Grant: Operating Grant

Influenza viruses continue to pose a severe threat worldwide. The major difficulty in defending against influenza virus infection is the high genetic variability of the virus. This results in the rapid generation of reassortant viruses that can escape the acquired immunity against previous virus strains or gain resistance to antiviral agents. During virus infection, virus-host interactions determine the virus life cycle and pathogenesis. One important strategy from the virus perspective is to activate cellular signaling pathways and hijack the cellular machinery to augment viral replication and propagation. Thus, cellular events that are essential for efficient virus replication and propagation might be the target for anti-influenza interventions. The proposed research is designed to focus on the cellular function, specifically, to dissect how influenza virus infection leads to the activation of cellular Phosphatidylinositol 3-kinases (PI3K)/Akt signaling pathway, which is essential for efficient virus replication and propagation. The rationale is that a missing cellular function is more difficult for the virus to adapt to, and should affect virus infection independent of the virus strain and antigenic properties. The knowledge gained from this research will increase understanding of the pathogenesis of influenza virus and provide new insights for the development of antiviral therapeutics for this emerging disease.