Being an obligate intracellular parasite with a limited number of proteins, Influenza A Virus (IAV) heavily depends on host proteins to complete a successful replication cycle. There is a tremendous body of literature on host factors required for efficient production of viral progeny as well as on host proteins that have suppressive roles on IAV infection. Through interaction with these host proteins, IAV evolved ways to evade such restriction factors and also manipulate host-cell signaling pathways for its own benefit, e.g. inhibition of interferon mediated antiviral response by the viral protein NS1. My specific focus is trying to further investigate the biology of IAV infection in context of host cell metabolism and possible manipulation of metabolic pathways by IAV, in order to identify targets for novel anti-viral strategies.
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