Journal
JOURNAL OF VIROLOGY
Volume 82, Issue 22, Pages 11461-11466Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01071-08
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Funding
- EU [LSHMCT-2004-503359]
- Federal Government of Germany
- BMBF Zoonose
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During H5N1 influenza virus infection, proinflammatory cytokines are markedly elevated in the lungs of infected hosts. The significance of this dysregulated cytokine response in H5N1-mediated pathogenesis remains to be determined. To investigate the influence of hypercytokinemia, or cytokine storm, a transgenic mouse technology was used. The classical NF-kappa B pathway regulates the induction of most proinflammatory cytokines. Deletion of the p50 subunit leads to a markedly reduced expression of the NF-kappa B-regulated cytokines and chemokines. Here we show that H5N1 influenza virus infection of this transgenic mouse model resulted in a lack of hypercytokinemia but not in altered pathogenesis.
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