Genetic stability of equine arteritis virus during horizontal and vertical transmission in an outbreak of equine viral arteritis.
Abstract: An imported carrier stallion (A) from Europe was implicated in causing an extensive outbreak of equine viral arteritis (EVA) on a Warmblood breeding farm in Pennsylvania, USA. Strains of equine arteritis virus (EAV) present in the semen of two carrier stallions (A and G) on the farm were compared to those in tissues of foals born during the outbreak, as well as viruses present in the semen of two other stallions that became persistently infected carriers of EAV following infection during the outbreak. The 2822 bp segment encompassing ORFs 2-7 (nt 9807-12628; which encode the G(S), GP3, GP4, G(L), M and N proteins, respectively) was directly amplified by RT-PCR from semen samples and foal tissues. Nucleotide and phylogenetic analyses confirmed that virus present in the semen of stallion A initiated the outbreak. The genomes of viruses present in most foal tissues (10/11) and serum from an acutely infected mare collected during the outbreak were identical to that of virus present in the lung of the first foal that died of EVA. Virus in the placenta of one foal differed by one nucleotide (99.9% identity) from the predominant outbreak virus. The relative genetic stability of viruses that circulated during the outbreak contrasts markedly with the heterogeneous virus populations variously present in the semen of persistently infected stallions on the farm. These findings are consistent with the hypothesis that the carrier stallion can be a source of genetic diversity of EAV, and that outbreaks of EVA can be initiated by the horizontal aerosol transmission of specific viral variants that occur in the semen of particular carrier stallions.
Publication Date: 1999-08-31 PubMed ID: 10466790DOI: 10.1099/0022-1317-80-8-1949Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
- Research Support
- U.S. Gov't
- Non-P.H.S.
Summary
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The research study focuses on investigating the genetic stability of equine arteritis virus (EAV) during an outbreak of equine viral arteritis (EVA) in a breeding farm. The study identifies the source of the viral outbreak and establishes that carrier stallions can contribute to the genetic diversity of EAV.
Outbreak Initiation and Virus Comparison
- The study began by identifying that a stallion, imported from Europe, triggered an extensive EVA outbreak in a Pennsylvania breeding farm.
- Samples were collected from two already existing carrier stallions on the farm and compared with viral strains found in the foals born during the outbreak. This also included comparisons with viruses from stallions that became infected and subsequently carriers of the EAV during the outbreak.
Methodology and Analysis
- The researchers analyzed a specific segment of the virus – ORFs 2-7, directly amplified by RT-PCR from semen samples and foal tissues. This segment helps produce specific viral proteins, crucial for the virus’s structure and functioning.
- Through nucleotide and phylogenetic analyses, they were able to confirm that the virus present in Stallion A initiated the outbreak.
- In addition, the study found that most viral genomes present in the foal tissues and serum from a mare during the outbreak were identical to the first foal that died due to EVA.
Observations and Conclusion
- Interestingly, the virus found in the placenta of one foal was slightly different, differing by one nucleotide (99.9% identical) from the main outbreak virus.
- The researchers observed significant genetic stability in the outbreak viruses compared to the heterogeneous, or diverse, virus populations usually present in persistently infected stallions.
- This study, therefore, supports the theory that carrier stallions can be sources of genetic diversity of EAV, and specific viral variants present in the semen of such stallions can begin outbreaks of EVA through horizontal aerosol transmission.
Cite This Article
APA
Balasuriya UBR, Hedges JF, Nadler SA, McCollum WH, Timoney PJ, MacLachlan NJ.
(1999).
Genetic stability of equine arteritis virus during horizontal and vertical transmission in an outbreak of equine viral arteritis.
J Gen Virol, 80 ( Pt 8), 1949-1958.
https://doi.org/10.1099/0022-1317-80-8-1949 Publication
Researcher Affiliations
- Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine1, and Department of Nematology, College of Agriculture and Environmental Sciences2, University of California, Davis, CA 95616, USA.
- Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine1, and Department of Nematology, College of Agriculture and Environmental Sciences2, University of California, Davis, CA 95616, USA.
- Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine1, and Department of Nematology, College of Agriculture and Environmental Sciences2, University of California, Davis, CA 95616, USA.
- Department of Veterinary Science, Gluck Equine Research Center, University of Kentucky, Lexington, KY 40546, USA3.
- Department of Veterinary Science, Gluck Equine Research Center, University of Kentucky, Lexington, KY 40546, USA3.
- Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine1, and Department of Nematology, College of Agriculture and Environmental Sciences2, University of California, Davis, CA 95616, USA.
MeSH Terms
- Amino Acid Sequence
- Animals
- Arterivirus Infections / epidemiology
- Arterivirus Infections / transmission
- Arterivirus Infections / veterinary
- Arterivirus Infections / virology
- Base Sequence
- Carrier State
- DNA, Viral
- Disease Outbreaks
- Disease Transmission, Infectious
- Equartevirus / classification
- Equartevirus / genetics
- Genetic Heterogeneity
- Glycoproteins
- Horse Diseases / epidemiology
- Horse Diseases / transmission
- Horse Diseases / virology
- Horses
- Infectious Disease Transmission, Vertical
- Male
- Molecular Sequence Data
- Nucleocapsid Proteins / genetics
- Phylogeny
- Sequence Analysis
- Viral Envelope Proteins / genetics
- Viral Proteins / genetics
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