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Virulence. 2011 Nov-Dec;2(6):542-6. doi: 10.4161/viru.2.6.17812. Epub 2011 Nov 1.

The influenza A virus protein PB1-F2: killing two birds with one stone?

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  • 1Department of Microbiology, Mount Sinai School of Medicine, New York, NY, USA.

Abstract

PB1-F2 is a 90 amino acid protein that is expressed from the +1 open reading frame in the PB1 gene of some influenza A viruses. The PB1-F2 protein has been shown to contribute to viral pathogenicity, but the molecular mechanisms for mediating virulence have been unclear. Previous reports demonstrate that PB1-F2 promotes cell death, causes immunopathology and increases pro-inflammatory responses. Our group has identified a single point mutation from asparagine (N) to serine (S) at position 66 in the PB1-F2 protein that dramatically increases the virulence of highly pathogenic avian H5N1 influenza viruses and of the 1918 pandemic strain. In search for the mechanism by which PB1-F2 N66S increases pathogenicity, we have identified and characterized a novel function of PB1-F2, i.e. interferon antagonism, both in vitro and in the mouse model. Here, we discuss a hypothesis for a possible molecular link between the pro-apoptotic and anti-interferon functions of PB1-F2.

PMID:
21971186
[PubMed - indexed for MEDLINE]
PMCID:
PMC3260547
Free PMC Article
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