Abstract
West Nile virus (WNV) continues to cause outbreaks of severe neuroinvasive disease in humans and other vertebrate animals in the United States, Europe, and other regions of the world. This review discusses our understanding of the interactions between virus and host that occur in the central nervous system (CNS), the outcome of which can be protection, viral pathogenesis, or immunopathogenesis. We will focus on defining the current state of knowledge of WNV entry, tropism, and host immune response in the CNS, all of which affect the balance between injury and successful clearance.
Highlights
West Nile virus (WNV) is a mosquito borne, neurotropic, positive-stranded, enveloped RNA virus in the Flaviviridae family
WNV infection of neurons can result in caspase 3-dependent apoptosis, which likely contributes to central nervous system (CNS) dysfunction and pathogenesis of severe disease
While no significant difference in peripheral or CNS tissue viral burden was observed in WNV-infected caspase 3−/− mice, these animals were more resistant to lethal WNV infection due to reduced neuronal cell death in the cerebral cortex, brain stem, and cerebellum [68]
Summary
West Nile virus (WNV) is a mosquito borne, neurotropic, positive-stranded, enveloped RNA virus in the Flaviviridae family. WNV is maintained in an Viruses 2012, 4 enzootic cycle between mosquitoes and birds, and infects and causes disease in vertebrate animals including horses and humans. While the majority of human infections are asymptomatic, WNV can cause a severe febrile illness and neuroinvasive syndrome characterized by meningitis, encephalitis, and/or acute flaccid paralysis [5,6,7]. An association of single nucleotide polymorphisms (SNP) between symptomatic and asymptomatic WNV infections and IRF3 and Mx1 innate immune response and effector genes has been reported [20]; genetic variation in the interferon (IFN) response pathway appears to correlate with the risk of symptomatic WNV infection in humans. We will summarize our understanding of the host-virus interface in the CNS and how this determines WNV disease pathogenesis and clinical outcome
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