West Nile Encephalitis Virus Infection: Viral Pathogenesis and the Host Immune Response

West Nile virus is a neurotropic flavivirus that has emerged globally as a significant cause of viral encephalitis in humans. Infection of humans is associated with a febrile illness that can progress to meningitis and encephalitis with symptoms including cognitive dysfunction and flaccid paralysis. Following its introduction to the United States in 1999, West Nile virus rapidly disseminated across North America. Outbreaks of West Nile virus fever and neuroinvasive disease now occur annually in the United States, with about 23,000 diagnosed human cases between 1999 and 2006, and likely millions of undiagnosed infections. At present no vaccines or specific therapies for West Nile virus are currently approved for humans.

The emergence of West Nile virus in the Western hemisphere and the corresponding increase in disease burden has been accompanied by intensive study. West Nile Encephalitis Virus Infection: Viral Pathogenesis and the Host Immune Response focuses on recent studies that have identified key steps in the molecular pathogenesis of West Nile virus infection. After introducing the scale of the global problem, the genetic diversity, and the clinical syndromes, the initial chapters describe our most up-to-date understanding of the pathogenesis steps in animals and the viral sequence determinants that mediate virulence. Subsequent chapters focus on the earliest innate host immune response that controls West Nile virus spread and include recent experiments on pathogen recognition receptors, IFN antiviral cascades, and mechanisms of West Nile virus antagonism. The book explores in detail the host-pathogen interface, and analyzes the latest data describing how a balance between host protective responses, host immunopathology, West Nile-induced pathology, and West Nile virusВ immune evasion determines infection outcome. Finally, the book concludes with novel approaches and prospects for human vaccines and therapeutics.

About the Editor:

Dr. Michael S. Diamond is Associate Professor in the Division of Infectious Diseases at Washington University Medical School, St. Louis, MO, uSA.