FREE SHIPPING over $40
OVER 10000 FIVE-STAR REVIEWS
5% OFF ALL SUBSCRIPTIONS
100% HAPPINESS GUARANTEE
Analyze Diet
0
Journal of virology2012; 86(22); 12407-12410; doi: 10.1128/JVI.01698-12

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.

Abstract: We investigated the correlation between in vitro susceptibility of CD3(+) T lymphocytes to equine arteritis virus (EAV) infection and establishment of persistent infection among 14 stallions following natural infections. The data showed that carrier stallions with a CD3(+) T lymphocyte susceptibility phenotype to in vitro EAV infection may be at higher risk of becoming carriers than those that lack this phenotype (P = 0.0002).
Get Full Text
Publication Date: 2012-08-29 PubMed ID: 22933293PubMed Central: PMC3486460DOI: 10.1128/JVI.01698-12Google Scholar: Lookup
The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
LinkedInCopy
  • Journal Article
  • Research Support
  • Non-U.S. Gov't

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.

The study examines the relationship between the natural vulnerability of certain white blood cells (CD3(+) T lymphocytes) to equine arteritis virus (EAV) infection and the likelihood of horses developing a persistent infection after initial exposure to the virus.

Research Objective

  • The study aimed to explore the connection between the in vitro (in a controlled environment outside a living organism) susceptibility of certain white blood cells (CD3(+) T lymphocytes) to equine arteritis virus (EAV) infection and the predisposition of horses to develop a long-term infection following natural exposure to the virus.

Methodology

  • To achieve the objective, the researchers investigated 14 naturally infected stallions (male horses). The natural infections in these stallions served as actual biological settings for the study.

Results

  • The research showed that stallions whose CD3(+) T lymphocytes exhibited susceptibility to EAV infection in vitro were more likely to become carriers of the virus. In other words, these stallions developed a persistent infection rather than completely recovering after initial exposure.
  • The study findings showed a significant association (P=0.0002, signifying a very low probability that the results happened by chance) between the CD3(+) T lymphocyte susceptibility phenotype and the potential for a stallion to become a carrier of EAV. A ‘phenotype’ is the set of observable characteristics or traits resulting from the interaction of its genotype (set of genes) with the environment.
  • Stallions that did not display this phenotype (i.e., their CD3(+) T lymphocytes did not show in vitro vulnerability to EAV) were at a lower risk of becoming carriers.

Significance

  • The research findings could have important implications for understanding why some horses become carriers of EAV—a condition that can have serious health consequences for the horse population—while others can resist the virus.
  • If this genetic predisposition to becoming virus carriers can be identified through testing, it could potentially lead to preventive measures or treatments to control the spread of EAV within the horse population.

Cite This Article

APA
Go YY, Bailey E, Timoney PJ, Shuck KM, Balasuriya UB. (2012). 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, 86(22), 12407-12410. https://doi.org/10.1128/JVI.01698-12

Publication

Journal of virology
ISSN: 1098-5514
NlmUniqueID: 0113724
Country: United States
Language: English
Volume: 86
Issue: 22
Pages: 12407-12410

Researcher Affiliations

Go, Yun Young
  • Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, Kentucky, USA.
Bailey, Ernest
    Timoney, Peter J
      Shuck, Kathleen M
        Balasuriya, Udeni B R

          MeSH Terms

          • Animals
          • Arterivirus Infections / metabolism
          • Arterivirus Infections / transmission
          • Arterivirus Infections / virology
          • CD3 Complex / biosynthesis
          • Carrier State / veterinary
          • Equartevirus / metabolism
          • Genetic Predisposition to Disease
          • Haplotypes
          • Horse Diseases / virology
          • Horses
          • In Vitro Techniques
          • Male
          • Microscopy, Fluorescence / methods
          • Phenotype
          • Risk
          • T-Lymphocytes / virology

