Journal
CELLULAR MICROBIOLOGY
Volume 11, Issue 6, Pages 863-871Publisher
WILEY
DOI: 10.1111/j.1462-5822.2009.01309.x
Keywords
-
Categories
Funding
- University of Muenster Medical School
- Deutsche Forschungsgemeinschaft [EH-235/1-1]
- Fonds der Chemischen Industrie
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available