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West Nile virus

Thursday 11 March 2004

Since the mid-1990s, West Nile virus (WNV) has emerged as a significant agent of arboviral encephalitis in several regions of the world.

In 1999, WNV was introduced into the northeastern United States and was associated with an outbreak of encephalitis affecting humans, birds and horses.

Subsequently, the virus has spread across the country, and across southern Canada, and in 2002 and 2003 was associated with the largest outbreaks of arboviral encephalitis recorded in the Western hemisphere.

Interestingly, the more recent spread of WNV into Mexico, Central America and the Caribbean has not been associated with the high levels of clinical disease observed in North America.

West Nile virus is an arthropod-borne virus (arbovirus) of the flavivirus group, which also includes viruses that cause dengue fever, Eastern encephalitis, and yellow fever.

West Nile virus has a broad geographic distribution in the Old World, with outbreaks in Africa, the Middle East, Europe, Southeast Asia, and Australia.

This virus was first detected in the United States in 1999 during an outbreak in New York City in which there were 62 cases of encephalitis and seven deaths.56,57 West Nile virus is transmitted by mosquitoes to birds and to mammals.

Wild birds develop prolonged viremia and are the major reservoir for the virus. Humans are usually incidental hosts. Virus has also been transmitted by transplanted organs.

West Nile virus infection is usually asymptomatic, but in 20% of infected individuals, it gives rise to a mild, short-lived febrile illness associated with headache and myalgia. A maculopapular rash is seen in approximately half the cases.

CNS complications (meningitis, encephalitis, meningoencephalitis) are not frequent, occurring in about one in 150 clinically apparent infections. They manifest as acute flaccid paralysis, clinically indistinguishable from polio.

There is a mortality of about 10% in patients with meningoencephalitis and long-term cognitive and neurologic impairment in many survivors. Perivascular and leptomeningeal chronic inflammation, microglial nodules, and neuronophagia predominantly involving the temporal lobes and brain stem have been observed in the brains of patients who died of West Nile virus infection.

Immunosuppressed persons and the elderly appear to be at the greatest risk for severe disease. Rare complications include hepatitis, myocarditis, and pancreatitis.

The pathogenesis of severe CNS disease is not yet clear. Limited studies in animal models suggest that West Nile virus envelope proteins may be important for CNS tropism and that macrophage depletion may predispose to CNS disease.


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- Beasley DW. Recent advances in the molecular biology of west nile virus. Curr Mol Med. 2005 Dec;5(8):835-50. PMID: 16375717

- Arroyo J, Miller CA, Catalan J, Monath TP. Yellow fever vector live-virus vaccines: West Nile virus vaccine development. Trends Mol Med. 2001 Aug;7(8):350-4. PMID: 11516995