Saint Louis encephalitis

Saint Louis encephalitis
Electron micrograph of "Saint Louis encephalitis virus" seen in a mosquito salivary gland
SymptomsMild illness, including fever and headache.
(if severe) High fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions and spastic paralysis
CausesSaint Louis encephalitis virus
Diagnostic methodBlood test, spinal fluid test,clinical presentation
Differential diagnosisJapanese encephalitis,Herpes simplex encephalitis, Eastern equine encephalitis, Zika virus, Ehrlichiosis
PreventionNo vaccine
TreatmentSupportive care
Saint Louis encephalitis virus
Virus classification e
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Kitrinoviricota
Class: Flasuviricetes
Order: Amarillovirales
Family: Flaviviridae
Genus: Flavivirus
Species:
Saint Louis encephalitis virus
Synonyms
  • St. Louis encephalitis virus[1]
  • St. Louis virus[2]

Saint Louis encephalitis is a disease caused by the mosquito-borne Saint Louis encephalitis virus.[3]

Saint Louis encephalitis virus is related to Japanese encephalitis virus and is a member of the family Flaviviridae.[3] This disease mainly affects the United States, including Hawaii.[4]

Occasional cases have been reported from Canada, Mexico and the Caribbean, including the Greater Antilles, Trinidad and Tobago, and Jamaica.[4]

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. Elderly people are more likely to have a fatal infection.[5][6][7]

Cause

The cause of this condition is Saint Louis encephalitis virus, which is a Flavivirus, a single-stranded RNA virus .[6]Flaviviruses have positive-sense, single-stranded RNA genomes which are non-segmented and around 10–11 kbp in length.[8] In general, the genome encodes three structural proteins (Capsid, prM, and Envelope) and seven non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5).[9] The genomic RNA is modified at the 5′ end of positive-strand genomic RNA with a cap-1 structure (me7-GpppA-me2).[10]

Transmission

Culex pipiens

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.[11]

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. [12][13]

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,[12][13] though very rarely it has occurred via blood transfusion.

Mechanism

The pathophysiology of Saint Louis encephalitis occurs via replication in the local lymph nodes (near mosquito bite).[6]

In terms of family Flaviviridae replication, this happens via creating an antigenome as a template for genome RNA to be produced. Replication complexes are isolated in membranous structures inside the endoplasmic reticulum. Serine protease, an RNA helicase and an RNA-dependent RNA polymerase is among the enzymes (replication). As for virion assembly, this happens by budding through intracellular membranes. [14]

Diagnosis

In terms of the diagnosis of Saint Louis encephalitis the following is done when an individual is suspected of infection:[15]


Differential diagnosis

The DDx of this infection is as follows:[6]

Treatment

The management of this condition is limited to supportive care with intravenous fluids.[6]

There are no vaccines or any other treatments specifically for Saint Louis encephalitis virus, although one study showed that early use of interferon alfa-2b may decrease the severity of complications.[16]

Epidemiology

In the United States an average of more than 100 cases of Saint Louis encephalitis are recorded annually. In temperate areas of the United States, Saint Louis encephalitis cases occur primarily in the late summer. In the southern United States where the climate is milder Saint Louis encephalitis can occur year-round.[17][18]

History

St. Louis (city)

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.[19][20]

Over 1,000 cases were reported to the local health departments and the newly constituted National Institutes of Health of the United States was appealed to for epidemiological and investigative expertise.[21]

The previously unknown virus that caused the epidemic was isolated by the NIH team first in monkeys and then in white mice.[22]

Evolution

Five evolutionary genetic studies of SLE virus have been published of which four[23][24][25][26] focused on phylogeny, genetic variation, and recombination dynamics by sequencing the envelope protein gene and parts of other genes.A recent evolutionary study[27] 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.[28] 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 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[26] 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).

Another study estimated the evolutionary rate to be 4.1 × 10−4 substitutions/site/year (95% confidence internal 2.5-5.7 × 10−4 substitutions/site/year),[29] the virus seems to have evolved in northern Mexico and then spread northwards with migrating birds.

References

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  2. ICTV 5th Report Francki, R. I. B., Fauquet, C. M., Knudson, D. L. & Brown, F. (eds)(1991). Classification and nomenclature of viruses. Fifthreport of the International Committee on Taxonomy of Viruses. Archives of Virology Supplementum 2, p226 https://ictv.global/ictv/proposals/ICTV%205th%20Report.pdf Archived 2023-03-09 at the Wayback Machine
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