Neurological Progress
West Nile virus neuroinvasive disease
Article first published online: 18 SEP 2006
DOI: 10.1002/ana.20959
Copyright © 2006 American Neurological Association
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How to Cite
Davis, L. E., DeBiasi, R., Goade, D. E., Haaland, K. Y., Harrington, J. A., Harnar, J. B., Pergam, S. A., King, M. K., DeMasters, B. K. and Tyler, K. L. (2006), West Nile virus neuroinvasive disease. Ann Neurol., 60: 286–300. doi: 10.1002/ana.20959
Publication History
- Issue published online: 18 SEP 2006
- Article first published online: 18 SEP 2006
- Manuscript Accepted: 24 JUL 2006
- Manuscript Revised: 19 JUL 2006
- Manuscript Received: 19 APR 2006
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Abstract
Since 1999, there have been nearly 20,000 cases of confirmed symptomatic West Nile virus (WNV) infection in the United States, and it is likely that more than 1 million people have been infected by the virus. WNV is now the most common cause of epidemic viral encephalitis in the United States, and it will likely remain an important cause of neurological disease for the foreseeable future. Clinical syndromes produced by WNV infection include asymptomatic infection, West Nile Fever, and West Nile neuroinvasive disease (WNND). WNND includes syndromes of meningitis, encephalitis, and acute flaccid paralysis/poliomyelitis. The clinical, laboratory, and diagnostic features of these syndromes are reviewed here. Many patients with WNND have normal neuroimaging studies, but abnormalities may be present in areas including the basal ganglia, thalamus, cerebellum, and brainstem. Cerebrospinal fluid invariably shows a pleocytosis, with a predominance of neutrophils in up to half the patients. Diagnosis of WNND depends predominantly on demonstration of WNV-specific IgM antibodies in cerebrospinal fluid. Recent studies suggest that some WNV-infected patients have persistent WNV IgM serum and/or cerebrospinal fluid antibody responses, and this may require revision of current serodiagnostic criteria. Although there is no proven therapy for WNND, several vaccines and antiviral therapy with antibodies, antisense oligonucleotides, and interferon preparations are currently undergoing human clinical trials. Recovery from neurological sequelae of WNV infection including cognitive deficits and weakness may be prolonged and incomplete. Ann Neurol 2006;60:286–300

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