tumor necrosis factor- (TNF-α), are absolutely dependent on activation of PI3K [9] . Although the nuclear factor kappa B (NF-B) pathway has been shown to contribute to the transcriptional activation of type I interferon by PRRSV [15] , one study shows that NF-B is more likely related to induction of inflammatory cytokines such as TNF- and IL-6, rather than type I interferon, after influenza A virus infection and CpG ODN stimulation [9] . This discrepancy may be due to the cell types and viruses used in different studies since different cell types and different viruses exhibit distinct features in the induction of type I interferon pathway. Virus replication and viral infectivity are usually not essential to the induction of type I interferon since both UV-inactivated and heat-inactivated influenza A viruses induce more abundant interferon- than their live virus counterparts [16] .