Is flavivirus resistance interferon type I‐independent?

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Abstract
Interferon type I comprises a group of major virus‐inducible host antiviral factors that control infection with a great number of human and animal viruses. They are ubiquitously expressed cytokines that interfere with virus replication within different cell types by activating a number of host genes and several parallel antiviral pathways. Two major intracellular actors of IFN‐I‐induced antiviral states are ribonucleic acid‐dependent protein kinase and 2′‐5′‐oligoadenylate synthetases/RNase L, both being induced by IFN‐I and activated by viral double stranded ribonucleic acid. In addition, Mx proteins and ribonucleic acid‐specific adenosine deaminase have also been implicated in IFN‐I‐induced antiviral responses to some RNA viruses. Viruses, in turn, have evolved different strategies to escape a control imposed by IFN‐I and by IFN‐I‐induced antiviral factors. The fatal outcome of virus infection as well as the efficiency of IFN‐I‐based antiviral therapies in its prevention, are determined by complex interactions between viral virulence factors and cellular antiviral IFN‐I inducible factors. In the light of these facts and current knowledge on IFN‐I involvement in flavivirus infection, I discuss a possible role of IFN‐I signalling in resistance to flavivirus infection in a model of congenic mouse strains that express different levels of susceptibility/resistance to common flaviviruses. Specifically, this review emphasizes importance of fully operative 2′‐5′‐oligoadenylate synthetases/RNase L pathway for the IFN‐I‐induced stimulation of flavivirus resistance conferred by Flv.