[Frontiers in Bioscience 14, 3024-3040, January 1, 2009]
The host immunologic response to West Nile encephalitis virus
Michael S. Diamond1,2,3, Erin Mehlhop1, Theodore Oliphant3, Melanie A. Samuel3
1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, 2Department of Medicine,, Washington University School of Medicine, St. Louis, MO, 3Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO
TABLE OF CONTENTS
West Nile encephalitis virus (WNV) is a small, enveloped, mosquito-transmitted, positive-polarity RNA virus of the Flaviviridae family. This virus is closely related to other arthropod-borne viruses that cause human disease including Dengue, Yellow fever, and Japanese encephalitis viruses. WNV cycles in nature between mosquitoes and birds, but also infects human, horses, and other vertebrates. In humans, WNV disseminates to the central nervous system (CNS) and causes severe disease primarily in the immunocompromised and elderly. Experimental studies have made significant progress in dissecting the viral and host factors that determine the pathogenesis and outcome of WNV infection. This review will focus on the interactions between WNV and the protective and pathogenic host immune responses.