RESUMO
Phylogenetic analysis of 20 strains of Venezuelan equine encephalitis (VEE) virus subtype IE isolated from 1961 to 1996 in Mexico and throughout Central America showed that VEE virus subtype IE was monophyletic with respect to other VEE virus subtypes. Nonetheless, there were at least three distinct geographically separated VEE virus IE genotypes: northwestern Panama, Pacific coast (Mexico/Guatemala), and Gulf/Caribbean coast (Mexico/Belize). Strains from the Caribbean coast of Guatemala, Honduras, and Nicaragua may cluster with the Gulf/Caribbean genotype, but additional isolates from the region between Guatemala and Panama will be required to firmly establish their phylogenetic position. Viruses associated with two separate equine epizootics in Mexico in the 1990s were phylogenetically related to nonepizootic viruses from neighboring Guatemala and may represent the emergence or re-emergence of equine-virulent VEE virus subtype IE in Middle America.
Assuntos
Vírus da Encefalite Equina Venezuelana/classificação , Vírus da Encefalite Equina Venezuelana/genética , Encefalomielite Equina Venezuelana/veterinária , Doenças dos Cavalos/virologia , Adulto , Sequência de Aminoácidos , Animais , América Central , Criança , Vírus da Encefalite Equina Venezuelana/isolamento & purificação , Encefalomielite Equina Venezuelana/virologia , Cavalos , Humanos , Recém-Nascido , México , Dados de Sequência Molecular , Filogenia , Precursores de Proteínas/química , Precursores de Proteínas/genética , Proteínas do Envelope Viral/química , Proteínas do Envelope Viral/genéticaRESUMO
Venezuelan equine encephalitis (VEE) epidemics and equine epizootics occurred periodically in the Americas from the 1920s until the early 1970s, when the causative viruses, subtypes IAB and IC, were postulated to have become extinct. Recent outbreaks in Columbia and Venezuela have renewed interest in the source of epidemic/epizootic viruses and their mechanism of interepizootic maintenance. We performed phylogenetic analyses of VEE virus isolates spanning the entire temporal and geographic range of strains available, using 857-nucleotide reverse transcription-PCR products including the E3 and E2 genes. Analyses indicated that epidemic/epizootic viruses are closely related to four distinct, enzootic subtype ID-like lineages. One of these lineages, which occurs in Columbia, Peru, and Venezuela, also included all of the epidemic/epizootic isolates; the remaining three ID-like lineages, which occur in Panama, Peru, Florida, coastal Ecuador, and southwestern Columbia, were apparently not associated with epizootic VEE emergence. Within the Columbia/Peru/Venezuela lineage, three distinct monophyletic groups of epidemic/epizootic viruses were delineated, indicating that VEE emergence has occurred independently at least three times (convergent evolution). Representative, complete E2 amino acid sequences were compared to identify potential determinants of equine virulence and epizootic emergence. Amino acids implicated previously in laboratory mouse attenuation generally did not vary among the natural isolates that we examined, indicating that they probably are not involved in equine virulence changes associated with VEE emergence. Most informative amino acids correlated with phylogenetic relationships rather than phenotypic characteristics, suggesting that VEE emergence has resulted from several distinct combinations of mutations that generate viruses with similar antigenic and equine virulence phenotypes.