Systemic and Ophthalmic Manifestations of West Nile Virus Infection

Yos Priestley; Marcia Thiel; Steven B. Koevary


Expert Rev Ophthalmol. 2008;3(3):279-292. 

In This Article

Epidemiology & Risk Factors

West Nile virus was first isolated in the West Nile district of Uganda in 1937 from the blood of a febrile woman[3] and was first identified as a cause of meningoencephalitis during an outbreak in an Israeli nursing home in 1957. Since then, outbreaks have been reported throughout the world, with the first infection in the USA reported in August 1999 in the New York City (NY, USA) area.[4] While it is not known with certainty how the virus reached the western hemisphere, its close homology (>99.8%) to an isolate found in Israel suggests that it arrived from the Middle East.[5] Furthermore, the only strains of WNV found to be fatal in both birds and humans are found in the USA and Israel.[6]

Since its arrival in the USA, WNV has gradually spread westward. In 2000, 21 cases of disease were reported in three states on the East Coast and, by the following year, 66 cases were reported in ten states. In 2002, the number of virus infections and states affected jumped dramatically to 4156 and 39, respectively.[7] According to the US Centers for Disease Control (CDC) website, there have been a total of 27,573 reported cases of WNV infections since its initial incursion in 1999 through 2007, including 1083 fatalities in a total of 43 states.[92] It is estimated that over 750,000 have gone undiagnosed.[92]

General risk factors for contracting WNV include the time of year and geographical region. In temperate regions, incidence peaks in August or September owing to the high number of mosquitoes, while those living in the South appear to be at risk year-round because of their perennially warmer weather patterns. As mentioned previously, while the virus has been reported in most states, it is generally thought that risk increases for individuals who spend appreciable time in areas where mosquito-borne viruses are common, such as the East Coast and the Midwest. Individuals who work outdoors are also thought to be at an increased risk.[6,8,93]

Patients with the following conditions were reported to have an increased risk of developing severe WNV disease: diabetes mellitus, hypertension, HIV, rheumatoid arthritis, coronary disease, cancer, organ transplant recipients on immunosuppressive therapy, patients on mechanical ventilation, history of stroke, and alcoholism.[2,4,6,9,10,11] Patients with diabetes were also reported to be at increased risk of developing ischemic maculopathy.[12] Advanced age has also been linked to severe WNV disease.[4,6,13] A study by Chowers et al. found an elevated risk of neuroinvasive disease in patients 70 years of age or over.[14] Children have also been shown to be at greater risk primarily because they tend to spend more time outdoors during high-risk times of the year.[15] In keeping with the association of more severe disease with increasing age, children generally seem to experience fewer complications and morbidity from WNV infection than do adults greater than 18 years of age.[15]

A study by Glass et al. suggested that there might be a genetic basis for human susceptibility. A genetic mutation of CCR5, a chemokine receptor, results in the creation of the CCR5Δ32 allele. While this mutation was shown to be beneficial in protecting T cells from being infected by HIV,[16] the study by Glass et al. suggests that it also increases the risk of fatal WNV infection.[17] Among patients with confirmed WNV infection, 4-8% were homozygous for CCR5Δ32; by contrast, only approximately 1% of the general population in the USA is homozygous for the mutated allele.[18] Patients who are homozygous for CCR5Δ32 also had a higher mortality rate than those who did not carry the mutation. This mutation appears most commonly in Caucasian populations. In light of the foregoing, patients with HIV-1 who receive CCR5 antagonist therapy are at increased risk of developing severe WNV infection.[18]


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