West Nile virus is a flavivirus that is now the primary cause of arbovirus encephalitis in the United States. Most patients have mild or no symptoms. About 1 out of 150 patients develop a severe infection involving the central nervous system. Diagnosis is by serologic testing. Treatment is supportive with close monitoring for severe infection.
West Nile virus was first introduced into the United States in 1999 in New York City. It is now present in all 48 contiguous states, southern Canada, Mexico, Central and South America and Caribbean Islands. West Nile virus also is widely distributed in Africa, Middle East, southern Europe, Russia, India, and Indonesia.
West Nile virus is present in many species of birds. Many infected birds are asymptomatic but others, especially crows and jays, become sick and die and thus possibly are an indicator of disease in an area. Horses infected by West Nile virus may become fatally ill, and equine cases also are an indication of West Nile virus transmission in a locality. An equine vaccine is available. Viral transmission is mainly by the Culex mosquito, but the virus also may be transmitted by blood transfusion, organ transplantation, or occasionally transplacentally to a fetus.
Symptoms and Signs of West Nile Virus
Most (4 out of 5) patients with West Nile virus infection have no symptoms. About 1 in 5 develop fever along with other symptoms such as headache, body aches, joint pain, vomiting, diarrhea, or maculopapular rash. About 1 in 150 patients develop severe central nervous system involvement with encephalitis, meningitis, or flaccid paralysis (1). Symptoms of central nervous system infection include high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, vision loss, numbness, and paralysis. Severe illness can affect any age, but those > 60 years and those with certain chronic medical conditions (eg, diabetes) or immunocompromising conditions are at greater risk. Mortality is about 10% in people with severe central nervous system involvement (2).
West Nile virus acute flaccid paralysis is clinically and pathologically identical to that in poliomyelitis, with damage of anterior horn cells. Acute flaccid paralysis can occur without fever or apparent viral prodrome and often presents as isolated limb paresis or paralysis and may progress to respiratory paralysis requiring mechanical ventilation.
Most people with typical fever and myalgia recover completely, but fatigue and weakness can last for weeks or months. Patients who recover from West Nile virus encephalitis or acute flaccid paralysis often have residual neurologic deficits.
Symptoms and signs references
1. Centers for Disease Control and Prevention: West Nile Virus: About West Nile. May 15, 2024. Accessed June 18, 2025.
2. Centers for Disease Control and Prevention: West Nile Virus: Clinical Signs and Symptoms of West Nile Virus Disease. May 15, 2024. Accessed June 18, 2025.
Diagnosis of West Nile Virus
Serologic testing
Reverse transcriptase-polymerase chain reaction (RT-PCR)
West Nile virus infection is diagnosed by finding West Nile virus-specific IgM antibodies in the serum or cerebrospinal fluid (CSF). These antibodies are usually detectable 3 to 8 days after onset of illness and persist for 30 to 90 days, but longer persistence has been documented. False-positive serologic results may result from cross-reactive antibodies due to infection with other flaviviruses, recent immunization with flavivirus vaccines (yellow fever or Japanese encephalitis), or from nonspecific reactivity.
CSF studies are consistent with viral meningitis, showing elevated protein levels and white blood cell counts. There is usually an early predominance of neutrophils that transitions to lymphocytic predominance over time.
Plaque-reduction neutralization tests (PRNTs) done in reference laboratories, including some state public health laboratories and the Centers for Disease Control and Prevention (CDC), can help determine the specific infecting flavivirus, including West Nile virus. PRNTs can also confirm acute infection by demonstrating a fourfold or greater change in West Nile virus-specific neutralizing antibody titer between acute- and convalescent-phase serum samples collected 2 to 3 weeks apart.
Viral cultures and tests to detect viral RNA (eg, RT-PCR) in serum or CSF are performed to confirm infection.
Treatment of West Nile Virus
Supportive care
Supportive care for severe West Nile virus illness includes:
Close monitoring of patients with encephalitis for the development of elevated intracranial pressure and seizures
Close monitoring of patients with encephalitis or acute flaccid paralysis for inability to protect their airway
Mechanical ventilation, if needed
Acute respiratory failure may develop rapidly, and prolonged ventilatory support may be required.
Prevention of West Nile Virus
Community-level mosquito control programs
Personal protective measures to avoid mosquito bites
No West Nile virus vaccines are available for use in humans.
Personal protective measures to decrease exposure to infected mosquitoes, including diethyltoluamide (DEET), mosquito netting, and protective attire, should be used.to decrease exposure to infected mosquitoes, including diethyltoluamide (DEET), mosquito netting, and protective attire, should be used.
Blood and some organ donors are screened for West Nile virus by nucleic acid–based tests. Healthcare professionals should remain vigilant for the possible transmission of West Nile virus through blood transfusion or organ transplantation.
There is no evidence that humans acquire West Nile virus infection from handling dead or infected birds, but the CDC recommends wearing gloves when handling dead birds (or any animal).
Key Points
West Nile virus is spread among birds and transmitted to humans by the bite of an infected mosquito.
Most patients have mild or no symptoms, but some develop a severe infection involving the central nervous system.
Diagnosis is by serologic testing for West Nile virus–specific IgM or by plaque reduction neutralization tests demonstrating a significant rise between acute and convalescent IgG pairs.
Patients who develop severe infection should be closely monitored for elevated intracranial pressure, inability to protect their airway, and respiratory failure requiring mechanical ventilation.
More Information
The following English-language resource may be useful. Please note that The Manual is not responsible for the content of this resource.
Clark MB, Schaefer TJ. West Nile Virus. [Updated 2023 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK544246/
