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About West Nile Virus (WNV)

West Nile Virus (WNV) is a mosquito-transmitted member of the genus Flavivirus in the family Flaviridae. It was discovered in northwest Uganda in 1937, but was not viewed as a potentially important public health threat until it was associated with epidemics of fever and encephalitis in the Middle East in the 1950’s. It was associated with sporadic outbreaks of human disease across portions of Africa, the Middle East, India, Europe and Asia; by the mid to late 1990's outbreaks began occurring more frequently.

The first domestically-acquired human cases of West Nile Virus disease in the Western Hemisphere were detected in New York City in 1999. WNV rapidly spread and by 2005 had established sustained transmission from Canada to southern Argentina. West Nile Virus has become enzootic in all 48 contiguous United States and evidence of transmission in the form of infected humans, mosquitoes, birds, horses, or other mammals has been reported from 96% of U.S. counties.

Today, West Nile Virus is the leading cause of mosquito-borne disease in the continental United States.  It is most commonly spread to people by the bite of an infected mosquito. Cases of WNV occur during mosquito season, which starts in the summer and continues through fall. There are no vaccines to prevent or medications to treat WNV in people. Fortunately, most people infected with WNV do not feel sick. About 1 in 5 people who are infected develop a fever and other symptoms. About 1 out of 150 infected people develop a serious, sometimes fatal, illness. You can reduce your risk of WNV by using insect repellent and wearing long-sleeved shirts and long pants to prevent mosquito bites.

Anyone who lives in or travels to areas where West Nile virus activity has been identified is at risk of getting the disease.

West Nile Virus is considered endemic (native) in New York State and is generally found in at least part of the state each summer. See the New York State weekly arboviral surveillance report. Most people are infected in summer to early fall. While chances of anyone becoming seriously ill are small, people over 50 years of age are at the highest risk for severe illness.

No symptoms in most people. Most people (8 out of 10) infected with West Nile virus do not develop any symptoms.

Febrile illness (fever) in some people. About 1 in 5 people who are infected develop a fever with other symptoms such as headache, body aches, joint pains, vomiting, diarrhea, or rash. Most people with febrile illness due to West Nile virus recover completely, but fatigue and weakness can last for weeks or months.

Serious symptoms in a few people. About 1 in 150 people who are infected develop a severe illness affecting the central nervous system such as encephalitis (inflammation of the brain) or meningitis (inflammation of the membranes that surround the brain and spinal cord).

  • Symptoms of severe illness include high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, vision loss, numbness and paralysis.
  • Severe illness can occur in people of any age; however, people over 60 years of age are at greater risk for severe illness if they are infected (1 in 50 people). People with certain medical conditions, such as cancer, diabetes, hypertension, kidney disease, and people who have received organ transplants, are also at greater risk.
  • Recovery from severe illness might take several weeks or months. Some effects to the central nervous system might be permanent.
  • About 1 out of 10 people who develop severe illness affecting the central nervous system die.


  • See your healthcare provider if you develop the symptoms described above.
  • Your healthcare provider can order tests to look for West Nile virus infection.


  • No vaccine or specific medicines are available for West Nile virus infection.
  • Over-the-counter pain relievers can be used to reduce fever and relieve some symptoms
  • In severe cases, patients often need to be hospitalized to receive supportive treatment, such as intravenous fluids, pain medication, and nursing care.
  • If you think you or a family member might have West Nile virus disease, talk with your health care provider.

Reducing exposure to mosquitos is the best prevention for West Nile Virus:

  • Use an approved insect repellent containing picaridin, DEET, oil of lemon eucalyptus (not for children under three), or products that contain the active ingredient IR3535.
  • Visit the EPA site to search by product and duration of effectiveness.
  • Make sure windows have screens. Repair or replace screens that have tears or holes.
  • Eliminate any standing water from your property and dispose of containers that can collect water. Standing water is a violation of the New York City Health Code.
  • Make sure roof gutters are clean and drained properly.
  • Clean and chlorinate swimming pools, outdoor saunas and hot tubs. Keep them empty or covered if not in use. Drain water that collects in pool covers.

