Venezuelan Equine Encephalitis Virus
Venezuelan equine encephalitis (VEE) is an alphavirus; other alphaviruses include eastern equine encephalitis, western equine encephalitis, Chikungunya fever, Semliki Forest disease, Barmah Forest fever, and Ross River fever. These viruses can be easily produced in large amounts and aerosolized for biological weapons purposes. As a biological agent, VEE viruses are relatively stable, and can potentially injury thousands. Additionally, the VEE virus is susceptible to genetic manipulations, which may enhance its infectiousness and virulence for biological weapons purposes.
There are more than a dozen different subtypes and varieties of the viruses belonging to the Venezuelan equine encephalitis (VEE) complex and eight serologically distinct types. The VEE viruses divide into two groups: epizootic and enzootic. Enzootic diseases affect small numbers of the animal population while epizootic diseases cause epidemics that transmit from animal to human hosts. The enzootic strains of VEE include subtypes I, varieties D-F, and subtypes II-VI usually affect equine in the tropical climate of Florida, Mexico, and South and Central America with rare human illness. Epizootic strains of VEE are subtype I, varieties A-B and C, and cause all severe outbreaks of illness in equiades (horses, mules, and donkeys) with humans a spillover hosts. The equine hosts act as an amplification host for the VEE virus, and mosquitoes spread the virus between equine hosts and to human hosts. In natural human epidemics, severe and often fatal encephalitis in Equidae always precedes that in humans.
History of VEE Virus
The Venezuelan equine encephalitis virus was first isolated and fully characterized in 1938. In 1943, the first description of VEE infection in humans was recorded. It was determined that specific human case was acquired as an aerosolized virus. In 1952, the first natural case of human VEE infection was reported in Colombia. The first human case of VEE in the US was reported in 1968.
In October 1962, an outbreak began with a clinical case of VEE documented in the Zulia state of Venezuela by Lake Maracaibo. The outbreak spread east and west. By the end of 1963, 14,000 human cases of VEE were documented in Venezuela and neighboring Colombia. Human cases continued to appear until 1966.
Another outbreak of VEE virus occurred between 1969 and 1972 that affected hundreds of thousands of equine and tens of thousands of humans. The virus spread from Central America to Mexico and into the Southern part of the United States. The last case of VEE infection was identified in the Guajira Peninsula region of Venezuela in 1973; afterwards, many experts speculated that the disease was extinct. Between December 1992 and December 1993, however, 26 cases of VEE infection were reported in Venezuela. Many humans in the area developed mild flu-like symptoms, and when tested, VEE antibodies were found in their blood samples.
In 1995, another outbreak of VEE struck western Venezuela and eastern Colombia. This was the first major outbreak of VEE in over two decades. The virus spread westwards through Falcon State into Zulia State. Between August and October, over 10,000 suspected cases of VEE were recorded with 11 deaths in Zulia State. In September and October 1995, a large number of human cases were reported in the La Guajira Department of Colombia. Throughout 1995, roughly 75,000 human cases were reported with fatalities surpassing 300.
History of VEE as a Biological Weapons Agent
All three equine encephalitis fevers, Venezuelan Equine Encephalitis, Western Equine Encephalitis, and Eastern Equine Encephalitis, are potential biological weapons agents. VEE is a particularly appealing agent due to its infectiousness (only 10-100 pathogens are needed to infect a person) and its effectiveness as an incapacitating agent. VEE infections are rarely fatal but cause severe symptoms similar to influenza and hence can be difficult to diagnose. Encephalitis fevers cause inflammation of the brain and long-term side effects such as nervous system damage. A potential biological attack using VEE virus would be through the aerosolized route, but would be most effective during periods when mosquitoes are most active. VEE can also be disseminated in a stable liquid or dried form.
The United States weaponized VEE as an offensive incapacitating agent before the termination of its biological weapons program. The Soviet Union also weaponized VEE as an incapacitating agent. According to Ken Alibek (formerly Kanatjan Alikbekov), the former deputy chief of Biopreparat, Soviet scientists experimented with splicing VEE genome into smallpox viruses. The results were a recombinant smallpox-VEE chimera virus that resembled smallpox under a microscope but produced different symptoms in its hosts. In 1959, a freeze-dried vile containing VEE was accidentally dropped by Soviet medical personnel in a stairwell and infected 20 laboratory staff. This laboratory accident and others demonstrate the infectiousness of aerosolized VEE.
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