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Journal of comparative pathology1994; 111(4); 383-388; doi: 10.1016/s0021-9975(05)80096-9

Resistance of castrated male horses to attempted establishment of the carrier state with equine arteritis virus.

Abstract: Twelve geldings all became infected when inoculated intranasally with the KY-84 strain of equine arteritis virus (EAV), a strain previously shown to be capable of establishing the carrier state in the stallion. With the exception of one animal that showed no effects other than pyrexia, all of the geldings developed clinical signs characteristic of equine viral arteritis (EVA). The geldings were febrile for varying periods within the range of 2-10 days after inoculation. Viraemia occurred from day 2 onwards, for periods varying from 9 to at least 19 days. Nasal shedding of virus began 2-4 days after inoculation and persisted for periods ranging from 7-14 days. All geldings "seroconverted" to EAV by day 11, with serum neutralization titres ranging from 8 to 64. The titres ranged from 8 to 32 after 4 weeks. Low concentrations of EAV were detected in the kidney and blood of one gelding killed 30 days after inoculation and in the blood of another killed after 57 days. Virus was not isolated from any tissue or fluid sample collected from the remaining 10 geldings, all of which were killed between days 30 and 148. The findings confirm that persistent EAV infection is unlikely to occur in geldings and support the results of previous studies, which demonstrated that testosterone plays an essential role in the establishment and maintenance of the carrier state.
Publication Date: 1994-11-01 PubMed ID: 7884055DOI: 10.1016/s0021-9975(05)80096-9Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This research studied the resistance of castrated male horses (geldings) to the equine arteritis virus (EAV), demonstrating that geldings are less likely to harbor a persistent infection of EAV due to the role of testosterone in the establishment and maintenance of the virus carrier state.

Study Method and Procedure

  • The authors tested the vulnerability of twelve geldings to EAV by intranasally inoculating them with the KY-84 strain of the virus. This strain had previously been shown to be capable of creating a persistent carrier state in stallions.
  • Following the inoculation, the researchers monitored the animals for clinical signs of equine viral arteritis (EVA), periods of fever or viremia (the presence of viruses in the blood), and nasal shedding of the virus. These observations were made to assess the course of infection and the body’s response to the virus.

Observations and Results

  • Except for one horse that only developed a fever, all of the geldings presented with characteristic clinical signs of EVA.
  • The infected geldings experienced periods of fever ranging from 2 to 10 days post inoculation. Viremia was observed from day 2 onwards, lasting between 9 to at least 19 days. Nasal shedding of the virus began 2-4 days after inoculation, indicating the period of active infection and potential contagion, and continued for 7 to 14 days.
  • All geldings had seroconverted to EAV by day 11, showing an immune response against the virus. The serum neutralization titres, a measure of the immune response, ranged from 8 to 64. After 4 weeks, the titres were between 8 and 32, indicating a gradual decrease in the immune response over time.
  • Trace amounts of EAV were found in the kidney and blood of one horse euthanized 30 days after inoculation, and in the blood of another horse euthanized after 57 days. However, no virus was isolated from any tissue or fluid sample collected from the remaining ten geldings, all of which were euthanized between days 30 and 148.

Research Conclusion

  • The researchers concluded that the lack of EAV persistence in geldings supports previous studies indicating testosterone’s essential role in establishing and maintaining the viral carrier state. This finding indicates that castrated male horses are less likely to become long-term carriers of EAV, potentially contributing to disease control strategies.

Cite This Article

APA
McCollum WH, Little TV, Timoney PJ, Swerczek TW. (1994). Resistance of castrated male horses to attempted establishment of the carrier state with equine arteritis virus. J Comp Pathol, 111(4), 383-388. https://doi.org/10.1016/s0021-9975(05)80096-9

Publication

ISSN: 0021-9975
NlmUniqueID: 0102444
Country: England
Language: English
Volume: 111
Issue: 4
Pages: 383-388

Researcher Affiliations

McCollum, W H
  • Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington 40546-0099.
Little, T V
    Timoney, P J
      Swerczek, T W

        MeSH Terms

        • Animals
        • Antibodies, Viral / blood
        • Arterivirus Infections / immunology
        • Arterivirus Infections / veterinary
        • Arterivirus Infections / virology
        • Carrier State / veterinary
        • Carrier State / virology
        • Equartevirus / immunology
        • Equartevirus / isolation & purification
        • Horse Diseases / immunology
        • Horse Diseases / virology
        • Horses
        • Male
        • Neutralization Tests
        • Orchiectomy / veterinary