          References

          This article includes 16 references
          1. Balasuriya UB. Serologic and molecular characterization of an abortigenic strain of equine arteritis virus isolated from infective frozen semen and an aborted equine fetus.. J. Am. Vet. Med. Assoc. 213:1586–1589.
            pubmed: 9838958
          2. Balasuriya UB, MacLachlan NJ. Equine viral arteritis. p 153–164 In Sellon DC, Long MT. (ed), Equine infectious diseases. Saunders Elsevier, St. Louis, MO.
          3. Balasuriya UB, MacLachlan NJ. The immune response to equine arteritis virus: potential lessons for other arteriviruses.. Vet. Immunol. Immunopathol. 102:107–129.
            pubmed: 15507299
          4. Cavanagh D. Nidovirales: a new order comprising Coronaviridae and Arteriviridae.. Arch. Virol. 142:629–633.
            pubmed: 9349308
          5. Go YY. Genome-wide association study among four horse breeds identifies a common haplotype associated with the in vitro CD3+ T cell susceptibility/resistance to equine arteritis virus infection.. J. Virol. 85:13174–13184.
            pmc: PMC3233183pubmed: 21994447
          6. Go YY. Complex interactions between the major and minor envelope proteins of equine arteritis virus determine its tropism for equine CD3+ T lymphocytes and CD14+ monocytes.. J. Virol. 84:4898–4911.
            pmc: PMC2863813pubmed: 20219931
          7. Holyoak GR, Balasuriya UB, Broaddus CC, Timoney PJ. Equine viral arteritis: current status and prevention.. Theriogenology 70:403–414.
            pubmed: 18502495
          8. Hullinger PJ, Gardner IA, Hietala SK, Ferraro GL, MacLachlan NJ. Seroprevalence of antibodies against equine arteritis virus in horses residing in the United States and imported horses.. J. Am. Vet. Med. Assoc. 219:946–949.
            pubmed: 11601790
          9. McCollum WH, Little TV, Timoney PJ, Swerczek TW. Resistance of castrated male horses to attempted establishment of the carrier state with equine arteritis virus.. J. Comp. Pathol. 111:383–388.
            pubmed: 7884055
          10. OIE. OIE manual of diagnostic tests and vaccines for terrestrial animals, 6th ed., vol 2. Office Internationale des Epizooties, Paris, France.
          11. Snijder EJ, Meulenberg JJ. The molecular biology of arteriviruses.. J. Gen. Virol. 79:961–979.
            pubmed: 9603311
          12. Timoney PJ. Factors influencing the international spread of equine diseases.. Vet. Clin. North Am. Equine Pract. 16:537–551.
            pubmed: 11219348
          13. Timoney PJ. The increasing significance of international trade in equids and its influence on the spread of infectious diseases.. Ann. N. Y. Acad. Sci. 916:55–60.
            pubmed: 11193671
          14. Timoney PJ, McCollum WH. Equine viral arteritis.. Vet. Clin. North Am. 9:295–309.
            pmc: PMC7134676pubmed: 8395325
          15. Timoney PJ. The carrier state in equine arteritis virus infection in the stallion with specific emphasis on the venereal mode of virus transmission.. J. Reprod. Fertil Suppl. 35:95–102.
            pubmed: 2824772
          16. Timoney PJ, McCollum WH, Roberts AW, Murphy TW. Demonstration of the carrier state in naturally acquired equine arteritis virus infection in the stallion.. Res. Vet. Sci. 41:279–280.
            pubmed: 3022363

          Citations

          This article has been cited 10 times.
          1. Thieulent CJ, Sarkar S, Carossino M, Bhowmik M, Zhu H, Balasuriya UBR. Cell Surface Vimentin Is an Attachment Factor That Facilitates Equine Arteritis Virus Infection In Vitro. Viruses 2026 Jan 15;18(1).
            doi: 10.3390/v18010113pubmed: 41600875google scholar: lookup
          2. Thieulent CJ, Carossino M, Balasuriya UBR, Graves K, Bailey E, Eberth J, Canisso IF, Andrews FM, Keowen ML, Go YY. Development of a TaqMan(®) Allelic Discrimination qPCR Assay for Rapid Detection of Equine CXCL16 Allelic Variants Associated With the Establishment of Long-Term Equine Arteritis Virus Carrier State in Stallions. Front Genet 2022;13:871875.
            doi: 10.3389/fgene.2022.871875pubmed: 35495124google scholar: lookup
          3. 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
          4. 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
          5. 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).
            doi: 10.1128/JVI.00015-18pubmed: 29444949google scholar: lookup
          6. Carossino M, Wagner B, Loynachan AT, Cook RF, Canisso IF, Chelvarajan L, Edwards CL, Nam B, Timoney JF, Timoney PJ, Balasuriya UBR. Equine Arteritis Virus Elicits a Mucosal Antibody Response in the Reproductive Tract of Persistently Infected Stallions. Clin Vaccine Immunol 2017 Oct;24(10).
            doi: 10.1128/CVI.00215-17pubmed: 28814389google scholar: lookup
          7. 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
          8. 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
          9. Balasuriya UB, Zhang J, Go YY, MacLachlan NJ. Experiences with infectious cDNA clones of equine arteritis virus: lessons learned and insights gained. Virology 2014 Aug;462-463:388-403.
            doi: 10.1016/j.virol.2014.04.029pubmed: 24913633google scholar: lookup
          10. 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
          Subscribe to our newsletter
          Join 99,658 horse owners like you who receive our email updates on horse health and nutrition.