West Nile virus, that is. A widespread outbreak in the U.S. has attracted renewed attention to the virus, which acquired its name from West Nile, Uganda, although there is no evidence that it originated there. Unfair, isn’t it? The virus was first isolated in Omogo, West Nile district, Uganda, in 1937, by researchers at the Yellow Fever Research Institute, then based in Entebbe. According to a 1940 article by Smithburn et al. in the American Journal of Tropical Medicine and Hygiene:
In attempting to isolate virus numerous persons were seen who were suffering either from an illness suggesting yellow fever, or from pyrexia of unknown cause. From many such persons blood was drawn, and as soon as possible thereafter the serum was in oculated intracerebrally2 into mice. Subinoculations were done from mice which became ill. In this manner several transmissible infective agents were isolated.
The purpose of this paper is to report the isolation of one such agent, which we call the West Nile virus, and to describe some of its properties. Although this virus was isolated from the blood of a human being, the circumstances of its isolation were such that nothing is known regarding the illness produced by the virus in the human subject.
That the virus was identified in West Nile should, if anything, be a testament to the medical contributions that have been made from the region, but it is more likely to have inspired notoriety. West Nile virus outbreaks have occurred all over the world, but the virus was not identified in North America until 1999.
West Nile virus is carried by mosquitoes, which acquire the virus from infected birds. In rare cases (only about 1 in 150 cases), severe viral infection is characterized by “high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, vision loss, numbness and paralysis“, according to the CDC. Up to 80% of those infected, however, do not experience any symptoms.
Current map of West Nile activity in the U.S.: