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Journal of virology1999; 73(5); 3672-3681; doi: 10.1128/JVI.73.5.3672-3681.1999

Genetic divergence with emergence of novel phenotypic variants of equine arteritis virus during persistent infection of stallions.

Abstract: The persistently infected carrier stallion is the critical natural reservoir of equine arteritis virus (EAV), as venereal infection of mares frequently occurs after breeding to such stallions. Two Thoroughbred stallions that were infected during the 1984 outbreak of equine viral arteritis in central Kentucky subsequently became long-term EAV carriers. EAV genomes amplified from the semen of these two stallions were compared by sequence analysis of the six 3' open reading frames (ORFs 2 through 7), which encode the four known structural proteins and two uncharacterized glycoproteins. The major variants of the EAV population that sequentially arose within the reproductive tract of each carrier stallion varied by approximately 1% per year, and the heterogeneity of the viral quasispecies increased during the course of long-term persistent infection. The various ORFs of the dominant EAV variants evolved independently, and there was apparently strong selective pressure on the uncharacterized GP3 protein during persistent infection. Amino acid changes also occurred in the V1 variable region of the GL protein. This region has been previously identified as a crucial neutralization domain, and selective pressures exerted on the V1 region during persistent EAV infection led to the emergence of virus variants with distinct neutralization properties. Thus, evolution of the EAV quasispecies that occurs during persistent infection of the stallion clearly can influence viral phenotypic properties such as neutralization and perhaps virulence.
Publication Date: 1999-04-10 PubMed ID: 10196259PubMed Central: PMC104142DOI: 10.1128/JVI.73.5.3672-3681.1999Google Scholar: Lookup
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  • Journal Article
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  • Non-U.S. Gov't
  • Research Support
  • U.S. Gov't
  • Non-P.H.S.
  • Research Support
  • U.S. Gov't
  • P.H.S.

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 article investigates the genetic changes that happen to the Equine Arteritis Virus (EAV) during long-term persistent infection in stallions, and how these mutations could impact the virus’s characteristics like disease-causing ability and how the immune system recognizes it.

Introduction

  • The study focuses on the Equine Arteritis Virus (EAV) that persists in infected carrier stallions – male horses. These horses serve as the natural reservoir for this virus.
  • Infection from these carrier stallions to mares often takes place via sexual transmission.
  • The study examined two Thoroughbred stallions that became long-term carriers of EAV after an outbreak in 1984 in central Kentucky.

Methods: Genetic Analysis

  • Researchers compared and analyzed EAV genomes amplified from the semen of the two carrier stallions.
  • They specifically examined six 3′ open reading frames (parts of the virus’s genes that can be translated into proteins) that encode four known structural proteins and two glycoproteins that are not yet fully characterized.

Findings: Genetic Variations

  • The major genetic variants of the EAV population within the reproductive tract of each stallion changed approximately 1% annually.
  • The diversity of the viral quasispecies – groups of viruses related by similar genetic makeup – increased during long-term persistent infection.
  • The evolution of these quasispecies has a clear influence on the characteristics of the virus.

Findings: Protein Evolution

  • The different genes of the dominant EAV variants evolved independently, with strong selective pressure specific to the uncharacterized GP3 protein.
  • Changes happened to the amino acids in the V1 variable region of the GL protein. This region is vital as it determines the neutralization domain – an area targeted by the immune system.
  • The selective pressures on the V1 region during persistent EAV infection led to the emergence of virus variants with unique neutralization properties.

Implications

  • The research implies that the genetic mutations happening to EAV during persistent infection can greatly influence the virus’s phenotypic attributes, such as its ability to neutralize and possibly its virulence – the severity or harmfulness of a disease.
  • This helps expand our understanding of how viruses adapt and evolve within their hosts and how these changes impact their potential threat to other individuals.

Cite This Article

APA
Hedges JF, Balasuriya UB, Timoney PJ, McCollum WH, MacLachlan NJ. (1999). Genetic divergence with emergence of novel phenotypic variants of equine arteritis virus during persistent infection of stallions. J Virol, 73(5), 3672-3681. https://doi.org/10.1128/JVI.73.5.3672-3681.1999

Publication

ISSN: 0022-538X
NlmUniqueID: 0113724
Country: United States
Language: English
Volume: 73
Issue: 5
Pages: 3672-3681

Researcher Affiliations

Hedges, J F
  • Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, California 95616, USA.
Balasuriya, U B
    Timoney, P J
      McCollum, W H
        MacLachlan, N J

          MeSH Terms

          • Amino Acid Sequence
          • Animals
          • Arterivirus Infections / epidemiology
          • Arterivirus Infections / veterinary
          • Arterivirus Infections / virology
          • Base Sequence
          • Carrier State
          • DNA, Viral
          • Disease Outbreaks
          • Equartevirus / classification
          • Equartevirus / genetics
          • Equartevirus / immunology
          • Genetic Variation
          • Horse Diseases / epidemiology
          • Horse Diseases / virology
          • Horses
          • Immunophenotyping
          • Male
          • Mice
          • Molecular Sequence Data
          • Neutralization Tests
          • Phenotype
          • Phylogeny
          • Semen / virology
          • Sequence Homology, Amino Acid
          • Viral Proteins / genetics
          • Virus Latency

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