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| Saint Louis encephalitis virus | |
|---|---|
_virus_EM_PHIL_1871_lores.JPG) | |
| Electron micrograph of Saint Louis encephalitis virus seen in amosquitosalivary gland | |
Virus classification | |
| (unranked): | Virus |
| Realm: | Riboviria |
| Kingdom: | Orthornavirae |
| Phylum: | Kitrinoviricota |
| Class: | Flasuviricetes |
| Order: | Amarillovirales |
| Family: | Flaviviridae |
| Genus: | Orthoflavivirus |
| Species: | Orthoflavivirus louisense |
| Synonyms | |
| Saint Louis encephalitis | |
|---|---|
| Specialty | Infectious diseases  |
Saint Louis encephalitis is a disease caused by themosquito-borneSaint Louis encephalitis virus. Saint Louis encephalitis virus is a member of the familyFlaviviridae related toWest Nile virus andJapanese encephalitis virus. Saint Louis encephalitis virus is endemic to the New World and is present from southern Canada to Argentina, from the east coast and west coast of the United States, and in the Caribbean Islands.[3]
In 1933, an outbreak of encephalitis occurred inSt. Louis,Missouri, and the neighboringSt. Louis County[4] with over 1,000 cases reported and 197 deaths.[5] The newly constitutedNational Institutes of Health of the United States was appealed to for epidemiological and investigative expertise.[5] The previously unknown virus that caused the epidemic was isolated by the NIH team first in monkeys and then in white mice.[6]
Several human epidemics of Saint Louis encephalitis with more than 100 cases occurred between 1937 and 1990 inIllinois,Indiana,Ohio,Missouri,Mississippi,Texas, andFlorida.[3]
On August 8, 2001, an outbreak of this disease prompted an emergency alert in Louisiana after 63 cases were reported.[7]
SinceWest Nile virus was introduced to the United States, incidence of Saint Louis encephalitis has decreased significantly and, in some parts of the United States, West Nile virus has replaced Saint Louis encephalitis virus.[8]
The majority of infections do not result in disease[3][8] or cause mild illness, includingfever andheadache. In more severe cases, symptoms may include headache, high fever, neck stiffness,stupor, disorientation,coma, tremors, occasional convulsions and spasticparalysis. Case fatality rate ranges from4–27%.[8] Severe cases are more likely in individuals over 75 years old who were not previously exposed to infection.[3]
There are novaccines or treatments specifically for Saint Louis encephalitis, although one study showed that early use ofinterferon alfa-2b may decrease the severity of complications.[9]
Saint Louis encephalitis virus circulates betweenmosquitoes, primarily from the genusCulex, andbirds, mainly in the ordersPasseriformes andColumbiformes.[3][10] The most common vector of this disease within the genusCulex isCulex pipiens, also known as the common or northern house mosquito,[11] andCulex quinquefasciatus, the southern house mosquito.[3][10] Other Culex vectors includeCulex tarsalis, primarily in the western United States, andCulex nigripalpis in Florida.[10] The Saint Louis encephalitis virus requires temperatures above 22°C to replicate in mosquitoes.[3]
Humans are dead end hosts for Saint Louis encephalitis virus, while infected mosquitoes can transmit the Saint Louis encephalitis virus to humans during the feeding process, humans cannot transmit the virus back into a mosquito.[10]
Between 1976 and 2001, an average of 57 cases of Saint Louis encephalitis were recorded by the CDC.[3] Between 2003 and 2023, an average of 14 cases of Saint Louis encephalitis cases were recorded by the CDC.[12] Human cases of Saint Louis encephalitis occur primarily in the late summer or early fall. Urban outbreaks are more likely to occur when a dry summer follows a warmer spring and water remains pooled in drainage systems where Culex breed.[3]
Five evolutionary genetic studies of SLE virus have been published of which four[13][14][15][16] focused onphylogeny,genetic variation, andrecombination dynamics by sequencing theenvelope protein gene and parts of other genes.
A recent evolutionary study[17] based on 23 new fullopen reading frame sequences (near-completegenomes) found that theNorth American strains belonged to a singleclade. 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 theeffective 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 theAmericas, and a split from the ancestral South American strains around 1892.[18] Scans for natural selection showed that mostcodons of the SLE virusORF were evolvingneutrally or undernegative selection. Positive selection was statistically detected only at one single codon coding foramino acids belonging to the hypothesizedN-linkedglycosylation site of theenvelope protein. Nevertheless, the latter can be due to selectionin vitro (laboratory) rather thanin vivo (host). In an independent study, 14 out of 106 examinedenvelope gene sequences were found not to contain a specific codon at position 156 coding for this glycosylation site (Ser→Phe/Tyr).[16]
Another study estimated the evolutionary rate to be4.1 × 10−4 substitutions/site/year (95% confidenceinternal 2.5-5.7 × 10−4 substitutions/site/year).[19]