West Nile Virus in the United States

The first domestically-acquired human cases of WNV disease in the Western Hemisphere were detected in New York City in 1999. WNV rapidly spread during the following years, and by 2005 had established sustained transmission foci in much of the hemisphere with an overall distribution that extended from central Canada to southern Argentina. WNV transmission persists across this large, ecologically-diverse expanse, and as a result this virus is recognized as the most widely distributed arbovirus in the world.

WNV has become enzootic in all 48 contiguous United States and evidence of transmission in the form of infected humans, mosquitoes, birds, horses, or other mammals has been reported from 96% of U.S. counties. This extensive distribution is due to the ability of WNV to establish and persist in the wide variety of ecosystems present across the country.

West Nile Virus in the U.S: Current Year Data

Current season data are updated every week from May through December. Due to delays in reporting, state, territorial, and local health departments may have more up-to-date information than what is presented here.

Latest Update: August 22, 2023

Total Human WNV Disease Cases (since May 1, 2023) 247
Neuroinvasive WNV Disease 169
States Reporting WNV Cases 34
West Nile Virus: Historical Data (1999 - 2022)

ArboNET is a national arboviral surveillance system managed by CDC and state health departments. ArboNET collects data on arboviral infections among people, veterinary animals, mosquitoes, dead birds, and sentinel animals. Explore Data 1999 - 2022

2022 Data

The 2022 data are preliminary and subject to change. Data are current as of June 13, 2023.

Human West Nile Disease Cases Neuroinvasive Disease Cases All Cases
Total Cases 816 1,126
Hospitalizations 763 854
Deaths 89 90
Month Reported Cases in 2022
January 4
February 4
March 1
April 3
May 7
June 28
July 106
August 458
September 397
October 97
November 18
December 3

West Nile in NYC

2022 Human Cases in NYC

  WNV Neuroinvasive Disease WNV Fever Blood Donors (Asymptomatic)
All NYC 36 9 2
Bronx 1 0 0
Brooklyn 12 3 1
Manhattan 6 0 0
Queens 11 2 1
Staten Island 6 4


  • West Nile Neuroinvasive Disease: Cases of West Nile encephalitis, meningitis or acute flaccid paralysis (severe muscle weakness associated with West Nile virus infection).
  • West Nile Fever: Cases with West Nile virus infection associated with mild to moderate illness but no evidence of central nervous system involvement.
  • Blood Donors: Blood donors are people who had no symptoms at the time of donating blood (people with symptoms are deferred from donating) through a blood collection agency, but whose blood tested positive when screened for the presence of West Nile virus.

Human Cases: Healthcare providers in New York City are required to report all patients hospitalized with viral encephalitis and meningitis to the Department of Health & Mental Hygiene. Blood and spinal fluid specimens are tested for West Nile virus by the New York City Department of Health & Mental Hygiene.

Borough reported for human cases is determined by where the case patient resides and may not always reflect where the case patient was actually infected.

2022 Positive Mosquito Pools in NYC

Borough Positive WNV Mosquito Pools
All NYC 1,555
Bronx 203
Brooklyn 291
Manhattan 80
Queens 509
Staten Island 472


Mosquito Pools: Mosquitoes are collected from over 90 locations Citywide and tested by the New York City Department of Health & Mental Hygiene.

While the Health Department's surveillance efforts are able to confirm evidence of West Nile virus in mosquitoes in the above mentioned areas, given the widespread presence of the virus, it should be protected against in all areas of New York City where the virus is just as likely to be detected. Residents of New York City can help reduce the risk of West Nile virus by eliminating areas of standing water and by taking precautions against mosquitoes.

WNV for Healthcare Providers


West Nile virus (WNV) disease should be considered in any person with a febrile or acute neurologic illness who has had recent exposure to mosquitoes, blood transfusion, or organ transplantation, especially during the summer months in areas where virus activity has been reported. The diagnosis should also be considered in any infant born to a mother infected with WNV during pregnancy or while breastfeeding.

