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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">A Novel Cytotoxic Sequence Contributes to Influenza A Viral Protein PB1-F2 Pathogenicity and Predisposition to Secondary Bacterial Infection</title><author><name sortKey="Alymova, Irina V" sort="Alymova, Irina V" uniqKey="Alymova I" first="Irina V." last="Alymova">Irina V. Alymova</name><affiliation><nlm:aff id="aff1">Influenza Division, National Center for Immunization & Respiratory Diseases, Centers for Disease Control & Prevention, Atlanta, Georgia, USA</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Samarasinghe, Amali" sort="Samarasinghe, Amali" uniqKey="Samarasinghe A" first="Amali" last="Samarasinghe">Amali Samarasinghe</name><affiliation><nlm:aff id="aff5">Department of Pediatrics, University of Tennessee Health Sciences Center, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Vogel, Peter" sort="Vogel, Peter" uniqKey="Vogel P" first="Peter" last="Vogel">Peter Vogel</name><affiliation><nlm:aff id="aff3">Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Green, Amanda M" sort="Green, Amanda M" uniqKey="Green A" first="Amanda M." last="Green">Amanda M. Green</name><affiliation><nlm:aff id="aff2">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Weinlich, Ricardo" sort="Weinlich, Ricardo" uniqKey="Weinlich R" first="Ricardo" last="Weinlich">Ricardo Weinlich</name><affiliation><nlm:aff id="aff4">Department of Immunology, 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="aff2">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation><affiliation><nlm:aff id="aff5">Department of Pediatrics, University of Tennessee Health Sciences Center, Memphis, Tennessee, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24173220</idno><idno type="pmc">3911746</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3911746</idno><idno type="RBID">PMC:3911746</idno><idno type="doi">10.1128/JVI.01373-13</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000675</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000675</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">A Novel Cytotoxic Sequence Contributes to Influenza A Viral Protein PB1-F2 Pathogenicity and Predisposition to Secondary Bacterial Infection</title><author><name sortKey="Alymova, Irina V" sort="Alymova, Irina V" uniqKey="Alymova I" first="Irina V." last="Alymova">Irina V. Alymova</name><affiliation><nlm:aff id="aff1">Influenza Division, National Center for Immunization & Respiratory Diseases, Centers for Disease Control & Prevention, Atlanta, Georgia, USA</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Samarasinghe, Amali" sort="Samarasinghe, Amali" uniqKey="Samarasinghe A" first="Amali" last="Samarasinghe">Amali Samarasinghe</name><affiliation><nlm:aff id="aff5">Department of Pediatrics, University of Tennessee Health Sciences Center, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Vogel, Peter" sort="Vogel, Peter" uniqKey="Vogel P" first="Peter" last="Vogel">Peter Vogel</name><affiliation><nlm:aff id="aff3">Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Green, Amanda M" sort="Green, Amanda M" uniqKey="Green A" first="Amanda M." last="Green">Amanda M. Green</name><affiliation><nlm:aff id="aff2">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Weinlich, Ricardo" sort="Weinlich, Ricardo" uniqKey="Weinlich R" first="Ricardo" last="Weinlich">Ricardo Weinlich</name><affiliation><nlm:aff id="aff4">Department of Immunology, 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="aff2">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</nlm:aff></affiliation><affiliation><nlm:aff id="aff5">Department of Pediatrics, University of Tennessee Health Sciences Center, Memphis, Tennessee, 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="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Enhancement of cell death is a distinguishing feature of H1N1 influenza virus A/Puerto Rico/8/34 protein PB1-F2. Comparing the sequences (amino acids [aa] 61 to 87 using PB1-F2 amino acid numbering) of the PB1-F2-derived C-terminal peptides from influenza A viruses inducing high or low levels of cell death, we identified a unique I68, L69, and V70 motif in A/Puerto Rico/8/34 PB1-F2 responsible for promotion of the peptide's cytotoxicity and permeabilization of the mitochondrial membrane. When administered to mice, a 27-mer PB1-F2-derived C-terminal peptide with this amino acid motif caused significantly greater weight loss and pulmonary inflammation than the peptide without it (due to I68T, L69Q, and V70G mutations). Similar to the wild-type peptide, A/Puerto Rico/8/34 elicited significantly higher levels of macrophages, neutrophils, and cytokines in the bronchoalveolar lavage fluid of mice than its mutant counterpart 7 days after infection. Additionally, infection of mice with A/Puerto Rico/8/34 significantly enhanced the levels of morphologically transformed epithelial and immune mononuclear cells recruited in the airways compared with the mutant virus. In the mouse bacterial superinfection model, both peptide and virus with the I68, L69, and V70 sequence accelerated development of pneumococcal pneumonia, as reflected by increased levels of viral and bacterial lung titers and by greater mortality. Here we provide evidence suggesting that the newly identified cytotoxic sequence I68, L69, and V70 of A/Puerto Rico/8/34 PB1-F2 contributes to the pathogenesis of both primary viral and secondary bacterial infections.