West Nile virus is a member of the flavivirus genus within the Japanese encephalitis antigenic complex of the family Flaviviridae [2]. It was first isolated in a woman in the West Nile district of Uganda in 1937 and later identified in birds in the Nile delta [2]. The virus is maintained in nature through a mosquito-bird-mosquito transmission cycle, with birds serving as reservoir hosts [2].
Disease overview
West Nile virus is a flavivirus responsible for substantial morbidity and mortality in birds, horses, and humans across multiple continents [1][2]. It was historically confined to Africa, Europe, the Middle East, and Asia, causing mainly mild febrile illness, but became more virulent and spread to North America in the late 1990s [1][2]. In the United States it is now the most common arboviral disease and has generated the three largest neuroinvasive outbreaks on record [3][4]. No licensed human vaccine exists, and prevention relies on mosquito control and exposure reduction [1][4].
Read the full clinical and epidemiological profile 6
Human infection is frequently asymptomatic but can range to rare encephalitis, paralysis, and death [1][2]. Among neuroinvasive disease cases in the United States, common acute symptoms include fever, nausea or vomiting, fatigue, headache, altered mental status, and focal weakness, with pooled mortality near 9% and frequent ICU admission [3]. West Nile fever develops in about 25% of infections with prolonged symptoms, while neuroinvasive disease occurs in under 1% but carries roughly 10% fatality and considerable long-term morbidity such as persistent weakness after paralysis [3][4].
WNV epidemics were originally localized to Europe, Africa, the Middle East, and parts of Asia, with human infections reported worldwide for over 50 years [1][2]. The 1999 introduction via New York produced a dramatic outbreak that spread across the continental United States and subsequently throughout the Americas [2][4]. The largest outbreaks occurred in Greece, Israel, Romania, Russia, and the USA, often along major bird migratory routes [2]. Since 1999 the contiguous US has reported 16,196 neuroinvasive cases and 1,549 deaths, with incidence highest in the Midwest from mid-July to early September [4].
Human infection most often follows bites from infected mosquitoes, which acquire the virus by feeding on viremic birds and later inject it via salivary glands during blood meals [2]. The virus is maintained in a mosquito-bird-mosquito cycle, with Culex mosquitoes as principal vectors and vertical transmission sustaining mosquito populations [2]. Less common routes include contact with infected animal tissues, organ transplant, blood transfusion, breast milk, and one reported transplacental case [2].
During outbreaks, emphasis shifts to aggressive adult mosquito control to lower abundances of infected biting mosquitoes [4].
- 1 Rossi SL et al. West Nile virus. Clin Lab Med. 2010 Mar. PMID: 20513541. doi: 10.1016/j.cll.2009.10.006. PubMed: https://pubmed.ncbi.nlm.nih.gov/20513541/
- 2 World Health Organization. West Nile virus [Internet]. cited 23 Oct 2026. Available from: https://www.who.int/news-room/fact-sheets/detail/west-nile-virus
- 3 Roberts JA et al. Clinical, Prognostic, and Longitudinal Functional and Neuropsychological Features of West Nile Virus Neuroinvasive Disease in the United States: A Systematic Review and Meta-Analysis. Ann Neurol. 2025 Jul. PMID: 40008684. doi: 10.1002/ana.27220. PubMed: https://pubmed.ncbi.nlm.nih.gov/40008684/
- 4 Petersen LR et al. West Nile virus: review of the literature. JAMA. 2013 Jul 17. PMID: 23860989. doi: 10.1001/jama.2013.8042. PubMed: https://pubmed.ncbi.nlm.nih.gov/23860989/
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Literature links are provided for discovery and do not alter or validate the surveillance series above.
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