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Description

Western equine encephalitis (WEE) is a rare mosquito-borne viral disease caused by a alphavirus, which circulates between birds and Culex tarsalis mosquitoes, primarily in western North America. Western equine encephalitis virus is the causative agent of the relatively uncommon viral disease Western equine encephalitis.[1][2][3] Diagnosis is based on clinical presentation and confirmed via serologic testing or PCR. No specific antiviral therapy currently exists; management is supportive, including hospitalization for severe cases.[4][2]

Presentation

The presentation for individuals with WEE is as follows:[2] fever, headache, nausea, neck stiffness, myalgias, chills, malaise and vomiting.

Complications

As to the possible complications in WEE there are the following:[2] seizures, meningitis and coma.

Virology

An alphavirus of the family Togaviridae, the WEE virus is an arbovirus (arthropod-borne virus) transmitted by mosquitoes of the genera Culex and Culiseta.[1] WEE is a recombinant virus between two other alphaviruses, an ancestral Sindbis virus-like virus, and an ancestral Eastern equine encephalitis virus-like virus. There have been 700 confirmed cases in the U.S. since 1964. This virus contains an envelope that is made up of glycoproteins and nucleic acids. The virus is transmitted to people and horses by bites from infected mosquitoes (Culex tarsalis and Aedes taeniorhynchus) and birds during wet, summer months.[5][6]

Mechanism

In terms of the pathogenesis of WEE begins when the virus is inoculated into host by mosquito bite. The virus first replicates locally in lymph nodes before entering the bloodstream, causing a systemic infection. If the viral load is high enough, WEEV enters the blood-brain barrier to invade the CNS. Once inside the brain, the virus replicates rapidly within and destroys neurons and glial cells. This damage, combined with the subsequent massive infiltration of inflammatory cells and release of cytokines triggers severe swelling and inflammation of the brain.[7][2][8]

Diagnosis

In terms of the evaluation of WEE we find the following:[2] Computed tomography, MRI and lumbar puncture.

Differential diagnosis

As to the differential diagnosis we find that for WEE it would be the following:[2] Dengue, Herpes simplex encephalitis, Eastern equine encephalitis, Venezuelan equine encephalitis, Murray Valley encephalitis, Powassan Virus encephalitis, Enterovirus meningitis and Mycoplasma meningitis.

Prevention

There is currently no vaccine, therefore to avoid mosquito bites wear long sleeves, pants, and socks to cover your skin. Since mosquitoes can bite through thin fabrics, treat your clothes with repellents like permethrin, DEET, or other EPA-approved options to reduce the risk.[2]

Treatment

As to management of WEE there is no effective antiviral therapy, care is supportive.[2]

Epidemiology

According to the CDC, the geographic occurrence for this virus is almost worldwide, and tends to be more prevalent in places in and around swampy areas where human populations tend to be limited. In North America, WEE is seen primarily in U.S. states and Canadian provinces west of the Mississippi River.[5] The disease is also seen in countries of South America.[5]

History

WEE was discovered in 1930 when a number of horses in the San Joaquin Valley of California, U.S. died of a mysterious encephalitis. Karl Friedrich Meyer investigated but was not able to isolate the pathogen from necropsies of horses that had been dead for some time and needed samples from an animal in the earlier stages of disease. When the team heard of a horse that appeared to have encephalitis, they successfully isolated WEEV from the brain tissue.[9]

Research

In a 2025 article Harvard Medical School researchers have shown that a small number of mutations(one to three E2 glycoprotein substitutions are sufficient) in the spike protein of WEE virus can significantly alter its infectivity and virulence.These mutations may transform a benign strain into one capable of causing severe outbreaks in humans and horses.[10]

References

  1. 1.0 1.1 Ryan KJ; Ray CG, eds. (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 978-0-8385-8529-0.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 Simon, Leslie V.; Coffey, Ryan; Fischer, Michelle A. (2025). "Western Equine Encephalitis". StatPearls. StatPearls Publishing.
  3. "About Western Equine Encephalitis". Western Equine Encephalitis Virus. 17 May 2024. Retrieved 7 November 2025.
  4. "Western Equine Encephalitis". dhhs.ne.gov. Archived from the original on 31 August 2025. Retrieved 31 October 2025.
  5. 5.0 5.1 5.2 "Western Equine Encephalitis Fact Sheet - Minnesota Dept. of Health". www.health.state.mn.us. Archived from the original on 2019-01-21. Retrieved 2016-12-04.
  6. Strauss, J. H.; Strauss, E. G. (September 1994). "The alphaviruses: gene expression, replication, and evolution". Microbiological Reviews. 58 (3): 491–562. doi:10.1128/mr.58.3.491-562.1994. ISSN 0146-0749. PMC 372977. PMID 7968923.
  7. Chen, Zhuangzhuang; Li, Guozhong (February 2021). "Immune response and blood–brain barrier dysfunction during viral neuroinvasion". Innate Immunity. 27 (2): 109–117. doi:10.1177/1753425920954281. PMC 7882805. PMID 32903111.
  8. Salimi, Hamid; Cain, Matthew D.; Jiang, Xiaoping; Roth, Robyn A.; Beatty, Wandy L.; Sun, Chengqun; Klimstra, William B.; Hou, Jianghui; Klein, Robyn S. (11 February 2020). "Encephalitic Alphaviruses Exploit Caveola-Mediated Transcytosis at the Blood-Brain Barrier for Central Nervous System Entry". mBio. 11 (1): e02731–19. doi:10.1128/mBio.02731-19. ISSN 2150-7511. PMC 7018649. PMID 32047126.
  9. Sabin, Albert (1980). "Karl Friedrich Meyer: 1884–1974" (PDF). Biogr Mem Natl Acad Sci. 52. Washington, D.C.: 269–332. PMID 11620787. Archived (PDF) from the original on 2016-03-04. Retrieved 2025-05-28.
  10. Fan, Xiaoyi; Li, Wanyu; Oros, Jessica; Plante, Jessica A.; Mitchell, Brooke M.; Plung, Jesse S.; Basu, Himanish; Nagappan-Chettiar, Sivapratha; Boeckers, Joshua M.; Tjang, Laurentia V.; Mann, Colin J.; Brusic, Vesna; Buck, Tierra K.; Varnum, Haley; Yang, Pan; Malcolm, Linzy M.; Choi, So Yoen; Souza, William M. de; Chiu, Isaac M.; Umemori, Hisashi; Weaver, Scott C.; Plante, Kenneth S.; Abraham, Jonathan (29 May 2025). "Molecular basis for shifted receptor recognition by an encephalitic arbovirus". Cell. 188 (11): 2957–2973.e28. doi:10.1016/j.cell.2025.03.029. ISSN 0092-8674. PMC 12406711. PMID 40187345.