Repeated emergence of epidemic/epizootic Venezuelan equine encephalitis from a single genotype of enzootic subtype ID virus

Ann M. Powers, M. Steven Oberste, Aaron C. Brault, Rebeca Rico-Hesse, Shannon M. Schmura, Jonathan F. Smith, Wenli Kang, William P. Sweeney, Scott Weaver

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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.

Original languageEnglish (US)
Pages (from-to)6697-6705
Number of pages9
JournalJournal of Virology
Volume71
Issue number9
StatePublished - 1997

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Venezuelan Equine Encephalomyelitides
encephalitis
Genotype
Venezuela
Horses
Peru
Viruses
horses
viruses
genotype
Virulence
Venezuelan Equine Encephalitis Viruses
Panama
Ecuador
virulence
Amino Acids
Reverse Transcription
Disease Outbreaks
Amino Acid Sequence
Venezuelan equine encephalitis virus

ASJC Scopus subject areas

  • Immunology

Cite this

Powers, A. M., Oberste, M. S., Brault, A. C., Rico-Hesse, R., Schmura, S. M., Smith, J. F., ... Weaver, S. (1997). Repeated emergence of epidemic/epizootic Venezuelan equine encephalitis from a single genotype of enzootic subtype ID virus. Journal of Virology, 71(9), 6697-6705.

Repeated emergence of epidemic/epizootic Venezuelan equine encephalitis from a single genotype of enzootic subtype ID virus. / Powers, Ann M.; Oberste, M. Steven; Brault, Aaron C.; Rico-Hesse, Rebeca; Schmura, Shannon M.; Smith, Jonathan F.; Kang, Wenli; Sweeney, William P.; Weaver, Scott.

In: Journal of Virology, Vol. 71, No. 9, 1997, p. 6697-6705.

Research output: Contribution to journalArticle

Powers, AM, Oberste, MS, Brault, AC, Rico-Hesse, R, Schmura, SM, Smith, JF, Kang, W, Sweeney, WP & Weaver, S 1997, 'Repeated emergence of epidemic/epizootic Venezuelan equine encephalitis from a single genotype of enzootic subtype ID virus', Journal of Virology, vol. 71, no. 9, pp. 6697-6705.
Powers AM, Oberste MS, Brault AC, Rico-Hesse R, Schmura SM, Smith JF et al. Repeated emergence of epidemic/epizootic Venezuelan equine encephalitis from a single genotype of enzootic subtype ID virus. Journal of Virology. 1997;71(9):6697-6705.
Powers, Ann M. ; Oberste, M. Steven ; Brault, Aaron C. ; Rico-Hesse, Rebeca ; Schmura, Shannon M. ; Smith, Jonathan F. ; Kang, Wenli ; Sweeney, William P. ; Weaver, Scott. / Repeated emergence of epidemic/epizootic Venezuelan equine encephalitis from a single genotype of enzootic subtype ID virus. In: Journal of Virology. 1997 ; Vol. 71, No. 9. pp. 6697-6705.
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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.",
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