Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia
Identifieur interne : 000645 ( Pmc/Curation ); précédent : 000644; suivant : 000646Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia
Auteurs : Ashok K. Chockalingam [États-Unis] ; Danielle Hickman [États-Unis] ; Lindomar Pena [États-Unis] ; Jianqiang Ye [États-Unis] ; Andrea Ferrero [États-Unis] ; Jose R. Echenique [Argentine] ; Hongjun Chen [États-Unis] ; Troy Sutton [États-Unis] ; Daniel R. Perez [États-Unis]Source :
- Journal of Virology [ 0022-538X ] ; 2012.
Abstract
We investigated the synergism between influenza virus and
Url:
DOI: 10.1128/JVI.05809-11
PubMed: 22278240
PubMed Central: 3302490
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia</title>
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<author><name sortKey="Chen, Hongjun" sort="Chen, Hongjun" uniqKey="Chen H" first="Hongjun" last="Chen">Hongjun Chen</name>
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<author><name sortKey="Sutton, Troy" sort="Sutton, Troy" uniqKey="Sutton T" first="Troy" last="Sutton">Troy Sutton</name>
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<author><name sortKey="Perez, Daniel R" sort="Perez, Daniel R" uniqKey="Perez D" first="Daniel R." last="Perez">Daniel R. Perez</name>
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<series><title level="j">Journal of Virology</title>
<idno type="ISSN">0022-538X</idno>
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<front><div type="abstract" xml:lang="en"><p>We investigated the synergism between influenza virus and <named-content content-type="genus-species">Streptococcus pneumoniae</named-content>
, particularly the role of deletions in the stalk region of the neuraminidase (NA) of H2N2 and H9N2 avian influenza viruses. Deletions in the NA stalk (ΔNA) had no effect on NA activity or on the adherence of <named-content content-type="genus-species">S. pneumoniae</named-content>
to virus-infected human alveolar epithelial (A549) and mouse lung adenoma (LA-4) cells, although it delayed virus elution from turkey red blood cells. Sequential <named-content content-type="genus-species">S. pneumoniae</named-content>
infection of mice previously inoculated with isogenic recombinant H2N2 and H9N2 influenza viruses displayed severe pneumonia, elevated levels of intrapulmonary proinflammatory responses, and death. No differences between the WT and ΔNA mutant viruses were detected with respect to effects on postinfluenza pneumococcal pneumonia as measured by bacterial growth, lung inflammation, morbidity, mortality, and cytokine/chemokine concentrations. Differences were observed, however, in influenza virus-infected mice that were treated with oseltamivir prior to a challenge with <named-content content-type="genus-species">S. pneumoniae</named-content>
. Under these circumstances, mice infected with ΔNA viruses were associated with a better prognosis following a secondary bacterial challenge. These data suggest that the H2N2 and H9N2 subtypes of avian influenza A viruses can contribute to secondary bacterial pneumonia and deletions in the NA stalk may modulate its outcome in the context of antiviral therapy.</p>
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<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="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">22278240</article-id>
<article-id pub-id-type="pmc">3302490</article-id>
<article-id pub-id-type="publisher-id">05809-11</article-id>
<article-id pub-id-type="doi">10.1128/JVI.05809-11</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Pathogenesis and Immunity</subject>
</subj-group>
</article-categories>
<title-group><article-title>Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Chockalingam</surname>
<given-names>Ashok K.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Hickman</surname>
<given-names>Danielle</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Pena</surname>
<given-names>Lindomar</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ye</surname>
<given-names>Jianqiang</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ferrero</surname>
<given-names>Andrea</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Echenique</surname>
<given-names>Jose R.</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>b</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chen</surname>
<given-names>Hongjun</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Sutton</surname>
<given-names>Troy</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Perez</surname>
<given-names>Daniel R.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<aff id="aff1"><label>a</label>
Department of Veterinary Medicine, University of Maryland, College Park, Maryland, USA</aff>
<aff id="aff2"><label>b</label>
Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Ciudad Universitaria, Córdoba, Argentina</aff>
</contrib-group>
<author-notes><corresp>Address correspondence to Daniel R. Perez, <email>dperez1@umd.edu</email>
.</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>4</month>
<year>2012</year>
</pub-date>
<volume>86</volume>
<issue>7</issue>
<fpage>3564</fpage>
<lpage>3573</lpage>
<history><date date-type="received"><day>27</day>
<month>7</month>
<year>2011</year>
</date>
<date date-type="accepted"><day>6</day>
<month>1</month>
<year>2012</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2012, American Society for Microbiology. All Rights Reserved.</copyright-statement>
<copyright-year>2012</copyright-year>
<copyright-holder>American Society for Microbiology</copyright-holder>
</permissions>
<self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zjv00712003564.pdf"></self-uri>
<abstract><p>We investigated the synergism between influenza virus and <named-content content-type="genus-species">Streptococcus pneumoniae</named-content>
, particularly the role of deletions in the stalk region of the neuraminidase (NA) of H2N2 and H9N2 avian influenza viruses. Deletions in the NA stalk (ΔNA) had no effect on NA activity or on the adherence of <named-content content-type="genus-species">S. pneumoniae</named-content>
to virus-infected human alveolar epithelial (A549) and mouse lung adenoma (LA-4) cells, although it delayed virus elution from turkey red blood cells. Sequential <named-content content-type="genus-species">S. pneumoniae</named-content>
infection of mice previously inoculated with isogenic recombinant H2N2 and H9N2 influenza viruses displayed severe pneumonia, elevated levels of intrapulmonary proinflammatory responses, and death. No differences between the WT and ΔNA mutant viruses were detected with respect to effects on postinfluenza pneumococcal pneumonia as measured by bacterial growth, lung inflammation, morbidity, mortality, and cytokine/chemokine concentrations. Differences were observed, however, in influenza virus-infected mice that were treated with oseltamivir prior to a challenge with <named-content content-type="genus-species">S. pneumoniae</named-content>
. Under these circumstances, mice infected with ΔNA viruses were associated with a better prognosis following a secondary bacterial challenge. These data suggest that the H2N2 and H9N2 subtypes of avian influenza A viruses can contribute to secondary bacterial pneumonia and deletions in the NA stalk may modulate its outcome in the context of antiviral therapy.</p>
</abstract>
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</front>
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