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World J Virol. May 12, 2013; 2(2): 49-56
Published online May 12, 2013. doi: 10.5501/wjv.v2.i2.49
Innate host responses to West Nile virus: Implications for central nervous system immunopathology
Giada Rossini, Maria Paola Landini, Francesco Gelsomino, Vittorio Sambri, Stefania Varani
Giada Rossini, Maria Paola Landini, Unit of Clinical Microbiology, Regional Reference Centre for Microbiological Emergencies, St. Orsola University Hospital, 40138 Bologna, Italy
Maria Paola Landini, Francesco Gelsomino, Vittorio Sambri, Stefania Varani, Microbiology, Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, 40138 Bologna, Italy
Author contributions: Rossini G drafted the manuscript, revised the figures and critically revised the final version; Landini MP contributed to drafting the manuscript and the final revision; Gelsomino F contributed to drafting the manuscript and prepared the figures; Sambri V contributed to drafting the manuscript and critical revisions; Varani S designed and wrote the manuscript.
Supported by RFO of University of Bologna, the grant “Fondi Finalizzati Lab P3” from Regione Emilia-Romagna; the grant “Ricerca Finalizzata RF-2009-1539631” from the Italian Ministry of Health
Correspondence to: Stefania Varani, MD, PhD, Microbiology, Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Padiglione 11, St. Orsola-Malpighi University Hospital, via Massarenti 9, 40138 Bologna, Italy. stefania.varani@unibo.it
Telephone: +39-51-6363511 Fax: +39-51-307397
Received: December 5, 2012
Revised: January 19, 2013
Accepted: February 2, 2013
Published online: May 12, 2013
Abstract

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.

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