Activation of phosphatidylinositol 3-kinase signaling by the nonstructural NS1 protein is not conserved among type A and B influenza viruses

Recently it has been shown by several laboratories that the influenza A virus nonstructural protein 1 (A/NS1) binds and activates phosphatidylinositol 3-kinase (PI3K). This function of the protein is likely to prevent premature apoptosis induction during viral propagation. Here we show that the B/NS1 protein completely lacks the capacity to induce PI3K signaling. Thus, PI3K activation is another unique function of A/NS1 that is different from the action of its influenza B virus counterpart. Influenza A virus infections induce a variety of pro- and antiviral-acting signaling processes (12, 13). Very recently the phosphatidylinositol 3-kinase (PI3K) and its downstream ef-fector Akt/protein kinase B have been added to the list of influenza A virus-induced signaling mediators (5, 9, 18). PI3K is involved in a wide variety of cellular events, generating lipid signals downstream of receptors and influencing diverse cellu-lar pathways (20, 21). In the context of an influenza A virus infection, PI3K was identified as a perfect example of a seem-ingly antiviral signaling component that is misused by the viru