Serveur d'exploration H2N2

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Genetic evolution of the neuraminidase of influenza A (H3N2) viruses from 1968 to 2009 and its correspondence to haemagglutinin evolution

Identifieur interne : 000776 ( Ncbi/Merge ); précédent : 000775; suivant : 000777

Genetic evolution of the neuraminidase of influenza A (H3N2) viruses from 1968 to 2009 and its correspondence to haemagglutinin evolution

Auteurs : Kim B. Westgeest [Pays-Bas] ; Miranda De Graaf [Pays-Bas, Royaume-Uni] ; Mathieu Fourment [Singapour] ; Theo M. Bestebroer [Pays-Bas] ; Ruud Van Beek [Pays-Bas] ; Monique I. J. Spronken [Pays-Bas] ; Jan C. De Jong [Pays-Bas] ; Guus F. Rimmelzwaan [Pays-Bas] ; Colin A. Russell [Royaume-Uni, États-Unis] ; Albert D. M. E. Osterhaus [Pays-Bas] ; Gavin J. D. Smith [Singapour] ; Derek J. Smith [Pays-Bas, Royaume-Uni, États-Unis] ; Ron A. M. Fouchier [Pays-Bas]

Source :

RBID : PMC:3542130

Abstract

Each year, influenza viruses cause epidemics by evading pre-existing humoral immunity through mutations in the major glycoproteins: the haemagglutinin (HA) and the neuraminidase (NA). In 2004, the antigenic evolution of HA of human influenza A (H3N2) viruses was mapped (Smith et al., Science305, 371–376, 2004) from its introduction in humans in 1968 until 2003. The current study focused on the genetic evolution of NA and compared it with HA using the dataset of Smith and colleagues, updated to the epidemic of the 2009/2010 season. Phylogenetic trees and genetic maps were constructed to visualize the genetic evolution of NA and HA. The results revealed multiple reassortment events over the years. Overall rates of evolutionary change were lower for NA than for HA1 at the nucleotide level. Selection pressures were estimated, revealing an abundance of negatively selected sites and sparse positively selected sites. The differences found between the evolution of NA and HA1 warrant further analysis of the evolution of NA at the phenotypic level, as has been done previously for HA.


