Geographic distribution of Venezuelan equine encephalitis virus subtype IE genotypes in Central America and Mexico.

Abstract

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.Venezuelan equine encephalitis (VEE) virus, a member of the alphavirus genus of Togaviridae, is a major arboviral pathogen of the western hemisphere, causing large-scale outbreaks among humans and equines in tropical and subtropical regions of the Americas. 1 The VEE viruses have been classified into six major subtypes (I-VI) based on antigenic characteristics, with additional variants defined within subtypes I and III. 2 Variants IAB and IC are equine-virulent and have caused large equine outbreaks in northern South America throughout the latter two-thirds of the 20th century, including a 1969-1971 VEE virus subtype IAB epizootic that swept through Central America and Mexico, and into southern Texas in the United States. 3 The remaining VEE viruses (ID-IF and II-VI) are maintained in localized enzootic foci in close association with a preferred mosquito vector and small mammal host. The enzootic strains have traditionally been considered to be avirulent for equine species, based on experimental infections, but most are fully capable of causing human disease. 1 The VEE virus subtype IE has been isolated from mosquitoes or sentinel rodents in Mexico and throughout Central America. In the 1960s, there were several small-scale equine encephalitis outbreaks in northeastern Mexico, prior to the northward movement of VEE virus subtype IAB. 4,5 Although no etiologic agent was isolated, the outbreaks were clinically compatible with VEE virus etiology and it has been suggested that the local enzootic VEE virus IE strain was responsible. 5 In southeastern Mexico, human and equine VEE virus infections were detected serologically, 6-8 but virus isolates were obtained only from mosquitoes and from sentinel hamsters. 9 In 1993 and 1996, VEE virus subtype IE was isolated from diseased horses during two small-scale epizootics of equine encephalitis on the southwest coast of Mexico in Chiapas (1993) and Oaxaca (1996) states, resulting in a total of 160 known cases. The viruses isolated during those outbreaks were antigenically indistinguishable from other IE strains and partial nuc...

Positively Charged Amino Acid Substitutions in the E2 Envelope Glycoprotein Are Associated with the Emergence of Venezuelan Equine Encephalitis Virus

“…Previous data from partial PE2 sequences suggested that the enzootic isolate, 80U76, was the virus most closely related to the four epizootic IE virus strains (29). In contrast, our complete genomic sequences indicate that, in a pairwise comparison with the four epizootic Mexican IE viruses, enzootic strain 68U201 shared a greater nucleotide and amino acid sequence identity than the 1980 isolate that was made from the same sylvatic focus at La Avellana, Guatemala ( Table 1).…”

“…Previous sequencing studies of the N terminus of the PE2 envelope glycoprotein precursor gene of many enzootic and epizootic VEE subtype IE viruses indicated a high degree of genetic similarity (less than 1% nucleotide sequence divergence) between isolates obtained from the two recent Mexican outbreaks and enzootic isolates taken from sylvatic habitats on the Pacific Coast of Guatemala (29). Based on this high genetic similarity between enzootic and epizootic subtype IE VEEV, we hypothesized that the emergence of epizootic subtype IE viruses could have resulted in a similar manner as epizootic IAB or IC viruses, from enzootic progenitors.…”

The Use of Chimeric Venezuelan Equine Encephalitis Viruses as an Approach for the Molecular Identification of Natural Virulence Determinants

“…This is a significant finding considering that in 1993 and 1996, IE VEE viruses caused outbreaks of equine encephalitis in southern Mexico, with over 160 cases documented (21). Utilizing multiple approaches to characterize genotypic markers associated with virulence, chimeric viruses should be a useful approach for elucidating genetic determinants involved in pathogenesis, transmission, and evolution of the multiple subtypes and varieties of the VEE antigenic complex.…”

A DNA Vaccine for Venezuelan Equine Encephalitis Virus Delivered by Intramuscular Electroporation Elicits High Levels of Neutralizing Antibodies in Multiple Animal Models and Provides Protective Immunity to Mice and Nonhuman Primates

“…Naturally transmitted by mosquitoes through rodent hosts, VEEV is highly pathogenic for equines and humans and has sporadically caused widespread epidemics in North, Central, and South America (48). While most equine and human outbreaks have been caused by the epizootic IAB and IC subtypes of VEEV, isolated cases of disease caused in equines and humans by infection with the enzootic ID and IE subtypes have also been reported (10,32,50). Regardless of the variety, human infection with VEEV typically results in an acute, incapacitating, but self-limiting disease characterized by fever, headache, lymphopenia, myalgia, and malaise (3).…”