The influenza virus neuraminidase contributes to secondary bacterial pneumonia
Identifieur interne : 000533 ( Pmc/Corpus ); précédent : 000532; suivant : 000534The influenza virus neuraminidase contributes to secondary bacterial pneumonia
Auteurs : Ville T. Peltola ; K. Gopal Murti ; Jonathan A. MccullersSource :
- The Journal of infectious diseases [ 0022-1899 ] ; 2005.
Abstract
Secondary bacterial pneumonia is a common cause of death during influenza epidemics. We hypothesized that virus-specific factors could contribute to differences in annual excess mortality. A set of recombinant viruses with neuraminidases from representative influenza virus strains from the last 50 years was created and characterized. Their specific neuraminidase activities correlated with their ability to support secondary bacterial infections. Recombinant viruses with the 1957 and 1997 neuraminidases had the highest activities, while a virus with the 1968 neuraminidase had the lowest activity. The high activity of the 1957 neuraminidase, when compared to other neuraminidases, more strongly supported bacterial adherence in vitro and secondary pneumococcal pneumonia in a mouse model. These data lend support to our hypothesis that the neuraminidase of influenza viruses contributes to secondary bacterial infections and subsequent excess mortality.
Url:
DOI: 10.1086/430954
PubMed: 15962219
PubMed Central: 2715995
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<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">0413675</journal-id><journal-id journal-id-type="pubmed-jr-id">4830</journal-id><journal-id journal-id-type="nlm-ta">J Infect Dis</journal-id><journal-title>The Journal of infectious diseases</journal-title><issn pub-type="ppub">0022-1899</issn><issn pub-type="epub">1537-6613</issn></journal-meta><article-meta><article-id pub-id-type="pmid">15962219</article-id><article-id pub-id-type="pmc">2715995</article-id><article-id pub-id-type="doi">10.1086/430954</article-id><article-id pub-id-type="manuscript">NIHMS126352</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>The influenza virus neuraminidase contributes to secondary bacterial pneumonia</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Peltola</surname><given-names>Ville T.</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Murti</surname><given-names>K. Gopal</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>McCullers</surname><given-names>Jonathan A.</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib></contrib-group><aff id="A1"><label>1</label>Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, USA</aff><aff id="A2"><label>2</label>Department of Molecular Biotechnology, St. Jude Children's Research Hospital, Memphis, TN, USA</aff><author-notes><fn fn-type="present-address" id="FN1"><p id="P1">Present address of Dr. Peltola: Department of Pediatrics, Turku University Hospital, PL52, 20521 Turku, Finland.</p></fn><corresp id="CR1">Corresponding author: Jon McCullers Department of Infectious Diseases St. Jude Children's Research Hospital 332 N. Lauderdale St., Memphis, TN 38105−2794 (901) 495−5164 FAX: (901) 495−3099 <email>jon.mccullers@stjude.org</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>23</day><month>6</month><year>2009</year></pub-date><pub-date pub-type="epub"><day>8</day><month>6</month><year>2005</year></pub-date><pub-date pub-type="ppub"><day>15</day><month>7</month><year>2005</year></pub-date><pub-date pub-type="pmc-release"><day>27</day><month>7</month><year>2009</year></pub-date><volume>192</volume><issue>2</issue><fpage>249</fpage><lpage>257</lpage><abstract><p id="P2">Secondary bacterial pneumonia is a common cause of death during influenza epidemics. We hypothesized that virus-specific factors could contribute to differences in annual excess mortality. A set of recombinant viruses with neuraminidases from representative influenza virus strains from the last 50 years was created and characterized. Their specific neuraminidase activities correlated with their ability to support secondary bacterial infections. Recombinant viruses with the 1957 and 1997 neuraminidases had the highest activities, while a virus with the 1968 neuraminidase had the lowest activity. The high activity of the 1957 neuraminidase, when compared to other neuraminidases, more strongly supported bacterial adherence in vitro and secondary pneumococcal pneumonia in a mouse model. These data lend support to our hypothesis that the neuraminidase of influenza viruses contributes to secondary bacterial infections and subsequent excess mortality.</p></abstract><kwd-group><kwd>influenza virus</kwd><kwd>Streptococcus pneumoniae</kwd><kwd>pneumococcus</kwd><kwd>pneumonia</kwd><kwd>mouse model</kwd><kwd>neuraminidase</kwd><kwd>pandemic</kwd><kwd>synergism</kwd></kwd-group><contract-num rid="AI1">R01 AI066349-01</contract-num><contract-sponsor id="AI1">National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID</contract-sponsor></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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