title: PI3K signalling during influenza A virus infections.
abstract: 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 p85beta 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.
authors: Centre for Biomolecular Sciences, University of St Andrews, St Andrews, Fife, UK. bgh1@st-andrews.ac.uk
authors: B G
authors: BG
authors: Hale
authors: R E
authors: RE
authors: Randall
mesh_terms: D000998:Antiviral Agents; D004196:Disease Outbreaks; D004789:Enzyme Activation; D006801:Humans; D009980:Influenza A virus / Q000502:physiology*; D007251:Influenza, Human / Q000453:epidemiology / Q000503:physiopathology*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D015398:Signal Transduction; D017361:Viral Nonstructural Proteins / Q000502:physiology*; D014779:Virus Replication
chemical_list: D000998:Antiviral Agents; C085820:INS1 protein, influenza virus; D017361:Viral Nonstructural Proteins; D019869:Phosphatidylinositol 3-Kinases