-Astrid</forename>
                    <surname>Vernet</surname>
                  </persName>
                  <idno type="halauthorid">1695430</idno>
                  <affiliation ref="#struct-55917"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Mohammed</forename>
                    <forename type="middle">R</forename>
                    <surname>Njankouo</surname>
                  </persName>
                  <idno type="halauthorid">1695431</idno>
                  <affiliation ref="#struct-55917"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Kathleen</forename>
                    <surname>Victoir</surname>
                  </persName>
                  <idno type="halauthorid">709990</idno>
                  <affiliation ref="#struct-412971"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Jane</forename>
                    <forename type="middle">Francis</forename>
                    <surname>Akoachere</surname>
                  </persName>
                  <idno type="halauthorid">1695432</idno>
                  <affiliation ref="#struct-302471"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Damian</forename>
                    <surname>Anong</surname>
                  </persName>
                  <idno type="halauthorid">1695433</idno>
                  <affiliation ref="#struct-302471"></affiliation>
                </author>
                <author role="crp">                  <persName>                    <forename type="first">Richard</forename>
                    <surname>Njouom</surname>
                  </persName>
                  <email type="md5">ec8d6f20516c8f1fc929824f992ce55f</email>
                  <email type="domain">pasteur-yaounde.org</email>
                  <idno type="halauthorid">1695434</idno>
                  <affiliation ref="#struct-55917"></affiliation>
                </author>
              </analytic>
              <monogr>                <idno type="halJournalId" status="VALID">28700</idno>
                <idno type="issn">1932-6203</idno>
                <idno type="eissn">1932-6203</idno>
                <title level="j">PLoS ONE</title>
                <imprint>                  <publisher>Public Library of Science</publisher>
                  <biblScope unit="volume">12</biblScope>
                  <biblScope unit="issue">9</biblScope>
                  <biblScope unit="pp">e0184411</biblScope>
                  <date type="datePub">2017-09-06</date>
                </imprint>
              </monogr>
              <idno type="doi">10.1371/journal.pone.0184411</idno>
              <idno type="pubmed">28877235</idno>
              <idno type="pubmedcentral">PMC5587321</idno>
            </biblStruct>
          </sourceDesc>
          <profileDesc>            <langUsage>              <language ident="en">English</language>
            </langUsage>
            <textClass>              <keywords scheme="author">                <term xml:lang="en">Influenza</term>
                <term xml:lang="en">Vaccines</term>
                <term xml:lang="en">Influenza viruses</term>
                <term xml:lang="en">Viral vaccines</term>
                <term xml:lang="en">Antimicrobial resistance</term>
                <term xml:lang="en">DNA sequence analysis</term>
                <term xml:lang="en">Cameroon</term>
                <term xml:lang="en">Influenza A virus</term>
              </keywords>
              <classCode scheme="mesh">Cameroon</classCode>
              <classCode scheme="mesh">Epitopes</classCode>
              <classCode scheme="mesh">Phylogeny</classCode>
              <classCode scheme="mesh">RNA, Viral</classCode>
              <classCode scheme="mesh">Seasons</classCode>
              <classCode scheme="mesh">Evolution, Molecular</classCode>
              <classCode scheme="mesh">Glycosylation</classCode>
              <classCode scheme="mesh">Hemagglutinin Glycoproteins, Influenza Virus</classCode>
              <classCode scheme="mesh">Humans</classCode>
              <classCode scheme="mesh">Influenza A Virus, H3N2 Subtype</classCode>
              <classCode scheme="mesh">Influenza Vaccines</classCode>
              <classCode scheme="mesh">Influenza, Human</classCode>
              <classCode scheme="mesh">Mutation</classCode>
              <classCode scheme="halDomain" n="sdv.gen">Life Sciences [q-bio]/Genetics</classCode>
              <classCode scheme="halTypology" n="ART">Journal articles</classCode>
            </textClass>
            <abstract xml:lang="en">              <p>The first outbreak of influenza A(H3N2) occurred in 1968 and caused the third flu pandemic of the 20th century. It has affected multiple countries over time. The best strategy to reduce the burden of influenza is through vaccination whose efficacy varies with respect to the circulating strains. This study was performed to better understand the molecular evolution of influenza A(H3N2) and assess vaccine efficacy in Cameroon. Complete sequences of three gene segments were obtained from 2014 to 2016 influenza seasons in Cameroon. Hemagglutinin (HA), Neuraminidase (NA) and matrix (M) genes of 35 A(H3N2) virus strains were amplified and sequenced. Predicted vaccine efficacy was measured using the Pepitope model. Phylogenetic analysis of the HA gene showed that all Cameroonian strains had evolved away from the 3C.1-A/Texas/50/2012-like clade. Globally, 2014 virus strains clustered with the 2015-2016 vaccine strain, 3C.3a-A/Switzerland/9715293/2013, whereas 2015 and 2016 virus strains clustered with the 2016-2017 vaccine strain, 3C.2a-A/HongKong/4801/2014. In order to determine the genotypic drug susceptibility to neuraminidase inhibitors and amantadine, the NA and M2 protein coding sequences were analyzed. There was no strain with characteristic mutation for resistance to neuraminidase inhibitors, per contra; all strains possessed the substitution S31N, peculiar of resistance to adamantanes. There was drift in influenza A(H3N2) dominant epitopes B (2014 and 2015) to epitopes A (2016) with a theoretical efficiency in vaccine ranging from low to moderate. The presence of several antigenic site mutations among H3N2 virus strains between 2014-2016 influenza seasons in Cameroon confirms the progressing evolution of circulating H3N2 strains.</p>
            </abstract>
            <particDesc>              <org type="consortium">We are grateful to Yong Poovorawan and Nipaporn Tewawong for their helpful assistance in Pepitope calculation. We are also thankful to Matthieu Schoenhals for editing this manuscript</org>
            </particDesc>
          </profileDesc>
        </hal>
</record>

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Genetic and antigenic characterization of influenza A(H3N2) in Cameroon during the 2014-2016 influenza seasons

Genetic and antigenic characterization of influenza A(H3N2) in Cameroon during the 2014-2016 influenza seasons

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