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Deletions in the Neuraminidase Stalk Region of H2N2 and H9N2 Avian Influenza Virus Subtypes Do Not Affect Postinfluenza Secondary Bacterial Pneumonia
Author(s) -
Ashok Chockalingam,
Danielle Hickman,
Lindomar Pena,
Jianqiang Ye,
Andrea Ferrero,
José Echenique,
Hongjun Chen,
Troy C. Sutton,
Daniel R. Pérez
Publication year - 2012
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.05809-11
Subject(s) - neuraminidase , biology , streptococcus pneumoniae , virology , influenza a virus , virus , microbiology and biotechnology , neuraminidase inhibitor , proinflammatory cytokine , chemokine , pneumonia , context (archaeology) , stalk , immunology , inflammation , covid-19 , antibiotics , medicine , pathology , paleontology , disease , infectious disease (medical specialty) , horticulture
We investigated the synergism between influenza virus andStreptococcus pneumoniae , 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 ofS. pneumoniae to virus-infected human alveolar epithelial (A549) and mouse lung adenoma (LA-4) cells, although it delayed virus elution from turkey red blood cells. SequentialS. pneumoniae 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 withS. pneumoniae . 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.

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