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The probability of contracting these viruses and developing encephalitis vary widely among the different viruses with the incidence highest for the EEE virus and lowest for the VEE virus.
Because VEE virus has been recovered from pharyngeal cultures in 40% of patients[3] and aerosols of VEE virus have infected laboratory personnel, direct human-to-human transmission of VEE virus may be possible.
Kubes and Rios first isolated, identified, and named VEE virus, then sent the isolate to the United States for confirmation that the South American virus was antigenically distinct from the North American eastern and western equine encephalomyelitis viruses (5,6).
During epidemics and epizootics, VEE virus is transmitted rapidly among equines and from equines to humans by a variety of mosquito species.
VEE virus (VEEV; Togaviridae: Alphavirus) strains are categorized as either epizootic (associated with equine disease and major epidemics of human disease through equine amplification), or enzootic (not known to cause equine disease).
VEE virus subtype ID in Peru has not been previously associated with severe disease manifestations.
Virus isolates from horses in each location were nearly identical in sequence to 1995 isolates, which suggests natural persistence of subtype IC VEE virus (VEEV) strains in a genetically stable mode.