West Nile Virus: Pathogenesis and Therapeutic Options

6 April 2004 | Volume 140 Issue 7 | Pages 545-553

West Nile virus, a member of the family Flaviviridae, has spread throughout the United States. With more than 9000 cases and 200 deaths in 2003, West Nile virus has become the most common cause of viral encephalitis in several states. West Nile virus encephalitis is a zoonosis. The life cycle of the virus includes mainly birds as hosts and mosquitoes as vectors. Humans are accidental hosts, insufficient to support the life cycle of the virus because of low-grade, transient viremia. However, human-tohuman transmission through blood, organ transplantation, and lactation has been documented. The frequency of severe neurologic disease in the current epidemic suggests a more neurovirulent strain of virus than the one classically associated with West Nile fever. Several neurologic manifestations have been described, but the most characteristic presentation is encephalitis with weakness. Magnetic resonance imaging scans may be normal initially, but a characteristic pattern of involvement of deep gray matter nuclei can be recognized. Although results of polymerase chain reaction may be positive in the cerebrospinal fluid early in the course of the disease, diagnosis is based on serologic tests. Possible cross-reactivity with other members of the genus flavivirus mandates caution when serologic testing results are interpreted. Thus far, no therapeutic intervention has shown consistent clinical efficacy in West Nile virus disease. Several approaches, including interferon-2b and immunoglobulin with high titer against West Nile virus, offer promise based on animal models and limited clinical experience. New drugs with in vitro activity are being investigated, and a vaccine is being developed.

Author and Article Information

From the National Cancer Institute, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, and the Johns Hopkins University School of Medicine and Bloomberg School of Public Health, Baltimore, Maryland.

An edited summary of a Clinical Staff Conference held on 20 November 2002 at the National Institutes of Health, Bethesda, Maryland.

Acknowledgments: The authors acknowledge Dr. Henry Masur, Chief of Critical Care Medicine at the NIH Clinical Center, for making this conference possible.

Grant Support: There was no grant support for this conference or the preparation of this manuscript.

Potential Financial Conflicts of Interest: None disclosed.

Requests for Single Reprints: Juan Gea-Banacloche, MD, Experimental Transplantation and Immunology Branch, National Cancer Institute, 10 Center Drive, Room 12S227, Bethesda, MD 20892; e-mail, banacloj{at}mail.nih.gov.

Current Author Addresses: Dr. Gea-Banacloche: Experimental Transplantation and Immunology Branch, National Cancer Institute, 10 Center Drive, Room 12S227, Bethesda, MD 20892.

Dr. Johnson: The Johns Hopkins University School of Medicine & Bloomberg School of Public Health, 3103 North Charles Street, 2nd Floor, Baltimore, MD 21218-3803.

Dr. Bagic: EEG Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive, Room 5C101, Bethesda, MD 20892.

Dr. Butman: Diagnostic Radiology Department, Clinical Center, National Institutes of Health, 9000 Rockville Pike, Room 1C635, Bethesda, MD 20892.

Dr. Murray: Department of Laboratory Medicine, Clinical Center, National Institutes of Health, 9000 Rockville Pike, Room 2C385, Bethesda, MD 20892.

Dr. Guillet Agrawal: Department of Critical Care Medicine, Clinical Center, National Institutes of Health, 9000 Rockville Pike, Building 10, Room 7D43, Bethesda, MD 20892.