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Journal of virology1999; 73(5); 4266-4271; doi: 10.1128/JVI.73.5.4266-4271.1999

Genetic and phenotypic changes accompanying the emergence of epizootic subtype IC Venezuelan equine encephalitis viruses from an enzootic subtype ID progenitor.

Abstract: Recent studies have indicated that epizootic Venezuelan equine encephalitis (VEE) viruses can evolve from enzootic, subtype ID strains that circulate continuously in lowland tropical forests (A. M. Powers, M. S. Oberste, A. C. Brault, R. Rico-Hesse, S. M. Schmura, J. F. Smith, W. Kang, W. P. Sweeney, and S. C. Weaver, J. Virol. 71:6697-6705, 1997). To identify mutations associated with the phenotypic changes leading to epizootics, we sequenced the entire genomes of two subtype IC epizootic VEE virus strains isolated during a 1992-1993 Venezuelan outbreak and four sympatric, subtype ID enzootic strains closely related to the predicted epizootic progenitor. Analysis by maximum-parsimony phylogenetic methods revealed 25 nucleotide differences which were predicted to have accompanied the 1992 epizootic emergence; 7 of these encoded amino acid changes in the nsP1, nsP3, capsid, and E2 envelope glycoprotein, and 2 were mutations in the 3' untranslated genome region. Comparisons with the genomic sequences of IAB and other IC epizootic VEE virus strains revealed that only one of the seven amino acid changes associated with the 1992 emergence, a threonine-to-methionine change at position 360 of the nsP3 protein, accompanied another VEE virus emergence event. Two changes in the E2 envelope glycoprotein region believed to include the major antigenic determinants, both involving replacement of uncharged residues with arginine, are also candidates for epizootic determinants.
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Publication Date: 1999-04-10 PubMed ID: 10196323PubMed Central: PMC104206DOI: 10.1128/JVI.73.5.4266-4271.1999Google Scholar: Lookup
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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.

This research investigates the genetic alterations that may lead to the emergence of epidemic Venezuelan equine encephalitis (VEE) viruses from endemic forms. By comparing the genetic sequences of different VEE virus strains, the study found a number of significant nucleotide and amino acid changes which could be associated with the transformation of the virus.

Research Context and Methods

  • The researchers focused on understanding the evolution of epidemic Venezuelan equine encephalitis (VEE) viruses from endemic, subtype ID strains. The latter are known to circulate continuously in lowland tropical forests.
  • The entire genomes of two subtype IC epidemic VEE virus strains, isolated during a 1992-1993 outbreak in Venezuela, were sequenced. These were compared to four sympatric, subtype ID endemic strains believed to be closely related to the predicted epidemic progenitor.
  • Using maximum-parsimony phylogenetic methods, the researchers analysed the differences between these strains to identify the mutations associated with the change into epidemic strains.

Key Findings

  • The analysis revealed 25 different nucleotide mutations which were predicted to have accompanied the emergence of a 1992 epidemic. Among these, 7 were found to encode amino acid changes in four important components: nsP1, nsP3, the capsid, and E2 envelope glycoprotein.
  • Two mutations were located in the 3′ untranslated genome region. This part of the genome does not produce any protein on its own but has significant roles in other processes like nuclear export, translation and genome packaging.
  • Comparisons with the genomic sequences of other epidemic VEE viruses, such as IAB and other IC strains, showed that only one of the seven amino acid changes found in the 1992 epidemic, a threonine-to-methionine modification at position 360 of the nsP3 protein, accompanied another VEE virus emergence event.
  • Two other changes in the E2 envelope glycoprotein region – an area thought to include the major antigenic determinant – may also be linked to the development of epidemic disease. These changes both involve the replacement of uncharged residues with arginine.

Implications and Conclusions

  • The researchers identified certain genetic alterations that are likely associated with the transition of the VEE virus from being endemic to becoming epidemic. This understanding could be instrumental for future interventions to control virus transmission and potentially prevent future outbreaks.
  • This research also contributes to our overall understanding of virus evolution and how viruses might diverge from their ancestral strains to trigger larger-scale disease outbreaks.

Cite This Article

APA
Wang E, Barrera R, Boshell J, Ferro C, Freier JE, Navarro JC, Salas R, Vasquez C, Weaver SC. (1999). Genetic and phenotypic changes accompanying the emergence of epizootic subtype IC Venezuelan equine encephalitis viruses from an enzootic subtype ID progenitor. J Virol, 73(5), 4266-4271. https://doi.org/10.1128/JVI.73.5.4266-4271.1999

Publication

Journal of virology
ISSN: 0022-538X
NlmUniqueID: 0113724
Country: United States
Language: English
Volume: 73
Issue: 5
Pages: 4266-4271

Researcher Affiliations

Wang, E
  • Center for Tropical Diseases and Department of Pathology, University of Texas Medical Branch, Galveston, Texas 77555-0609, USA.
Barrera, R
    Boshell, J
      Ferro, C
        Freier, J E
          Navarro, J C
            Salas, R
              Vasquez, C
                Weaver, S C

                  MeSH Terms

                  • Amino Acid Sequence
                  • Animals
                  • Base Sequence
                  • Cell Line
                  • Cricetinae
                  • DNA, Viral
                  • Disease Outbreaks / veterinary
                  • Encephalitis Virus, Venezuelan Equine / classification
                  • Encephalitis Virus, Venezuelan Equine / genetics
                  • Encephalomyelitis, Venezuelan Equine / epidemiology
                  • Encephalomyelitis, Venezuelan Equine / veterinary
                  • Horse Diseases / epidemiology
                  • Horse Diseases / virology
                  • Horses
                  • Molecular Sequence Data
                  • Phenotype
                  • Phylogeny
                  • Sequence Analysis

                  Grant Funding

                  • AI39800 / NIAID NIH HHS

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