PI3K-Akt signaling and viral infection.
PI3K-Akt pathway is an important mechanism through which viral infection influences various cell functions. Activating PI3K-Akt signaling is a strategy employed by viruses to slow down apoptosis and prolong viral replication in both acute and persistent infection. It is also probable that prevention of cell death facilitates virus-induced carcinogenesis. Accumulating evidence suggests that the activity of PI3K or Akt is critical for survival of a few viruses. Adenovirus relies on PI3K-mediated organization of actin filament for active internalization. Non-segmented negative-sense RNA viruses require Akt to enhance synthesis of viral RNAs. On the other hand, PI3K-Akt signaling is associated with up-regulating interferon response. Higher PI3K-Akt activity might impede viral propagation due to activation of cellular defenses. Influenza A virus is an interesting case which requires active PI3K for penetration despite the negative effects of inducing immune response. Unlike most viruses, it was reported that VP1 protein of foot-and-mouth disease virus inhibits Akt to promote cell death. These reports confirm the multiple roles of PI3K-Akt pathway in viral infection. Here, more new information on the interaction between PI3K-Akt signaling and viral infection is discussed.
Ji
Wen-Tsai
WT
Department of Veterinary Medicine, National Pingtung University of Science and Technology, Pingtung 912, Taiwan.
Liu
Hung J
HJ
D000818:Animals; D006801:Humans; D008954:Models, Biological; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction; D014777:Virus Diseases / Q000201:enzymology* / Q000821:virology*; D018406:Virus Physiological Phenomena
D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt