{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T22:31:16Z","timestamp":1778797876246,"version":"3.51.4"},"reference-count":38,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2012,4,1]],"date-time":"2012-04-01T00:00:00Z","timestamp":1333238400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2012,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            We investigated the synergism between influenza virus and\n            <jats:named-content content-type=\"genus-species\">Streptococcus pneumoniae<\/jats:named-content>\n            , 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 (\u0394NA) had no effect on NA activity or on the adherence of\n            <jats:named-content content-type=\"genus-species\">S. pneumoniae<\/jats:named-content>\n            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\n            <jats:named-content content-type=\"genus-species\">S. pneumoniae<\/jats:named-content>\n            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 \u0394NA 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\n            <jats:named-content content-type=\"genus-species\">S. pneumoniae<\/jats:named-content>\n            . Under these circumstances, mice infected with \u0394NA 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.\n          <\/jats:p>","DOI":"10.1128\/jvi.05809-11","type":"journal-article","created":{"date-parts":[[2012,1,26]],"date-time":"2012-01-26T09:15:55Z","timestamp":1327569355000},"page":"3564-3573","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":21,"title":["Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia"],"prefix":"10.1128","volume":"86","author":[{"given":"Ashok K.","family":"Chockalingam","sequence":"first","affiliation":[{"name":"Department of Veterinary Medicine, University of Maryland, College Park, Maryland, 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