The Intracellular Signalling that Associated with Influenza A Virus Infection

Hany Khalil

Abstract

Influenza-A virus infection induces a variety of intracellular signalling pathways that are either antiviral or required to ensure efficient replication. A prominent cellular antiviral event is the activation of cascade that produces type I interferon’s (IFNs): IFN-α and IFN-β. Consequently, an appreciated number of antiviral proteins that encoded by so-called IFN stimulated genes are activated, such as Mx1, PKR and ISG-15 genes. Conversely, virus-supportive signalling processes activated upon infection are I kappa B kinase/nuclear factor kappa-light-chain-enhancer of activated B cells (IKK/ NF-κB), phosphatidylinositol-3- kinasee/Akt (PI3K/Akt), and the RNA activating factor-1(Raf-1). Specific inhibition of the latter signalling cascade leads to striking impairment of the replication of all influenza A viruses, as a result of nuclear retention of RNPs in late stages of the replication cycle. In this review, the intracellular signaling that associated with IAV infection will be highlighted to realize the appropriate therapeutically strategy against IAV infection.