Repeated emergence of epidemic/epizootic Venezuelan equine encephalitis from a single genotype of enzootic subtype ID virus.
Abstract: 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.
Publication Date: 1997-09-01 PubMed ID: 9261393PubMed Central: PMC191949DOI: 10.1128/JVI.71.9.6697-6705.1997Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
- Research Support
- U.S. Gov't
- P.H.S.
- Amino Acid Sequence
- Comparative Study
- Disease Etiology
- Disease Outbreaks
- Disease Transmission
- Epidemiology
- Equine Diseases
- Equine Health
- Equine Science
- Evolutionary Biology
- Genotyping
- Infectious Disease
- Molecular biology
- Pathogenesis
- Phylogenetic Analysis
- Public Health
- Veterinary Medicine
- Veterinary Research
- Virology
- Virus
Summary
This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.
The research article investigates the recurring emergence of Venezuelan equine encephalitis, known as VEE, from a single genotype of enzootic subtype ID virus. The study involves detailed phylogenetic analyses of VEE virus isolates across time and geography, and analyzes possible determinants for virus virulence and emergence.
Research Method
- The researchers carried out phylogenetic analyses on VEE virus isolates, which spanned across different timelines and geographic locations. For this, they used 857-nucleotide reverse transcription-PCR products, inclusive of the E3 and E2 genes.
- The main objective of this analysis was to examine how closely the epidemic/epizootic viruses were related to four distinct, enzootic subtype ID-like lineages.
Findings
- The analysis indicated that the epidemic/epizootic viruses were closely related to one of the subtypes, which was found in Columbia, Peru, and Venezuela. All the epidemic/epizootic isolates were included in this subtype, whereas the remaining three subtypes were not associated with the emergence of VEE.
- Within the Columbia/Peru/Venezuela lineage, three specific groups of epidemic/epizootic viruses were determined. This delineation showed that the emergence of VEE had occurred independently at least three times, indicating an occurrence of convergent evolution.
Amino Acid Analysis
- The researchers also compared representative, complete E2 amino acid sequences to identify possible determinants of the virus’s virulence and emergence in equines.
- They found that amino acids previously implicated in laboratory mouse attenuation generally did not vary among the natural isolates examined. This suggested that these amino acids are likely not involved in changes in equine virulence associated with VEE emergence.
- Most of the informative amino acids were found to correlate with the phylogenetic relationships rather than phenotypic characteristics. This suggests that VEE emergence resulted from several distinct combinations of mutations that produce viruses with similar antigenic and equine virulence phenotypes.
Cite This Article
APA
Powers AM, Oberste MS, Brault AC, Rico-Hesse R, Schmura SM, Smith JF, Kang W, Sweeney WP, Weaver SC.
(1997).
Repeated emergence of epidemic/epizootic Venezuelan equine encephalitis from a single genotype of enzootic subtype ID virus.
J Virol, 71(9), 6697-6705.
https://doi.org/10.1128/JVI.71.9.6697-6705.1997 Publication
Researcher Affiliations
- Center for Tropical Diseases, University of Texas Medical Branch, Galveston 77555, USA.
MeSH Terms
- Amino Acid Sequence
- Base Sequence
- Biological Evolution
- DNA, Viral
- Disease Outbreaks
- Encephalitis Virus, Venezuelan Equine / classification
- Encephalitis Virus, Venezuelan Equine / genetics
- Encephalomyelitis, Venezuelan Equine / epidemiology
- Encephalomyelitis, Venezuelan Equine / virology
- Genotype
- Molecular Sequence Data
- Phylogeny
- Sequence Homology, Amino Acid
- Viral Envelope Proteins / genetics
Grant Funding
- AI10984 / NIAID NIH HHS
- AI39508 / NIAID NIH HHS
- AI39800 / NIAID NIH HHS
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