A new player in a deadly game: influenza viruses and the PI3K/Akt signalling pathway
Version of Record online: 12 MAR 2009
© 2009 Blackwell Publishing Ltd
Volume 11, Issue 6, pages 863–871, June 2009
How to Cite
Ehrhardt, C. and Ludwig, S. (2009), A new player in a deadly game: influenza viruses and the PI3K/Akt signalling pathway. Cellular Microbiology, 11: 863–871. doi: 10.1111/j.1462-5822.2009.01309.x
- Issue online: 5 MAY 2009
- Version of Record online: 12 MAR 2009
- Received 11 January, 2009; revised 26 February, 2009; accepted 26 February, 2009.
Upon influenza A virus infection of cells, a wide variety of antiviral and virus-supportive signalling pathways are induced. Phosphatidylinositol-3-kinase (PI3K) is a recent addition to the growing list of signalling mediators that are activated by these viruses. Several studies have addressed the role of PI3K and the downstream effector protein kinase Akt in influenza A virus-infected cells. PI3K/Akt signalling is activated by diverse mechanisms in a biphasic manner and is required for multiple functions during infection. While the kinase supports activation of the interferon regulatory factor-3 during antiviral interferon induction, it also exhibits virus supportive functions. In fact, PI3K not only regulates a very early step during viral entry but also results in suppression of premature apoptosis at later stages of infection. The latter function is dependent on the expression of the viral non-structural protein-1 (A/NS1). It has been shown that PI3K activation occurs by direct interaction of A/NS1 with the p85 regulatory subunit and interaction sites of A/NS1 and p85 have now been mapped in detail. Here, we summarize the current knowledge on influenza virus-induced PI3K signalling and how this pathway supports viral propagation.