Recent work has demonstrated that the PI3K (phosphoinositide 3-kinase) signalling pathway is important for efficient influenza A virus replication. Activation of PI3K in virus-infected cells is mediated by the viral NS1 protein, which binds directly to the p85β regulatory subunit of PI3K and causes the PI3K-dependent phosphorylation of Akt (protein kinase B). Given that recombinant influenza A viruses unable to activate PI3K signalling are attenuated in tissue culture, the PI3K pathway could be a novel target for the development of future anti-influenza drugs.
Keywords:Akt, antiviral drug, influenza A virus, NS1 protein, phosphoinositide 3-kinase (PI3K), p85
© 2007 The Biochemical Society