Abstract
West Nile virus (WNV) is a neurotropic flavivirus that cycles between mosquitoes and birds but that can also infect humans, horses, and other vertebrate animals. In most humans, WNV infection remains subclinical. However, 20%–40% of those infected may develop WNV disease, with symptoms ranging from fever to meningoencephalitis. A large variety of WNV strains have been described worldwide. Based on their genetic differences, they have been classified into eight lineages; the pathogenic strains belong to lineages 1 and 2. Ten years ago, Beasley et al. (2002) found that dramatic differences exist in the virulence and neuroinvasion properties of lineage 1 and lineage 2 WNV strains. Further insights on how WNV interacts with its hosts have recently been gained; the virus acts either at the periphery or on the central nervous system (CNS), and these observed differences could help explain the differential virulence and neurovirulence of WNV strains. This review aims to summarize the current state of knowledge on factors that trigger WNV dissemination and CNS invasion as well as on the inflammatory response and CNS damage induced by WNV. Moreover, we will discuss how WNV strains differentially interact with the innate immune system and CNS cells, thus influencing WNV pathogenesis.
Highlights
West Nile virus (WNV) is a member of the Japanese encephalitis (JE) antigenic complex and belongs to the Flavivirus genus in the Flaviridae family, which includes other major human pathogens such as the Saint Louis encephalitis, Japanese encephalitis, yellow fever, and dengue viruses.Flaviviruses consist of enveloped particles that surround ssRNA+ genomes of about 11 kb
Infection is subclinical, but approximately 20%–40% of those infected may develop symptoms of WNV disease ranging from West Nile fever to meningoencephalitis or flaccid paralysis, and, less frequently, death [1,4,5,6]
We will discuss how genetically diverse WNV strains can differentially interact with the innate immune system and central nervous system (CNS) cells, influencing WNV pathogenesis
Summary
West Nile virus (WNV) is a member of the Japanese encephalitis (JE) antigenic complex and belongs to the Flavivirus genus in the Flaviridae family, which includes other major human pathogens such as the Saint Louis encephalitis, Japanese encephalitis, yellow fever, and dengue viruses. WNV is maintained in an enzootic cycle between mosquitoes and birds [3] but can infect and cause disease in other vertebrate animals, including horses and humans. A declining trend in the number of human WNV neuroinvasive cases has been observed since 2003, the USA suffered in 2012 from one of the most severe epidemics ever reported, which resulted in 5,674 cases and 286 deaths When WNV infection results in neuroinvasive disease, the virus induces inflammatory lesions and neuronal damage in several brain regions such as the hippocampus, the brainstem, the cerebellum, and the anterior horn of the spinal cord [1,5,37,38]. We will discuss how genetically diverse WNV strains can differentially interact with the innate immune system and CNS cells, influencing WNV pathogenesis
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