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Journal of General Virology (1999), 80, 1949-1958.
© 1999 Society for General Microbiology


Animal: RNA Viruses

Genetic stability of equine arteritis virus during horizontal and vertical transmission in an outbreak of equine viral arteritis

Udeni B. R. Balasuriya1, Jodi F. Hedges1, Steven A. Nadler2, William H. McCollum3, Peter J. Timoney3 and N. James MacLachlan1

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

Author for correspondence: James MacLachlan.Fax +1 530 754 8124. e-mail njmaclachlan{at}ucdavis.edu

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 GS, GP3, GP4, GL, 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.




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