25425 West Nile Virus Antibody, IgG & IgM (WNS)

​West Nile Virus Antibody IgG

West NIle Virus Antibody IgM

WNS Interpretation

​​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.

Positive test results may not be valid in persons who have received blood transfusions or other blood products within the past several months.

False-negative results due to competition by high levels of IgG, while theoretically possible, have not been observed.

False-positive results may occur in persons vaccinated for flaviviruses (eg, yellow fever, Japanese encephalitis, dengue)

False-positive results may occur in patients infected with other arboviruses, including flaviviruses (eg, dengue virus) and alphavirusis (eg, LaCrosse [California] Encephalitis virus, Eastern or Western equine encephalitis virus, St. Louis virus) and in persons previously infected with West Nile virus (WNV).

Because closely related arboviruses exhibit serologic cross-reactivity, it sometimes may be epidemiologically important to attempt to pinpoint the infecting virus by conducting cross-neutralization tests using an appropriate battery of closely related viruses.

WNV antibody results for cerebrospinal fluid (CSF) should be interpreted with caution. Complicating factors include low antibody levels found in CSF, passive transfer of antibody from blood, and contamination via a traumatic lumbar puncture.

​West Nile virus (WNV) is a mosquito-borne flavivirus (single-stranded RNA) that primarily infects birds but can also infect humans and horses. 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. In 2012, a total of 5674 cases of WNV were reported to the Centers for Disease Control and Prevention (CDC), among which 2873 (51%) were classified as neuroinvasive disease (eg, meningitis or encephalitis) and 286 (5%) cases resulted in death.​

Most people who are infected with WNV will not develop clinical signs 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. 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.

Laboratory diagnosis is best achieved by demonstration of specific IgG and IgM class antibodies in serum specimens. Polymerase chain reaction (PCR) tests (WNVP / West Nile Virus (WNV), Molecular Detection, PCR, Plasma) can detect WNV RNA in plasma specimens from patients with recent WNV infection (ie, 3 to 5 days following infection) when specific antibodies to the virus are not yet present. However, the likelihood of detection is relatively low as the sensitivity of PCR detection is approximately 55% in cerebrospinal fluid and approximately 10% in blood, from patients with known WNV infection.

The presence of IgG-class antibodies to West Nile virus (WNV) in serum indicates infection with WNV at some time in the past. By 3 weeks postinfection, virtually all infected persons should have developed IgG antibodies to WNV. If acute-phase infection is suspected, serum specimens drawn within approximately 7 days postinfection should be compared with a specimen drawn approximately 14 to 21 days postinfection to demonstrate rising IgG antibody levels between the 2 serum specimens.

Presence of specific IgM-class antibodies in a serum specimen is consistent with acute-phase infection with WNV. 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 following disease resolution and in some cases will be detectable for 12 months or longer.

The absence of IgM antibodies to WNV is consistent with lack of acute-phase infection with this virus. Specimens collected too early in the acute phase (eg, before 8 to 10 days postinfection) may be negative for IgM-specific antibodies to WNV. If WNV is suspected, a second specimen collected approximately 14 days postinfection should be tested.

In the very early stages of WNV infection, IgM may be detectable in cerebrospinal fluid (CSF) before it becomes detectable in serum.