        Citations

        This article has been cited 12 times.
        1. Carossino M, Dini P, Kalbfleisch TS, Loynachan AT, Canisso IF, Cook RF, Timoney PJ, Balasuriya UBR. Equine arteritis virus long-term persistence is orchestrated by CD8+ T lymphocyte transcription factors, inhibitory receptors, and the CXCL16/CXCR6 axis. PLoS Pathog 2019 Jul;15(7):e1007950.
          doi: 10.1371/journal.ppat.1007950pubmed: 31356622google scholar: lookup
        2. Nam B, Mekuria Z, Carossino M, Li G, Zheng Y, Zhang J, Cook RF, Shuck KM, Campos JR, Squires EL, Troedsson MHT, Timoney PJ, Balasuriya UBR. Intrahost Selection Pressure Drives Equine Arteritis Virus Evolution during Persistent Infection in the Stallion Reproductive Tract. J Virol 2019 Jun 15;93(12).
          doi: 10.1128/JVI.00045-19pubmed: 30918077google scholar: lookup
        3. Carossino M, Dini P, Kalbfleisch TS, Loynachan AT, Canisso IF, Shuck KM, Timoney PJ, Cook RF, Balasuriya UBR. Downregulation of MicroRNA eca-mir-128 in Seminal Exosomes and Enhanced Expression of CXCL16 in the Stallion Reproductive Tract Are Associated with Long-Term Persistence of Equine Arteritis Virus. J Virol 2018 May 1;92(9).
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        4. Carossino M, Loynachan AT, Canisso IF, Cook RF, Campos JR, Nam B, Go YY, Squires EL, Troedsson MHT, Swerczek T, Del Piero F, Bailey E, Timoney PJ, Balasuriya UBR. Equine Arteritis Virus Has Specific Tropism for Stromal Cells and CD8(+) T and CD21(+) B Lymphocytes but Not for Glandular Epithelium at the Primary Site of Persistent Infection in the Stallion Reproductive Tract. J Virol 2017 Jul 1;91(13).
          doi: 10.1128/JVI.00418-17pubmed: 28424285google scholar: lookup
        5. Sarkar S, Bailey E, Go YY, Cook RF, Kalbfleisch T, Eberth J, Chelvarajan RL, Shuck KM, Artiushin S, Timoney PJ, Balasuriya UB. Allelic Variation in CXCL16 Determines CD3+ T Lymphocyte Susceptibility to Equine Arteritis Virus Infection and Establishment of Long-Term Carrier State in the Stallion. PLoS Genet 2016 Dec;12(12):e1006467.
          doi: 10.1371/journal.pgen.1006467pubmed: 27930647google scholar: lookup
        6. Balasuriya UB, Go YY, MacLachlan NJ. Equine arteritis virus. Vet Microbiol 2013 Nov 29;167(1-2):93-122.
          doi: 10.1016/j.vetmic.2013.06.015pubmed: 23891306google scholar: lookup
        7. Go YY, Bailey E, Timoney PJ, Shuck KM, Balasuriya UB. Evidence that in vitro susceptibility of CD3+ T lymphocytes to equine arteritis virus infection reflects genetic predisposition of naturally infected stallions to become carriers of the virus. J Virol 2012 Nov;86(22):12407-10.
          doi: 10.1128/JVI.01698-12pubmed: 22933293google scholar: lookup
        8. Go YY, Bailey E, Cook DG, Coleman SJ, Macleod JN, Chen KC, Timoney PJ, Balasuriya UB. Genome-wide association study among four horse breeds identifies a common haplotype associated with in vitro CD3+ T cell susceptibility/resistance to equine arteritis virus infection. J Virol 2011 Dec;85(24):13174-84.
          doi: 10.1128/JVI.06068-11pubmed: 21994447google scholar: lookup
        9. Zhang J, Stein DA, Timoney PJ, Balasuriya UB. Curing of HeLa cells persistently infected with equine arteritis virus by a peptide-conjugated morpholino oligomer. Virus Res 2010 Jun;150(1-2):138-42.
        10. Zhang J, Timoney PJ, MacLachlan NJ, McCollum WH, Balasuriya UB. Persistent equine arteritis virus infection in HeLa cells. J Virol 2008 Sep;82(17):8456-64.
          doi: 10.1128/JVI.01249-08pubmed: 18579588google scholar: lookup
        11. Glaser AL, Chirnside ED, Horzinek MC, de Vries AA. Equine arteritis virus. Theriogenology 1997 Apr 15;47(6):1275-95.
          doi: 10.1016/s0093-691x(97)00107-6pubmed: 16728076google scholar: lookup
        12. Hedges JF, Balasuriya UB, Timoney PJ, McCollum WH, MacLachlan NJ. Genetic divergence with emergence of novel phenotypic variants of equine arteritis virus during persistent infection of stallions. J Virol 1999 May;73(5):3672-81.