</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">24173220</article-id><article-id pub-id-type="pmc">3911746</article-id><article-id pub-id-type="publisher-id">01373-13</article-id><article-id pub-id-type="doi">10.1128/JVI.01373-13</article-id><article-categories><subj-group subj-group-type="heading"><subject>Pathogenesis and Immunity</subject></subj-group></article-categories><title-group><article-title>A Novel Cytotoxic Sequence Contributes to Influenza A Viral Protein PB1-F2 Pathogenicity and Predisposition to Secondary Bacterial Infection</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Alymova</surname><given-names>Irina V.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Samarasinghe</surname><given-names>Amali</given-names></name><xref ref-type="aff" rid="aff5"><sup>e</sup></xref></contrib><contrib contrib-type="author"><name><surname>Vogel</surname><given-names>Peter</given-names></name><xref ref-type="aff" rid="aff3"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Green</surname><given-names>Amanda M.</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Weinlich</surname><given-names>Ricardo</given-names></name><xref ref-type="aff" rid="aff4"><sup>d</sup></xref></contrib><contrib contrib-type="author"><name><surname>McCullers</surname><given-names>Jonathan A.</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref><xref ref-type="aff" rid="aff5"><sup>e</sup></xref></contrib><aff id="aff1"><label>a</label>Influenza Division, National Center for Immunization & Respiratory Diseases, Centers for Disease Control & Prevention, Atlanta, Georgia, USA</aff><aff id="aff2"><label>b</label>Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</aff><aff id="aff3"><label>c</label>Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</aff><aff id="aff4"><label>d</label>Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA</aff><aff id="aff5"><label>e</label>Department of Pediatrics, University of Tennessee Health Sciences Center, Memphis, Tennessee, USA</aff></contrib-group><author-notes><corresp id="cor1">Address correspondence to Irina V. Alymova, <email>ialymova@cdc.gov</email>.</corresp></author-notes><pub-date pub-type="ppub"><month>1</month><year>2014</year></pub-date><volume>88</volume><issue>1</issue><fpage>503</fpage><lpage>515</lpage><history><date date-type="received"><day>22</day><month>5</month><year>2013</year></date><date date-type="accepted"><day>3</day><month>10</month><year>2013</year></date></history><permissions><copyright-statement>Copyright © 2014, American Society for Microbiology. All Rights Reserved.</copyright-statement><copyright-year>2014</copyright-year><copyright-holder>American Society for Microbiology</copyright-holder></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zjv00114000503.pdf"></self-uri><abstract><p>Enhancement of cell death is a distinguishing feature of H1N1 influenza virus A/Puerto Rico/8/34 protein PB1-F2. Comparing the sequences (amino acids [aa] 61 to 87 using PB1-F2 amino acid numbering) of the PB1-F2-derived C-terminal peptides from influenza A viruses inducing high or low levels of cell death, we identified a unique I68, L69, and V70 motif in A/Puerto Rico/8/34 PB1-F2 responsible for promotion of the peptide's cytotoxicity and permeabilization of the mitochondrial membrane. When administered to mice, a 27-mer PB1-F2-derived C-terminal peptide with this amino acid motif caused significantly greater weight loss and pulmonary inflammation than the peptide without it (due to I68T, L69Q, and V70G mutations). Similar to the wild-type peptide, A/Puerto Rico/8/34 elicited significantly higher levels of macrophages, neutrophils, and cytokines in the bronchoalveolar lavage fluid of mice than its mutant counterpart 7 days after infection. Additionally, infection of mice with A/Puerto Rico/8/34 significantly enhanced the levels of morphologically transformed epithelial and immune mononuclear cells recruited in the airways compared with the mutant virus. In the mouse bacterial superinfection model, both peptide and virus with the I68, L69, and V70 sequence accelerated development of pneumococcal pneumonia, as reflected by increased levels of viral and bacterial lung titers and by greater mortality. Here we provide evidence suggesting that the newly identified cytotoxic sequence I68, L69, and V70 of A/Puerto Rico/8/34 PB1-F2 contributes to the pathogenesis of both primary viral and secondary bacterial infections.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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