West Nile virus (WNV) is a mosquito-borne virus. It belongs to the family Flaviviridae, genus Flavivirus and Japanese encephalitis serocomplex along with Japanese encephalitis virus and St. Louis encephalitis virus.

WNV is a spherical enveloped virus with a diameter of around 50 nm. It contains single stranded RNA genome that encodes the capsid (C), envelop (E), pre-membrane (prM) and seven non-structural proteins.

The virus has 5 phylogenetic lineages, of which lineages 1 and 2 are associated with human outbreaks. Lineage 1 has been subdivided into three sublineages: 1a, 1b and 1c consisting of virus isolates from different geographic areas as mentioned:

 • 1a: Isolates from Western hemisphere, Africa, Europe and the Middle East

• 1b: Kunjin virus from Australasia

• 1c: Indian isolates

TRANSMISSION CYCLE

WNV is maintained in the nature in an enzootic transmission cycle between bird mosquito–bird. It can infect several vertebrates including human but many of them including humans suffer from severe disease and death. Those vertebrates also develop low level of viremia which is not sufficient enough to infect the mosquito and are considered as the dead end host.

Several bird species can be infected with the virus. WNV infection in some bird species like American crow leads to severe disease and death, in some species like house sparrows it leads to high viremia with less mortality. Several passerine birds are considered important for human transmission as they develop high viremia sufficient to infect mosquito.

Culex pipiens, C. quinquefasciatus and C. tarsalis species are the major vector of WNV transmission particularly between infected birds and humans.

The virus is primarily transmitted through mosquito bite. However, transmission of WNV has also been reported through transfusion of blood and its components, organ transplant and transplacental transmission.

EPIDEMIOLOGY

West Nile virus was first discovered in 1937 in the West Nile district of Uganda from a patient with a mild febrile illness. The virus is widely distributed throughout Africa, southern Europe, the Middle East, Eastern Russia, southwest Asia and Australia. Until 1990s, occasional human outbreaks were reported with mild febrile illness. Over the years, large human outbreaks were reported from several parts of Russia and Europe with more severe disease. In America, human cases started occurring since 1999, and then the virus spreads from New York to other states of USA and America. Since 1999 to 2015, near 44,000 WNV cases and 2000 deaths have been reported to CDC.

In India, the activity of WNV has been reported from birds, mosquitoes and humans as the virus has been isolated from all of them. Neutralizing antibodies to WNV has been detected in human sera collected from several eastern and western coastal states. Confirmed cases have been reported previously from Vellore and Kolar districts of Tamil Nadu.

Recently in 2010, WNV associated retinitis has been reported during a febrile outbreak in Tamil Nadu. In 2011, outbreak of WNV encephalitis was reported from Kerala.

PATHOGENESIS

WNV is inoculated onto the skin through bite of infected Culex mosquito. Then the virus replicates in keratinocytes and dendritic cells. These infected cells migrate to the draining lymph nodes and then to the bloodstream. Through blood, the virus reaches various organs and to the central nervous system. Systemic replication of WNV leads to high viral load in the blood. This induces the increased level of proinflammatory cytokines which facilitates the entry of virus by increasing the permeability as well as by disrupting the blood–brain barrier.

The gray matter of brain, brainstem and spinal cord are commonly affected by the virus. Pathologic changes in the brain can occur due to direct replication of the virus in the neuron or due to cytokine mediated. The risk of developing neuroinvasive disease occurs in 1 in 150–250 infected persons. Advanced age is one of the important risk factors for development of neuroinvasive disease.

CLINICAL MANIFESTATIONS

Incubation period ranges from 2 to 14 days. Majority of the patients (»80%) remain asymptomatic. Around 20–25% of infected individuals develop clinical manifestations. Majority of them develop self-limiting West Nile fever with acute onset of fever, headache, malaise, weakness. Macular rash appears towards defervescence, over torso and extremities and usually sparing the palm and sole.

The neurologic manifestations can be meningitis, encephalitis or paralysis. WNV meningitis is manifested by abrupt onset of fever, headache, meningeal signs. Severity of encephalitis ranges from disorientation to severe encephalopathy, coma and death.

Paralysis in WNV infection occurs due to destruction of anterior horn cells of the spinal cord leading to poliomyelitis like acute, asymmetrical flaccid paralysis. Involvement of other organs may manifest as choroiditis, myocarditis, hepatitis, pancreatitis, etc.

LAB DIAGNOSIS

 Serology: Detection of WNV-specific IgM antibody by IgM capture ELISA in CSF or serum is the mainstay of diagnosis. In patients with symptoms of neuroinvasive disease, IgM antibody in CSF is usually positive by the time symptoms appear, whereas in other patients it may take 8 days to develop. In serum, IgM may persist for 12–16 months after subsidence of symptoms. Therefore, IgM positivity in serum of asymptomatic patients may not be due to acute infection and can be due to past infection. However, demonstration of serocon version is diagnostic.

WNV infection can also be diagnosed by demonstration of fourfold change of antibody titer by hemagglutination inhibition (HAI), complement fixation test (CFT) or plaque reduction neutralization test (PRNT). However, these tests are not useful for patient diagnosis as they require both acute and convalescent serum samples at 2–3 weeks interval.

Isolation: The virus can be isolated in suckling mice brain or cell culture system as applicable for other arboviruses.

Molecular test: Detection of WNV RNA by nucleic acid amplification tests such as RT-PCR, NASBA has been developed. Molecular detection tests are used mostly as an adjunct to MAC-ELISA and useful in early part of illness and in immunocompromised patients where antibody development is poor or in case of screening for blood transfusion.

TREATMENT AND PREVENTION

 Treatment of WNV infection is mainly supportive like other acute encephalitic syndrome. Several immunotherapeutic agents and antiviral have been tried but no definitive advantages have been reported.

So far no human vaccine is available, and currently there is no progress in vaccine trial because of its doubtful marketing potential. Prevention mainly depends on the reduction in infected mosquito population.

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