Send to

Choose Destination
See comment in PubMed Commons below
World J Virol. 2013 May 12;2(2):49-56. doi: 10.5501/wjv.v2.i2.49.

Innate host responses to West Nile virus: Implications for central nervous system immunopathology.

Author information

Giada Rossini, Maria Paola Landini, Unit of Clinical Microbiology, Regional Reference Centre for Microbiological Emergencies, St. Orsola University Hospital, 40138 Bologna, Italy.


West Nile virus (WNV) is an emerging neurotropic flavivirus that has recently spread to America and Southern Europe via an enzootic/epizootic bird-mosquito-bird transmission cycle. The virus can occasionally infect humans through mosquito bites, and man-to-man transmission has also been reported via infected blood or organ donation. In the human host, WNV causes asymptomatic infection in about 70%-80% of cases, while < 1% of clinical cases progress to severe neuroinvasive disease; long-term neurological sequelae are common in more than 50% of these severe cases. The pathogenesis of the neuroinvasive form of WNV infection remains incompletely understood, and risk factors for developing severe clinical illness are largely unknown. The innate immune response plays a major role in the control of WNV replication, which is supported by the fact that the virus has developed numerous mechanisms to escape the control of antiviral interferons. However, exaggerated inflammatory responses lead to pathology, mainly involving the central nervous system. This brief review presents the salient features of innate host responses, WNV immunoevasion strategies, and WNV-induced immunopathology.


Antigen presenting cells; Central nervous system; Inflammation; Innate immunity; Interferon and cytokines; West Nile virus infection

PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Baishideng Publishing Group Inc. Icon for PubMed Central
    Loading ...
    Support Center