Saint Louis encephalitis

Saint Louis encephalitis is a disease caused by the mosquito-borne Saint Louis encephalitis virus. Saint Louis encephalitis virus is a member of the family Flaviviridae related to West Nile virus and Japanese 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 in St. Louis, Missouri, and the neighboring St. Louis County^[4] with over 1,000 cases reported and 197 deaths.^[5] The newly constituted National 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 in Illinois, Indiana, Ohio, Missouri, Mississippi, Texas, and Florida.^[3]

On August 8, 2001, an outbreak of this disease prompted an emergency alert in Louisiana after 63 cases were reported.^[7]

Since West 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, including fever and headache. In more severe cases, symptoms may include headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions and spastic paralysis. Case fatality rate ranges from 4–27%.^[8] Severe cases are more likely in individuals over 75 years old who were not previously exposed to infection.^[3]

There are no vaccines or treatments specifically for Saint Louis encephalitis, although one study showed that early use of interferon alfa-2b may decrease the severity of complications.^[9]

Saint Louis encephalitis virus circulates between mosquitoes, primarily from the genus Culex, and birds, mainly in the orders Passeriformes and Columbiformes.^[3][10] The most common vector of this disease within the genus Culex is Culex pipiens, also known as the common or northern house mosquito,^[11] and Culex quinquefasciatus, the southern house mosquito.^[3][10] Other Culex vectors include Culex tarsalis, primarily in the western United States, and Culex 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 on phylogeny, genetic variation, and recombination dynamics by sequencing the envelope protein gene and parts of other genes.

Un estudio evolutivo reciente ^{[ 17 ]} basado en 23 nuevas secuencias completas de marcos de lectura abiertos ( genomas casi completos ) encontró que las cepas norteamericanas pertenecían a un único clado . Las cepas fueron aisladas en diferentes momentos (de 1933 a 2001) lo que permitió estimar los tiempos de divergencia de los clados del virus SLE y la tasa evolutiva general. Además, este estudio encontró un aumento en el tamaño efectivo de la población del virus SLE alrededor de finales del siglo XIX que corresponde a la división del clado norteamericano más reciente, lo que sugiere una colonización hacia el norte del virus SLE en las Américas , y una separación de las cepas ancestrales sudamericanas alrededor de 1892. ^{[ 18 ]} Los análisis de selección natural mostraron que la mayoría de los codones del ORF del virus SLE estaban evolucionando de manera neutral o bajo selección negativa . La selección positiva se detectó estadísticamente solo en un único codón que codifica para aminoácidos pertenecientes al sitio de glicosilación N -ligada hipotetizado de la proteína de envoltura . Sin embargo, esto último puede deberse a la selección in vitro (laboratorio) en lugar de in vivo (huésped). En un estudio independiente, se encontró que 14 de las 106 secuencias de genes de envoltura examinadas no contenían un codón específico en la posición 156 que codificara este sitio de glicosilación ( Ser→Phe/Tyr ). ^{[ 16 ]}

Otro estudio estimó que la tasa evolutiva era de 4,1 × 10⁻⁴ ^{sustituciones} /sitio/año ( intervalo de confianza del 95%: 2,5-5,7 × 10⁻⁴ ^{sustituciones} /sitio/año ). ^{[ 19 ]}

• United States Centers for Disease Control and Prevention. Saint Louis encephalitis.
• St. Louis Encephalitis at eMedicine
• The Encephalitis Society - A Global resource on Encephalitis
• "St. Louis encephalitis virus". NCBI Taxonomy Browser. 11080.