The VEE virus strain that is pathogenic for humans is amplified in horses with equine disease occurring prior to human disease.
VEE virus typically cycles among rodents and the mosquito Culex melanoconion (birds may also be involved in some cycles).
The great Atacama Desert stretches along the Pacific coast from northern Chile and along coastal Peru nearly to the border with Ecuador; rare, but occasional, rainfall interrupts the barrenness of this parched, hostile environment permitting infrequent but noteworthy incursions of mosquitoes and epizoodemic VEE virus (4).
L) Historically, VEE virus has been a pathogen studied for aerosol release as a potential biologic weapon.
Human infections with VEE virus subtype IAB and IC produce more neurologic involvement and result in mortality rates as high as 0.
VEE virus was isolated from serum culture in Vero cells.
Equines serve as highly efficient amplification hosts for mosquitoborne transmission of 2 VEE virus
(VEEV) epidemic subtypes, IAB and IC.
The etiologic agent is VEE virus
(VEEV), a positive-sense RNA virus in the family Togaviridae and genus Alphavirus.
To assess the impact of continuing circulation of VEE virus
(VEEV) on human and animal populations, serologic and viral isolation studies were conducted in 2000 to 2001 in Chiapas State.
Localization of a protective epitope on a Venezuelan equine encephalomyelitis (VEE) virus peptide that protects mice from both epizootic and enzootic VEE virus
challenge and it immunogenic in horses.