Clinical Presentation

An estimated 70-80% of human WNV infections are subclinical or asymptomatic. Most symptomatic persons experience an acute systemic febrile illness that often includes headache, weakness, myalgia, or arthralgia; gastrointestinal symptoms and a transient maculopapular rash also are commonly reported.

Less than 1% of infected persons develop neuroinvasive disease, which typically manifests as meningitis, encephalitis, or acute flaccid paralysis.

  • WNV meningitis is clinically indistinguishable from viral meningitis due to other etiologies and typically presents with fever, headache, and nuchal rigidity.
  • WNV encephalitis is a more severe clinical syndrome that usually manifests with fever and altered mental status, seizures, focal neurologic deficits, or movement disorders such as tremor or parkinsonism.
  • WNV acute flaccid paralysis is usually clinically and pathologically identical to poliovirus-associated poliomyelitis, with damage of anterior horn cells, and may progress to respiratory paralysis requiring mechanical ventilation. WNV poliomyelitis often presents as isolated limb paresis or paralysis and can occur without fever or apparent viral prodrome. WNV-associated Guillain-Barré syndrome and radiculopathy have also been reported and can be distinguished from WNV poliomyelitis by clinical manifestations and electrophysiologic testing.

Rarely, cardiac dysrhythmias, myocarditis, rhabdomyolysis, optic neuritis, uveitis, chorioretinitis, orchitis, pancreatitis, and hepatitis have been described in patients with WNV disease.

Clinical Evaluation

Routine clinical laboratory studies are generally nonspecific. In patients with neuroinvasive disease, cerebrospinal fluid (CSF) examination generally shows lymphocytic pleocytosis, but neutrophils may predominate early in the course of illness. Brain magnetic resonance imaging is frequently normal, but signal abnormalities in the basal ganglia, thalamus, and brainstem may be seen in patients with encephalitis, and in the anterior spinal cord in patients with poliomyelitis.


Most patients with non-neuroinvasive WNV disease or WNV meningitis recover completely, but fatigue, malaise, and weakness can linger for weeks or months. Patients who recover from WNV encephalitis or poliomyelitis often have residual neurologic deficits. Among patients with neuroinvasive disease, the overall case-fatality ratio is approximately 10%, but it is significantly higher for patients with WNV encephalitis and poliomyelitis than WNV meningitis.

Recent studies have raised questions about the possible persistence of WNV infection and subsequent renal disease. More information is available here.

Supportive care remains the mainstay of treatment for WN virus infection.

Supportive therapy may include pain control for headaches; if nausea and vomiting are present, antiemetic therapy and rehydration may be beneficial. Patients with encephalitis should be monitored for signs and symptoms of elevated intracranial pressure and seizures. In some patients, particularly those with poliomyelitis-like symptoms, airway protection and ventilatory support may be needed. In patients with WN fever, there is no clear role for treatments other than supportive care.

Potential Therapeutic Agents

There are certain agents that may be of potential benefit for treatment of patients with WN virus neuroinvasive disease; however, data are conflicting, and the risks and benefits of using one of these agents must be determined on a case-by-case basis. These agents include:

  • Corticosteroids – The rationale for corticosteroid therapy in the setting of WNV is to inhibit pro-inflammatory mediators that may contribute to the pathogenesis of WNV in the CNS. Several individual case reports have described clinical improvement after administration of high-dose corticosteroids for a variety of neurological complications of WN virus infection (eg, acute flaccid paralysis, opsoclonus myoclonus ataxia). However, in a nonrandomized series of patients with neuroinvasive disease, no difference was noted in the duration of hospitalization for the 18 patients treated with prednisone or other steroids compared with untreated patients.
  • Intravenous immunoglobulin – There is a theoretical benefit of administering intravenous immunoglobulin (IVIG) in patients with WN virus neuroinvasive disease who have humoral deficiencies. In the United States and Europe, high titer neutralizing antibodies have been demonstrated in plasma as a consequence of recurring WN virus outbreaks, and animal studies suggested there may be a potential role for the use of IVIG for the prevention and treatment of WN virus infection.

