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J. Virol. doi:10.1128/JVI.01071-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Role of hypercytokinemia in NF-B p50 deficient mice after H5N1 influenza A virus infection

Friedrich-Loeffler-Institut, Institute of Immunology, Paul-Ehrlich Str. 28, D-72076 Tübingen, Germany

^* To whom correspondence should be addressed. Email: oliver.planz{at}fli.bund.de.

	Abstract

During H5N1 influenza virus infection pro-inflammatory 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-kappaB pathway regulates the induction of most pro-inflammatory cytokines. Deletion of the p50 subunit leads to a markedly reduced expression of the NF-kappaB 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.