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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Naturally Occurring Swine Influenza A Virus PB1-F2 Phenotypes That Contribute to Superinfection with Gram-Positive Respiratory Pathogens</title><author><name sortKey="Weeks Gorospe, Jenni N" sort="Weeks Gorospe, Jenni N" uniqKey="Weeks Gorospe J" first="Jenni N." last="Weeks-Gorospe">Jenni N. Weeks-Gorospe</name><affiliation><nlm:aff id="aff1">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Hurtig, Heather R" sort="Hurtig, Heather R" uniqKey="Hurtig H" first="Heather R." last="Hurtig">Heather R. Hurtig</name><affiliation><nlm:aff id="aff2">Division of Basic Biomedical Sciences, University of South Dakota, Vermillion, South Dakota, USA</nlm:aff></affiliation></author><author><name sortKey="Iverson, Amy R" sort="Iverson, Amy R" uniqKey="Iverson A" first="Amy R." last="Iverson">Amy R. Iverson</name><affiliation><nlm:aff id="aff1">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Schuneman, Margaret J" sort="Schuneman, Margaret J" uniqKey="Schuneman M" first="Margaret J." last="Schuneman">Margaret J. Schuneman</name><affiliation><nlm:aff id="aff2">Division of Basic Biomedical Sciences, University of South Dakota, Vermillion, South Dakota, USA</nlm:aff></affiliation></author><author><name sortKey="Webby, Richard J" sort="Webby, Richard J" uniqKey="Webby R" first="Richard J." last="Webby">Richard J. Webby</name><affiliation><nlm:aff id="aff1">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Mccullers, Jonathan A" sort="Mccullers, Jonathan A" uniqKey="Mccullers J" first="Jonathan A." last="Mccullers">Jonathan A. Mccullers</name><affiliation><nlm:aff id="aff1">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Huber, Victor C" sort="Huber, Victor C" uniqKey="Huber V" first="Victor C." last="Huber">Victor C. Huber</name><affiliation><nlm:aff id="aff2">Division of Basic Biomedical Sciences, University of South Dakota, Vermillion, South Dakota, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22674997</idno><idno type="pmc">3416121</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3416121</idno><idno type="RBID">PMC:3416121</idno><idno type="doi">10.1128/JVI.00369-12</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">000651</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000651</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Naturally Occurring Swine Influenza A Virus PB1-F2 Phenotypes That Contribute to Superinfection with Gram-Positive Respiratory Pathogens</title><author><name sortKey="Weeks Gorospe, Jenni N" sort="Weeks Gorospe, Jenni N" uniqKey="Weeks Gorospe J" first="Jenni N." last="Weeks-Gorospe">Jenni N. Weeks-Gorospe</name><affiliation><nlm:aff id="aff1">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Hurtig, Heather R" sort="Hurtig, Heather R" uniqKey="Hurtig H" first="Heather R." last="Hurtig">Heather R. Hurtig</name><affiliation><nlm:aff id="aff2">Division of Basic Biomedical Sciences, University of South Dakota, Vermillion, South Dakota, USA</nlm:aff></affiliation></author><author><name sortKey="Iverson, Amy R" sort="Iverson, Amy R" uniqKey="Iverson A" first="Amy R." last="Iverson">Amy R. Iverson</name><affiliation><nlm:aff id="aff1">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Schuneman, Margaret J" sort="Schuneman, Margaret J" uniqKey="Schuneman M" first="Margaret J." last="Schuneman">Margaret J. Schuneman</name><affiliation><nlm:aff id="aff2">Division of Basic Biomedical Sciences, University of South Dakota, Vermillion, South Dakota, USA</nlm:aff></affiliation></author><author><name sortKey="Webby, Richard J" sort="Webby, Richard J" uniqKey="Webby R" first="Richard J." last="Webby">Richard J. Webby</name><affiliation><nlm:aff id="aff1">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Mccullers, Jonathan A" sort="Mccullers, Jonathan A" uniqKey="Mccullers J" first="Jonathan A." last="Mccullers">Jonathan A. Mccullers</name><affiliation><nlm:aff id="aff1">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Huber, Victor C" sort="Huber, Victor C" uniqKey="Huber V" first="Victor C." last="Huber">Victor C. Huber</name><affiliation><nlm:aff id="aff2">Division of Basic Biomedical Sciences, University of South Dakota, Vermillion, South Dakota, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Virology</title><idno type="ISSN">0022-538X</idno><idno type="eISSN">1098-5514</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>A combination of viral, bacterial, and host factors contributes to the severity and overall mortality associated with influenza virus-bacterium superinfections. To date, the virulence associated with the recently identified influenza virus protein PB1-F2 has been largely defined using models of primary influenza virus infection, with only limited assessment in models of <named-content content-type="genus-species">Streptococcus pneumoniae</named-content> superinfection. Specifically, these studies have incorporated isogenic viruses that differ in the PB1-F2 expressed, but there is still knowledge to be gained from evaluation of natural variants derived from a nonhuman host species (swine). Using this rationale, we developed the hypothesis that naturally occurring viruses expressing variants of genes, like the PB1-F2 gene, can be associated with the severity of secondary bacterial infections. To test this hypothesis, we selected viruses expressing variants