Saint Louis encephalitis is a disease caused by the mosquito-borne Saint Louis encephalitis virus. Saint Louis encephalitis virus is related to Japanese encephalitis virus and is a member of the family Flaviviridae. This disease mainly affects the United States, including Hawaii. Occasional cases have been reported from Canada, Mexico and the Caribbean, including the Greater Antilles, Trinidad and Tobago, and Jamaica. Signs and symptoms The majority of infections result in mild illness, including fever and headache. When infection is more severe the person may experience headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions and spastic paralysis. Fatality ranges from . Elderly people are more likely to have a fatal infection. Transmission Mosquitoes, primarily from the genus Culex, become infected by feeding on birds infected with the Saint Louis encephalitis virus. The most common vector of this disease within the genus Culex is Culex pipiens, also known as the common house mosquito. Infected mosquitoes then transmit the Saint Louis encephalitis virus to humans and animals during the feeding process. The Saint Louis encephalitis virus grows both in the infected mosquito and the infected bird, but does not make either one sick. Only infected mosquitoes can transmit Saint Louis encephalitis virus. Once a human has been infected with the virus it is not transmissible from that individual to other humans. Genetics Five evolutionary genetic studies of SLE virus have been published of which four focused on phylogeny, genetic variation, and recombination dynamics by sequencing the envelope protein gene and parts of other genes. A recent evolutionary study based on 23 new full open reading frame sequences (near-complete genomes) found that the North American strains belonged to a single clade. Strains were isolated at different points in time (from 1933 to 2001) which allowed for the estimation of divergence times of SLE virus clades and the overall evolutionary rate. Furthermore, this study found an increase in the effective population size of the SLE virus around the end of the 19th century that corresponds to the split of the latest North American clade, suggesting a northwards colonization of SLE virus in the Americas, and a split from the ancestral South American strains around 1892. Scans for natural selection showed that most codons of the SLE virus ORF were evolving neutrally or under negative selection. Positive selection was statistically detected only at one single codon coding for amino acids belonging to the