Url:
DOI: 10.1099/vir.0.043059-0
PubMed: 22718569
PubMed Central: 3542130

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PMC:3542130

Le document en format XML

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<title xml:lang="en" level="a" type="main">Genetic evolution of the neuraminidase of influenza A (H3N2) viruses from 1968 to 2009 and its correspondence to haemagglutinin evolution</title>
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<name sortKey="Smith, Derek J" sort="Smith, Derek J" uniqKey="Smith D" first="Derek J." last="Smith">Derek J. Smith</name>
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<name sortKey="Fouchier, Ron A M" sort="Fouchier, Ron A M" uniqKey="Fouchier R" first="Ron A. M." last="Fouchier">Ron A. M. Fouchier</name>
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<title level="j">The Journal of General Virology</title>
<idno type="ISSN">0022-1317</idno>
<idno type="eISSN">1465-2099</idno>
<imprint>
<date when="2012">2012</date>
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<div type="abstract" xml:lang="en">
<p>Each year, influenza viruses cause epidemics by evading pre-existing humoral immunity through mutations in the major glycoproteins: the haemagglutinin (HA) and the neuraminidase (NA). In 2004, the antigenic evolution of HA of human influenza A (H3N2) viruses was mapped (Smith
<italic>et al.</italic>
,
<italic>Science</italic>
<bold>305</bold>
, 371–376, 2004) from its introduction in humans in 1968 until 2003. The current study focused on the genetic evolution of NA and compared it with HA using the dataset of Smith and colleagues, updated to the epidemic of the 2009/2010 season. Phylogenetic trees and genetic maps were constructed to visualize the genetic evolution of NA and HA. The results revealed multiple reassortment events over the years. Overall rates of evolutionary change were lower for NA than for HA1 at the nucleotide level. Selection pressures were estimated, revealing an abundance of negatively selected sites and sparse positively selected sites. The differences found between the evolution of NA and HA1 warrant further analysis of the evolution of NA at the phenotypic level, as has been done previously for HA.</p>
</div>
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<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">J Gen Virol</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Gen. Virol</journal-id>
<journal-id journal-id-type="publisher-id">JGV</journal-id>
<journal-id journal-id-type="hwp">vir</journal-id>
<journal-title-group>
<journal-title>The Journal of General Virology</journal-title>
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<issn pub-type="ppub">0022-1317</issn>
<issn pub-type="epub">1465-2099</issn>
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<publisher-name>Society for General Microbiology</publisher-name>
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<article-id pub-id-type="pmc">3542130</article-id>
<article-id pub-id-type="publisher-id">043059</article-id>
<article-id pub-id-type="doi">10.1099/vir.0.043059-0</article-id>
<article-categories>
<subj-group subj-group-type="article-type">
<subject>Standard</subject>
</subj-group>
<subj-group subj-group-type="heading">
<subject>Animal</subject>
<subj-group subj-group-type="heading">
<subject>RNA viruses</subject>
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<title-group>
<article-title>Genetic evolution of the neuraminidase of influenza A (H3N2) viruses from 1968 to 2009 and its correspondence to haemagglutinin evolution</article-title>
<alt-title alt-title-type="recto-page-foot">
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<alt-title alt-title-type="verso-running-head">K. B. Westgeest and others</alt-title>
<alt-title alt-title-type="recto-running-head">Evolution of human H3N2 virus NA</alt-title>
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<contrib contrib-type="author">
<name>
<surname>Westgeest</surname>
<given-names>Kim B.</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>de Graaf</surname>
<given-names>Miranda</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
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<name>
<surname>Fourment</surname>
<given-names>Mathieu</given-names>
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<sup>3</sup>
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<surname>Bestebroer</surname>
<given-names>Theo M.</given-names>
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<sup>1</sup>
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<contrib contrib-type="author">
<name>
<surname>van Beek</surname>
<given-names>Ruud</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Spronken</surname>
<given-names>Monique I. J.</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>de Jong</surname>
<given-names>Jan C.</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Rimmelzwaan</surname>
<given-names>Guus F.</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Russell</surname>
<given-names>Colin A.</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff4">
<sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Osterhaus</surname>
<given-names>Albert D. M. E.</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Smith</surname>
<given-names>Gavin J. D.</given-names>
</name>
<xref ref-type="aff" rid="aff3">
<sup>3</sup>
</xref>
</contrib>
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<name>
<surname>Smith</surname>
<given-names>Derek J.</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff4">
<sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author" corresp="yes">
<name>
<surname>Fouchier</surname>
<given-names>Ron A. M.</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
</contrib>
<aff id="aff1">
<label>1</label>
Department of Virology, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands</aff>
<aff id="aff2">
<label>2</label>
Department of Zoology, University of Cambridge, Cambridge CB2 3EJ, UK</aff>
<aff id="aff3">
<label>3</label>
Program in Emerging Infectious Diseases, Duke-NUS Graduate Medical School, 8 College Road, Singapore 169857, Singapore</aff>
<aff id="aff4">
<label>4</label>
Fogarty International Center, National Institutes of Health, Bethesda, MD 20892, USA</aff>
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<author-notes>
<corresp id="cor1">
<bold>Correspondence</bold>
Ron A. M. Fouchier
<email xlink:href="r.fouchier@erasmusmc.nl">r.fouchier@erasmusmc.nl</email>
</corresp>
<fn id="fn1" fn-type="other">
<p>The GenBank/EMBL/DDBJ accession numbers for the sequences determined in this study are available in the supplementary data.</p>
</fn>
</author-notes>
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<month>9</month>
<year>2012</year>
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<month>9</month>
<year>2013</year>
</pub-date>
<pmc-comment> PMC Release delay is 12 months and 0 days and was based on the . </pmc-comment>
<volume>93</volume>
<issue>Pt 9</issue>
<fpage>1996</fpage>
<lpage>2007</lpage>
<history>
<date date-type="received">
<day>23</day>
<month>3</month>
<year>2012</year>
</date>
<date date-type="accepted">
<day>15</day>
<month>6</month>
<year>2012</year>
</date>
</history>
<permissions>
<copyright-statement>© 2012 SGM</copyright-statement>
</permissions>
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<p>Each year, influenza viruses cause epidemics by evading pre-existing humoral immunity through mutations in the major glycoproteins: the haemagglutinin (HA) and the neuraminidase (NA). In 2004, the antigenic evolution of HA of human influenza A (H3N2) viruses was mapped (Smith
<italic>et al.</italic>
,
<italic>Science</italic>
<bold>305</bold>
, 371–376, 2004) from its introduction in humans in 1968 until 2003. The current study focused on the genetic evolution of NA and compared it with HA using the dataset of Smith and colleagues, updated to the epidemic of the 2009/2010 season. Phylogenetic trees and genetic maps were constructed to visualize the genetic evolution of NA and HA. The results revealed multiple reassortment events over the years. Overall rates of evolutionary change were lower for NA than for HA1 at the nucleotide level. Selection pressures were estimated, revealing an abundance of negatively selected sites and sparse positively selected sites. The differences found between the evolution of NA and HA1 warrant further analysis of the evolution of NA at the phenotypic level, as has been done previously for HA.</p>
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<list>
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<li>Royaume-Uni</li>
<li>Singapour</li>
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