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West Nile virus (WNV) is a mosquito-borne flavivirus (single-stranded RNA) that primarily infects birds but occasionally infects horses and humans. WNV was first isolated in 1937 from an infected person in the West Nile district of Uganda. Until the viral infection was recognized in 1999 in birds in New York City, WNV was found only in the Eastern hemisphere, with wide distribution in Africa, Asia, the Middle East, and Europe.(1-3) In 2002, a total of 3,389 human cases of WNV infection were reported from 37 states (794 cases in Illinois); 2,354 (69%) presented with meningoencephalitis, 704 (21%) had West Nile fever, and 331 (10%) had an unspecified illness.(2) Overall, the WNV epidemic in the United States was the largest arboviral meningoencephalitis outbreak documented in the Western hemisphere. In addition, 33 cases of probable WNV infection occurred among persons who had received blood components in the month before illness onset.(3)
Most people who are infected with WNV will not have any type of illness. It is estimated that about 20% of those who become infected will develop West Nile fever with mild symptoms, including fever, headache, myalgia, and occasionally a skin rash on the trunk of the body. About 1 of 150 WNV infections (<1%) result in meningitis or encephalitis. Case fatality rates among patients hospitalized during recent outbreaks have ranged from 4% to 14%. Advanced age is the most important risk factor for death, and patients older than 70 years of age are at particularly high risk.(1)
Laboratory diagnosis of WNV is best achieved by demonstration of specific IgG and IgM class antibodies in serum specimens from patients. By the 8th day of illness, most infected persons will have detectable serum IgM antibody to WNV; in most cases it will be detectable for at least 1 to 2 months after onset of illness, in some cases it will be detectable for 12 months or longer. By 3 weeks postinfection, virtually all infected persons should have developed serum IgG antibodies to WNV.
The specific identification of WNV by detection of IgM in cerebrospinal fluid (CSF) is the recommended test to document central nervous system disease, but this test may be falsely negative in CSF collected <8 days after the onset of symptoms. PCR (LCWNV / West Nile Virus, Molecular Detection, PCR) can detect WNV RNA in specimens from patients with WNV infection when specific antibodies to the virus are not present. However, the likelihood of detection is relatively low as PCR sensitivity in CSF is approximately 55%, and in blood, about 10% in patients with known WNV infection.
Preferred test for the laboratory diagnosis of West Nile virus meningitis or encephalitis
A positive result is consistent with the acute phase of West Nile virus (WNV) meningitis or encephalitis. In the very early stages of acute WNV infection, IgM may be detectable in cerebrospinal fluid before it becomes detectable in serum.
A negative result may indicate the absence of disease. However, specimens drawn too early in the acute phase may be negative for IgM-specific antibodies to WNV. If WNV central nervous system (CNS) infection is suspected, a second specimen should be collected in 1 to 2 weeks and tested.
A positive result is consistent with CNS infection with WNV sometime in the past.
Test results should be used in conjunction with a clinical evaluation and other available diagnostic procedures.
The significance of negative test results in immunosuppressed patients is uncertain.
False-negative results due to competition by high levels of IgG, while theoretically possible, have not been observed.
West Nile virus antibody results for cerebrospinal (CSF) should be interpreted with caution. Complicating factors include low antibody levels found in CSF, passive transfer of antibody from blood, and contamination via bloody taps.
Cross-reactivity has been noted with some specimens containing IgM antibody to enteroviruses.
Reference values apply to all ages.
1. Petersen LR, Marafin AA: West Nile virus: a primer for the clinician. Ann Intern Med 2002;137:173-179
2. Petersen LR, Roehrig JT: West Nile virus: a reemerging global pathogen. Emerg Infect Dis 2001;7(4):611-614
3. Brinton MA: The molecular biology of West Nile virus: a new invader of the western hemisphere. Ann Rev Microbiol 2002;56:371-402
4. Centers for Disease Control and Prevention (CDC). Provisional surveillance summary of the West Nile virus epidemic. United States, January-November 2002. MMWR Morb Mortal Wkly Rep 2002;51(50):1129-1133
5. Centers for Disease Control and Prevention (CDC). Investigations of West Nile virus infections in recipients of blood transfusions. MMWR Morb Mortal Wkly Rep 2002;51(43):973-974