West Nile Virus History

West Nile Encephalitis

WNV is a flavivirus belonging taxonomically to the Japanese encephalitis serocomplex that includes the closely related St. Louis encephalitis (SLE) virus, Kunjin and Murray Valley encephalitis viruses, as well as others. WNV was first isolated in the West Nile Province of Uganda in 1937 (2). The first recorded epidemics occurred in Israel during 1951-1954 and in 1957. Epidemics have been reported in Europe in the Rhone delta of France in 1962 and in Romania in 1996 (3-5). The largest recorded epidemic occurred in South Africa in 1974 (6).

An outbreak of arboviral encephalitis in New York City and neighboring counties in New York state in late August and September 1999, was initially attributed to St. Louis encephalitis virus based on positive serologic findings in cerebrospinal fluid (CSF) and serum samples using a virus-specific IgM-capture enzyme-linked immunosorbent assay (ELISA).

The virus that caused the New York area outbreak has been definitively identified as a strain of WNV. The genomic sequences identified to date from human brain, virus isolates from zoo birds, dead crows, and mosquito pools are identical. SLE and West Nile viruses are antigenically related, and cross reactions are observed in most serologic tests. The isolation of viruses and genomic sequences from birds, mosquitoes, and human brain tissue permitted the discovery of West Nile virus in North America and prompted more specific testing. The limitations of serologic assays emphasize the importance of isolating the virus from entomologic, clinical, or veterinary material.

Although it is not known when and how West Nile virus was introduced into North America, international travel of infected persons to New York or transport by imported infected birds may have played a role. WNV can infect a wide range of vertebrates; in humans it usually produces either asymptomatic infection or mild febrile disease, but can cause severe and fatal infection in a small percentage of patients. Within its normal geographic distribution of Africa, the Middle East, western Asia, and Europe, WNV has not been documented to cause epizootics in birds; crows and other birds with antibodies to WNV are common, suggesting that asymptomatic or mild infection usually occurs among birds in those regions. Similarly, substantial bird virulence of SLE virus has not been reported. Therefore, an epizootic producing high mortality in crows and other bird species is unusual for either WNV or SLE virus. For both viruses, migratory birds may play an important role in the natural transmission cycles and spread. Like SLE virus, WNV is transmitted principally by Culex species mosquitoes, but also can be transmitted by Aedes, Anopheles, and other species. The predominance of urban Culex pipiens mosquitoes trapped during this outbreak suggests an important role for this species. Enhanced surveillance for early detection of virus activity in birds and mosquitoes will be crucial to guide control measures.

West Nile encephalitis References

1. CDC. Case definitions for infectious conditions under public health surveillance. MMWR 1997;46(RR-10):12-3.

2. Smithburn KC, Hughes TP, Burke AW, Paul JH. A neurotropic virus isolated from the blood of a native of Uganda. Am J Trop Med Hyg 1940;20:471.

3. Klingberg MA, Jasinka-Klingberg W, Goldblum N. Certain aspects of the epidemiology and distribution of immunity of West Nile virus in Israel. In: Proceeding of the 6th International Congress of Tropical Medicine, 1959;5:132.

4. Panther R, Hannoun C, Beytout D, Mouchet J. Epidemiology of West Nile virus. In: Human Illness: focus on Camargue [French]. Vol 3. Ann Inst Pasteur 1968;115:435.

5. Tsai TF, Popovici F, Cernescu C, Campbell GL, Nedelcu NI. West Nile encephalitis epidemic in southeastern Romania. Lancet 1998;352:767-71.

6. McIntosh BM, Jupp PG, Dos Santos I, Meenehan GM. Epidemics of West Nile and Sindbis viruses in South Africa with Culex (Culex) univittatus Theobold as vector. S Afr J Sci 1976;72:295.

Information developed by Centers for Disease Control and Prevention, National Center for Infectious Diseases, Division of Vector-Borne Infectious Diseases, 1300 Rampart Road, Colorado State University Foothills Research Campus, P.O. Box 2087, Fort Collins, Colorado 80522, USA; telephone: (970)221-6400; fax: (970)221-6476.

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