Venezuelan equine encephalitis virus

Venezuelan equine encephalitis virus
Virus classification
Group:	Group IV ((+)ssRNA)
Family:	Togaviridae
Genus:	Alphavirus
Species:	Venezuelan equine encephalitis virus

Venezuelan equine encephalitis virus
Classification and external resources
ICD-10	A92.2
ICD-9	066.2
MeSH	D004685

Venezuelan equine encephalitis virus is a mosquito-borne viral pathogen that causes Venezuelan equine encephalitis or encephalomyelitis (VEE). VEE can affect all equine species, such as horses, donkeys, and zebras. After infection, equines may suddenly die or show progressive central nervous system disorders. Humans also can contract this disease. Healthy adults who become infected by the virus may experience flu-like symptoms, such as high fevers and headaches. People with weakened immune systems and the young and the elderly can become severely ill or die from this disease.

The virus that causes VEE is transmitted primarily by mosquitoes that bite an infected animal and then bite and feed on another animal or human. The speed with which the disease spreads depends on the subtype of the VEE virus and the density of mosquito populations. Enzootic subtypes of VEE are diseases endemic to certain areas. Generally these serotypes do not spread to other localities. Enzootic subtypes are associated with the rodent-mosquito transmission cycle. These forms of the virus can cause human illness but generally do not affect equine health.

Epizootic subtypes, on the other hand, can spread rapidly through large populations. These forms of the virus are highly pathogenic to equines and can also affect human health. Equines, rather than rodents, are the primary animal species that carry and spread the disease. Infected equines develop an enormous quantity of virus in their circulatory system. When a blood-feeding insect feeds on such animals, it picks up this virus and transmits it to other animals or humans. Although other animals, such as cattle, swine, and dogs, can become infected, they generally do not show signs of the disease or contribute to its spread.

The virion is spherical and approximately 70 nm in diameter. It has a lipid membrane with glycoprotein surface proteins spread around the outside. Surrounding the nuclear material is a nucleocapsid that has an icosohedral symmetry of T = 4, and is approximately 40 nm in diameter.

Viral subtypes

Serology testing performed on this virus has shown the presence of six different subtypes (classified I to VI). These have been given names, including Mucambo, Tonate, and Pixuna subtypes. There are seven different variants in subtype I, and three of these variants, A, B, and C are the epizootic strains.

Venezuelan equine encephalitis outbreaks

Outbreaks of Venezuelan equine encephalitis virus occurred in Central American and South American countries. This virus was isolated in 1938, and outbreaks have been reported in many different countries since then. Mexico, Colombia, Venezuela, and the United States are just some of the countries that have reported outbreaks. Between December 1992 and January 1993, the Venezuelan state of Trujillo experienced an outbreak of this virus. Overall, 28 cases of the disease were reported along with 12 deaths. June 1993 saw a bigger outbreak, as 55 humans died as well as 66 equine deaths. A much larger outbreak in Venezuela and Colombia occurred in 1995. On May 23, 1995, equine encephalitis-like cases were reported in the northwest portion of the country. Eventually, the outbreak spread more towards the north as well as to the south. The outbreak caused about 11,390 febrile cases in humans as well as 16 deaths. About 500 equine cases were reported with 475 deaths. An outbreak of this disease occurred on Colombia in September 1995. This outbreak resulted in 14,156 human cases that were attributable to Venezuelan equine encephalitis virus with 26 human deaths. A possible explanation for the serious outbreaks was the particularly heavy rain that had fallen. This could have caused increased numbers of mosquitoes that could serve as vectors for the disease. A more likely explanation is that deforestation caused a change in mosquito species. Culex taenopius mosquitos, which prefer rodents, were replaced by Ochlerotatus taeniorhynchus mosquitos, which are more likely to bite humans and large equines.

Use as a biological weapon

When the U.S. biological warfare program ended in 1969, VEE virus was one of seven standardized biological weapons it had developed.^[1]

Recent news

In April, 2009, the U.S. Army Medical Research Institute of Infectious Diseases at Fort Detrick reported that samples of Venezuelan equine encephalitis virus were discovered missing during an inventory of a group of samples left by a departed researcher. The report stated the samples were likely among those destroyed when a freezer malfunctioned.

Notes

1. ^ Croddy, Eric C. and Hart, C. Perez-Armendariz J., Chemical and Biological Warfare, (Google Books), Springer, 2002, pp. 30-31, (ISBN 0387950761), accessed October 24, 2008.

References

• APHIS. 1996. Venezuelan Equine Encephalomyelitis

"PAHO: Equine Encephalitis in the Event of a Disaster". http://www.paho.org/English/DD/PED/te_equi.htm. Retrieved 2007-03-17.  "PAHO Epidemiological Bulletin: Outbreak of Venezuelan Equine Encephalities". http://www.paho.org/english/sha/epibul_95-98/be954out.htm. Retrieved 2007-03-17.  "PATHINFO: Venezuelan Equine Encephalitis Virus". http://pathport.vbi.vt.edu/pathinfo/pathogens/VEEV_complex_Info.shtml. Retrieved 2007-03-17. 

• Esparza J, Sánchez A (1975). "Multiplication of Venezuelan Equine Encephalitis (Mucambo) virus in cultured mosquito cells". Arch Virol 49 (2–3): 273–80. doi:10.1007/BF01317545. PMID 813617. 

"Army: 3 vials of virus samples missing from Maryland facility". CNN. 2009-04-22. http://www.cnn.com/2009/US/04/22/missing.virus.sample/index.html. Retrieved 2009-04-23.