in PB1-F2 and evaluated outcomes from superinfection with three distinct Gram-positive respiratory pathogens: <named-content content-type="genus-species">Streptococcus pneumoniae</named-content>, <named-content content-type="genus-species">Staphylococcus aureus</named-content>, and <named-content content-type="genus-species">Streptococcus pyogenes</named-content>. Our results demonstrate that the amino acid residues 62L, 66S, 75R, 79R, and 82L, previously proposed as molecular signatures of PB1-F2 virulence for influenza viruses in the setting of bacterial superinfection, are broadly associated with enhanced pathogenicity in swine in a bacterium-specific manner. Furthermore, truncated PB1-F2 proteins can preferentially increase mortality when associated with <named-content content-type="genus-species">Streptococcus pyogenes</named-content> superinfection. These findings support efforts to increase influenza virus surveillance to consider viral genotypes that could be used to predict increased severity of superinfections with specific Gram-positive respiratory pathogens.</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>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Virol</journal-id><journal-id journal-id-type="iso-abbrev">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">22674997</article-id><article-id pub-id-type="pmc">3416121</article-id><article-id pub-id-type="publisher-id">00369-12</article-id><article-id pub-id-type="doi">10.1128/JVI.00369-12</article-id><article-categories><subj-group subj-group-type="heading"><subject>Pathogenesis and Immunity</subject></subj-group></article-categories><title-group><article-title>Naturally Occurring Swine Influenza A Virus PB1-F2 Phenotypes That Contribute to Superinfection with Gram-Positive Respiratory Pathogens</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Weeks-Gorospe</surname><given-names>Jenni N.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Hurtig</surname><given-names>Heather R.</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Iverson</surname><given-names>Amy R.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Schuneman</surname><given-names>Margaret J.</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Webby</surname><given-names>Richard J.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>McCullers</surname><given-names>Jonathan A.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Huber</surname><given-names>Victor C.</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><aff id="aff1"><label>a</label>Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</aff><aff id="aff2"><label>b</label>Division of Basic Biomedical Sciences, University of South Dakota, Vermillion, South Dakota, USA</aff></contrib-group><author-notes><corresp>Address correspondence to Victor C. Huber, <email>victor.huber@usd.edu</email>.</corresp></author-notes><pub-date pub-type="ppub"><month>9</month><year>2012</year></pub-date><volume>86</volume><issue>17</issue><fpage>9035</fpage><lpage>9043</lpage><history><date date-type="received"><day>13</day><month>2</month><year>2012</year></date><date date-type="accepted"><day>30</day><month>5</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="zjv01712009035.pdf"></self-uri><abstract><p>A combination of viral, bacterial, and host factors contributes to the severity and overall mortality associated with influenza virus-bacterium superinfections. To date, the virulence associated with the recently identified influenza virus protein PB1-F2 has been largely defined using models of primary influenza virus infection, with only limited assessment in models of <named-content content-type="genus-species">Streptococcus pneumoniae</named-content> superinfection. Specifically, these studies have incorporated isogenic viruses that differ in the PB1-F2 expressed, but there is still knowledge to be gained from evaluation of natural variants derived from a nonhuman host species (swine). Using this rationale, we developed the hypothesis that naturally occurring viruses expressing variants of genes, like the PB1-F2 gene, can be associated with the severity of secondary bacterial infections. To test this hypothesis, we selected viruses expressing variants in PB1-F2 and evaluated outcomes from superinfection with three distinct Gram-positive respiratory pathogens: <named-content content-type="genus-species">Streptococcus pneumoniae</named-content>, <named-content content-type="genus-species">Staphylococcus aureus</named-content>, and <named-content content-type="genus-species">Streptococcus pyogenes</named-content>. Our results demonstrate that the amino acid residues 62L, 66S, 75R, 79R, and 82L, previously proposed as molecular signatures of PB1-F2 virulence for influenza viruses in the setting of bacterial superinfection, are broadly associated with enhanced pathogenicity in swine in a bacterium-specific manner. Furthermore, truncated PB1-F2 proteins can preferentially increase mortality when associated with <named-content content-type="genus-species">Streptococcus pyogenes</named-content> superinfection. These findings support efforts to increase influenza virus surveillance to consider viral genotypes that could be used to predict increased severity of superinfections with specific Gram-positive respiratory pathogens.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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