West Nile virus (WNV) is an enveloped positive-stranded RNA virus that has emerged over the past decade in North America to cause epidemics of meningitis, encephalitis, and acute flaccid paralysis in humans. WNV has broad species specificity, and replicates efficiently in many cell types, including those of the innate immune and central nervous systems. Recent studies have defined the pathogen recognition receptor (PRR) and signaling pathways by which WNV is detected, and several effector mechanisms that contribute to protective cell-intrinsic immunity. This review focuses on recent advances in identifying the host sensors that detect WNV, the adaptor molecules and signaling pathways that regulate the induction of interferon (IFN)-dependent defenses, and the proteins that limit WNV replication, spread, and disease pathogenesis.
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