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The Journal of general virology1992; 73 ( Pt 12); 3301-3305; doi: 10.1099/0022-1317-73-12-3301

Molecular evidence for the origin of the widespread Venezuelan equine encephalitis epizootic of 1969 to 1972.

Abstract: Venezuelan equine encephalitis (VEE) virus is a mosquito-borne pathogen that has caused encephalitis in equine species and humans during sporadic outbreaks in the western hemisphere. The last, and most widespread, VEE outbreak occurred in South America, Central America, Mexico and the U.S.A. (Texas) during 1969 to 1972. We have cloned and sequenced the genome of a virulent VEE subtype I-AB virus, strain 71-180, isolated in Texas in 1971. Thirty-four nucleotide differences were detected between the genome of 71-180 virus and that of the subtype I-AB Trinidad donkey (TRD) virus isolated during the 1943 VEE epizootic in Trinidad. Fifteen nucleotide changes occurred in the non-structural genes, 16 in the structural genes and three in the 3' non-coding region. Only six of the nucleotide differences resulted in amino acid substitutions: one change in each of non-structural proteins nsP1 and nsP3, two in the E2 envelope glycoprotein, one in the 6K polypeptide and one in the E1 envelope glycoprotein. The close genetic relationship between 71-180 virus and TRD virus, commonly used for production of formalin-inactivated VEE vaccines, suggests that incompletely inactivated virulent vaccine virus may have been the source of this and other VEE outbreaks. Use of formalized virulent virus was discontinued during the 1969 to 1972 panzootic. No VEE epizootics have been reported since the introduction of the live attenuated TC-83 vaccine virus.
Publication Date: 1992-12-01 PubMed ID: 1469368DOI: 10.1099/0022-1317-73-12-3301Google Scholar: Lookup
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  • Historical Article
  • Journal Article
  • Research Support
  • U.S. Gov't
  • Non-P.H.S.

Summary

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This study investigates the origin of the Venezuelan equine encephalitis (VEE) virus outbreak that took place from 1969 to 1972, by analyzing the genome of a specific VEE virus strain isolated in Texas in 1971. The research suggests that the incomplete inactivation viral matter from vaccines may have contributed to the recurrence of VEE virus.

Details of the Research

  • The research focusses on the Venezuelan equine encephalitis (VEE) virus, a mosquito-carried disease-causing organism that primarily affects horses but can also infect humans, causing encephalitis.
  • By studying the genome of a virulent VEE subtype I-AB virus (strain 71-180, from Texas in 1971), the team hoped to determine the source of the widespread outbreak of the disease from 1969 to 1972 which occurred in South America, Central America, Mexico, and Texas, USA.

Findings from the Research

  • Analyses found 34 nucleotide differences between the genome of the 71-180 virus and that of another VEE subtype I-AB virus called the Trinidad donkey (TRD) virus that was isolated during a 1943 outbreak in Trinidad. Of these, 15 occurred in the non-structural genes of the virus, 16 in the structural genes, and three in the 3′ non-coding region.
  • Only six of these nucleotide changes actually led to changes in the amino acids that form the proteins that make up the virus. These changes occurred in both non-structural proteins and those that make up the exterior ‘envelope’ of the virus.

Implications and Conclusions from the Research

  • The genetic similarity between the 71-180 virus and the Trinidad donkey (TRD) virus, which was commonly used for producing formalin-inactivated VEE vaccines, raises the possibility that incomplete inactivation of the virus in the vaccine may actually have been a source of the VEE outbreaks.
  • The use of formalin-inactivated virulent virus in vaccines was stopped during the 1969 to 1972 epidemic, and since the introduction of a live, attenuated virus vaccine (TC-83), no further major outbreaks of VEE have been reported.

Cite This Article

APA
Kinney RM, Tsuchiya KR, Sneider JM, Trent DW. (1992). Molecular evidence for the origin of the widespread Venezuelan equine encephalitis epizootic of 1969 to 1972. J Gen Virol, 73 ( Pt 12), 3301-3305. https://doi.org/10.1099/0022-1317-73-12-3301

Publication

ISSN: 0022-1317
NlmUniqueID: 0077340
Country: England
Language: English
Volume: 73 ( Pt 12)
Pages: 3301-3305

Researcher Affiliations

Kinney, R M
  • Division of Vector-Borne Infectious Diseases, Centers for Disease Control, Fort Collins, Colorado 80522-2087.
Tsuchiya, K R
    Sneider, J M
      Trent, D W

        MeSH Terms

        • Animals
        • Encephalitis Virus, Venezuelan Equine / genetics
        • Encephalitis Virus, Venezuelan Equine / pathogenicity
        • Encephalitis, Arbovirus / microbiology
        • History, 20th Century
        • Humans
        • North America
        • Sequence Homology, Amino Acid
        • Sequence Homology, Nucleic Acid
        • South America

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