However, IVIG has been administered to immunocompromised patients with varied outcomes. In, a randomized, placebo-controlled safety trial in 62 patients with neuroinvasive disease (the majority who were immunocompetent) failed to find benefit of a high-titered IVIG derived from Israeli donors, although this trial was designed to determine safety and not efficacy.

Limited data have also suggested a potential benefit of interferon alfa therapy, but interferon should not be used for treatment of WNV infection given the toxicity associated with interferon and the limited data supporting its use. Alfa interferon was found to be effective against WNV in in-vitro and in animal models. In addition, rapid neurologic improvement was demonstrated in two patients with serologically confirmed WNV infection who presented with deteriorating mental status and progression to coma and were treated with standard interferon alfa-2b within 72 hours of presentation. However, it remains unclear if the change in clinical status in these patients was due to interferon or to spontaneous improvement, which has been documented in untreated WNV infection. In addition, another report described two patients who developed WN fever after mosquito exposure while receiving interferon alfa-2b and ribavirin for hepatitis C infection.

 There does not appear to be a role for treatment of WN virus disease with the following agents given lack of efficacy:

  • Ribavirin – The antiviral agent ribavirin has demonstrated in vitro activity against WN virus, but therapeutic efficacy has not been demonstrated. Ribavirin increased mortality in Syrian golden hamsters when administered two days after inoculation [3]. In addition, during an outbreak in Israel, ribavirin appeared to be ineffective and possibly detrimental when it was used in an uncontrolled, nonblinded fashion in some patients with WN virus neuroinvasive disease.
  • Acyclovir – There does not appear to be a role for acyclovir in the treatment of WN virus infection based upon data from retrospective case series. In one report that included 49 patients treated with acyclovir, the duration of hospitalization did not differ compared with untreated patients [16]. In another series of 165 patients with neuroinvasive disease, 94 patients were treated with acyclovir for a median of eight days, and there was no clinical benefit compared with untreated patients.
WNV Antibody Testing

Laboratory diagnosis is generally accomplished by testing of serum or cerebrospinal fluid (CSF) to detect WNV-specific IgM antibodies. Immunoassays for WNV-specific IgM are available commercially and through state public health laboratories.

WNV-specific IgM 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. Therefore, positive IgM antibodies occasionally may reflect a past infection. If serum is collected within 8 days of illness onset, the absence of detectable virus-specific IgM does not rule out the diagnosis of WNV infection, and the test may need to be repeated on a later sample.

The presence of WNV-specific IgM in blood or CSF provides good evidence of recent infection but may also result from cross-reactive antibodies after infection with other flaviviruses or from non-specific reactivity. According to product inserts for commercially available WNV IgM assays, all positive results obtained with these assays should be confirmed by neutralizing antibody testing of acute- and convalescent-phase serum specimens at a state public health laboratory or CDC.

WNV IgG antibodies generally are detected shortly after IgM antibodies and persist for many years following a symptomatic or asymptomatic infection. Therefore, the presence of IgG antibodies alone is only evidence of previous infection and clinically compatible cases with the presence of IgG, but not IgM, should be evaluated for other etiologic agents.

Plaque-reduction neutralization tests (PRNTs) performed in reference laboratories, including some state public health laboratories and CDC, can help determine the specific infecting flavivirus. PRNTs can also confirm acute infection by demonstrating a fourfold or greater change in WNV-specific neutralizing antibody titer between acute- and convalescent-phase serum samples collected 2 to 3 weeks apart.

Other testing for WNV disease

Viral cultures and tests to detect viral RNA (e.g., reverse transcriptase-polymerase chain reaction [RT-PCR]) can be performed on serum, CSF, and tissue specimens that are collected early in the course of illness and, if results are positive, can confirm an infection. However, the likelihood of detecting a WNV infection through molecular testing is fairly low. Immunohistochemistry (IHC) can detect WNV antigen in formalin-fixed tissue. Negative results of these tests do not rule out WNV infection. Viral culture, RT-PCR, and IHC can be requested through state public health laboratories or CDC.