St. Louis Encephalitis

Taxobox | color=violet
name = "St. Louis Encephalitis Virus"


image_caption =
virus_group = iv
familia = "Flaviviridae"
genus = "Flavivirus"
species = "St. Louis Encephalitis Virus"

St. Louis Encephalitis is a disease caused by the mosquito borne St. Louis Encephalitis virus. St. Louis encephalitis virus is related to Japanese encephalitis virus. This disease mainly affects the United States. Occasional cases have been reported from Canada and Mexico.

The name of the virus goes back to 1933 when within five weeks in autumn an encephalitis epidemic of explosive proportions broke out in the vicinity of St. Louis, Missouri and the neighboring St. Louis County. [Washington Post Magazine, October 8, 1933] Over 1,000 cases were reported to the local health departments and the newly constituted National Institute of Health was appealed to for epidemiological and investigative expertise. The previously unknown virus that caused the epidemic was isolated by the NIH team first in monkeys and then in white mice. [Edward A. Beeman: "Charles Armstrong, M.D.: A Biography", 2007 p. 305 also online [http://history.nih.gov/01Docs/historical/documents/ArmstrongBiography.pdf here (PDF)] ]

Mosquitoes, from the genus "Culex", become infected by feeding on birds infected with the St. Louis encephalitis virus. Infected mosquitoes then transmit the St. Louis encephalitis virus to humans and animals during the feeding process. The St. 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 St. Louis encephalitis virus. Once a human has been infected with the virus it is not transmissible from that individual to other humans.

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 3-30%, aged people are more likely to have a fatal infection.In the United States an average of 128 cases of St. Louis encephalitis are recorded annually. In temperate areas of the United States, St. Louis encephalitis cases occur primarily in the late summer or early fall. In the southern United States where the climate is milder St. Louis encephalitis can occur year round.

There is no vaccine or any other treatments specifically for St. Louis encephalitis virus.

Five evolutionary genetic studies of SLE virus have been published of which four [Kramer LD, Presser SB, Hardy JL, Jackson AO. (1997) Genotypic and phenotypic variation of selected Saint Louis encephalitis viral strains isolated in California. "American Journal of Tropical Medicine and Hygiene" 57(2):222–229. [http://www.ajtmh.org/cgi/content/abstract/57/2/222 Abstract] ] [Kramer LD, Chandler LJ. (2001) Phylogenetic analysis of the envelope gene of St. Louis encephalitis virus. "Archives of Virology" 146(12):2341–2355. doi: [http://dx.doi.org/10.1007/s007050170007 10.1007/s007050170007] ] [Twiddy SS, Holmes EC. (2003) The extent of homologous recombination in members of the genus "Flavivirus". "Journal of General Virology" 84:429-440. doi: [http://dx.doi.org/10.1099/vir.0.18660-0 10.1099/vir.0.18660-0] ] May FJ, Li L, Zhang S, Guzman H, Beasley DW, Tesh RB, Higgs S, Raj P, Bueno R Jr, Randle Y, Chandler L, Barrett AD. (2008) Genetic variation of St. Louis encephalitis virus. "Journal of General Virology" 89(8):1901-1910. doi: [http://dx.doi.org/10.1099/vir.0.2008/000190-0 10.1099/vir.0.2008/000190-0] ] focused on phylogeny, genetic variation, and recombination dynamics by sequencing the "envelope" protein gene and parts of other genes.

A recent evolutionary study [Baillie GJ, Kolokotronis SO, Waltari E, Maffei JG, Kramer LD, Perkins SL. (2008) Phylogenetic and evolutionary analyses of St. Louis encephalitis virus genomes. "Molecular Phylogenetics and Evolution" 47(2):717-728. doi: [http://dx.doi.org/10.1016/j.ympev.2008.02.015 10.1016/j.ympev.2008.02.015] ] 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 19^th century that corresponds to the split of the latest North American clade, suggesting a northwards colonization of SLE virus in the Americas. 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 on single codon coding for aminoacids belonging to the hypothesized "N"-linked glycosylation site of the "envelope" protein. Nevertheless, the latter can be due to selection "in vitro" (laboratory) rather than "in vivo" (host). In an independent study 14 out of 106 examined "envelope" gene sequences were found not to contain a specific codon at position 156 coding for this glycosylation site (Ser→Phe/Tyr).

References

*Centers for Disease Control and Prevention. [http://www.cdc.gov/ncidod/dvbid/arbor/sle_qa.htm CDC Answers Your Questions About St. Louis Encephalitis]

External links

* [http://www.encephalitisglobal.com Encephalitis Global Inc.] Offering information and support to encephalitis survivors, caregivers and loved ones.
* [http://www.emedicine.com/MED/topic3157.htm Online article at eMedicine.com] by Eleftherios Mylonakis, MD. (26 June, 2006)