tetano
Editor, Senior Moderator
J Virol. 2012 Jan 25. [Epub ahead of print]
Deletions in the neuraminidase stalk region of H2N2 and H9N2 avian influenza subtypes do not affect post-influenza secondary bacterial pneumonia.
Chockalingam AK, Hickman D, Pena L, Ye J, Ferrero A, Echenique JR, Chen H, Sutton T, Perez DR.
Source
Department of Veterinary Medicine, University of Maryland, College Park. 8075 Greenmead Drive, College Park, MD 20742, USA.
Abstract
We investigated the synergism between influenza and Streptococcus pneumoniae (Sp), 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 in adherence of Sp on virus-infected human alveolar epithelial (A549) and mouse lung adenoma (LA-4) cells, although it delayed virus elution from turkey red blood cells. Sequential Sp infection of mice previously inoculated with isogenic recombinant influenza H2N2 and H9N2 viruses displayed severe pneumonia, elevated levels of intrapulmonary pro-inflammatory responses and death. No differences between wt and ΔNA viruses were detected with respect to effects in post-influenza pneumococcal pneumonia as measured by bacterial growth, lung inflammation, morbidity, mortality, and cytokine/chemokine concentrations. Differences were observed, however, in influenza-infected mice that were treated with oseltamivir prior to challenge with Sp. Under these circumstances, mice infected with ΔNA viruses were associated with better prognosis following secondary bacterial challenge. These data suggest that the H2N2 and H9N2 subtype 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.
PMID:
22278240
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22278240
Deletions in the neuraminidase stalk region of H2N2 and H9N2 avian influenza subtypes do not affect post-influenza secondary bacterial pneumonia.
Chockalingam AK, Hickman D, Pena L, Ye J, Ferrero A, Echenique JR, Chen H, Sutton T, Perez DR.
Source
Department of Veterinary Medicine, University of Maryland, College Park. 8075 Greenmead Drive, College Park, MD 20742, USA.
Abstract
We investigated the synergism between influenza and Streptococcus pneumoniae (Sp), 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 in adherence of Sp on virus-infected human alveolar epithelial (A549) and mouse lung adenoma (LA-4) cells, although it delayed virus elution from turkey red blood cells. Sequential Sp infection of mice previously inoculated with isogenic recombinant influenza H2N2 and H9N2 viruses displayed severe pneumonia, elevated levels of intrapulmonary pro-inflammatory responses and death. No differences between wt and ΔNA viruses were detected with respect to effects in post-influenza pneumococcal pneumonia as measured by bacterial growth, lung inflammation, morbidity, mortality, and cytokine/chemokine concentrations. Differences were observed, however, in influenza-infected mice that were treated with oseltamivir prior to challenge with Sp. Under these circumstances, mice infected with ΔNA viruses were associated with better prognosis following secondary bacterial challenge. These data suggest that the H2N2 and H9N2 subtype 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.
PMID:
22278240
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22278240