Abstract
West Nile virus (WNV), a mosquito-borne, single-stranded flavivirus, has caused annual outbreaks of viral encephalitis in the United States since 1999. The virus induces acute infection with a clinical spectrum ranging from a mild flu-like febrile symptom to more severe neuroinvasive conditions, including meningitis, encephalitis, acute flaccid paralysis, and death. Some WNV convalescent patients also developed long-term neurological sequelae. Neither the treatment of WNV infection nor an approved vaccine is currently available for humans. Neuronal death in the central nervous system (CNS) is a hallmark of WNV-induced meningitis and encephalitis. However, the underlying mechanisms of WNV-induced neuronal damage are not well understood. In this review, we discuss current findings from studies of WNV infection in vitro in the CNS resident cells and the in vivo animal models, and provide insights into WNV-induced neuropathogenesis.
Highlights
West Nile virus (WNV), is a member of the family of Flaviviridae, genus Flavivirus, a group of plus-sense, single-stranded RNA viruses
These results suggest that WNV can directly trigger neuronal death in the absence of inflammatory cell types, such as T cells, microglia, and monocytes
Neuronal loss is a hallmark of WNV-induced meningitis and encephalitis
Summary
West Nile virus (WNV), is a member of the family of Flaviviridae, genus Flavivirus, a group of plus-sense, single-stranded RNA viruses. Parquet M et al [26] was the first to report apoptotic features in WNV-infected neurons, including cell shrinkage, chromatin condensation, and subdiploid DNA content [26] Autophagy, another type of programmed cell death pathway, is known to support viral growth following infection with other flaviviruses, such as dengue virus or Japanese encephalitis virus [27,28]. In the upper cervical cord dying neurons (A, hollow arrows) were encircled and phagocytized by inflammatory cells, mainly microglia (arrowheads) as an example of neuronophagia. It was found in Purkinje cells (B, hollow arrows) in the cerebellum and associated inflammation (Burgmann gliosis, arrows) in the surrounding area
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