FREE SHIPPING over $40
OVER 9000 FIVE-STAR REVIEWS
5% OFF ALL SUBSCRIPTIONS
100% HAPPINESS GUARANTEE
Analyze Diet
0
Home / Equine Research Bank / Sci Rep / Spread of equine arteritis virus among Hucul horses with dif...
Scientific reports2020; 10(1); 2909; doi: 10.1038/s41598-020-59870-y

Spread of equine arteritis virus among Hucul horses with different EqCXCL16 genotypes and analysis of viral quasispecies from semen of selected stallions.

Abstract: Equine arteritis virus (EAV) is maintained in the horse populations through persistently infected stallions. The aims of the study were to monitor the spread of EAV among Polish Hucul horses, to analyse the variability of circulating EAVs both between- and within-horses, and to identify allelic variants of the serving stallions EqCXCL16 gene that had been previously shown to strongly correlate with long-term EAV persistence in stallions. Serum samples (n = 221) from 62 horses including 46 mares and 16 stallions were collected on routine basis between December 2010 and May 2013 and tested for EAV antibodies. In addition, semen from 11 stallions was tested for EAV RNA. A full genomic sequence of EAV from selected breeding stallions was determined using next generation sequencing. The proportion of seropositive mares among the tested population increased from 7% to 92% during the study period, while the proportion of seropositive stallions remained similar (64 to 71%). The EAV genomes from different stallions were 94.7% to 99.6% identical to each other. A number (41 to 310) of single nucleotide variants were identified within EAV sequences from infected stallions. Four stallions possessed EqCXCL16S genotype correlated with development of long-term carrier status, three of which were persistent shedders and the shedder status of the remaining one was undetermined. None of the remaining 12 stallions with EqCXCL16R genotype was identified as a persistent shedder.
Get Full Text
Publication Date: 2020-02-19 PubMed ID: 32076048PubMed Central: PMC7031528DOI: 10.1038/s41598-020-59870-yGoogle 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.

This research observes the impact and spread of Equine arteritis virus (EAV) among a group of Polish Hucul horses, while also investigating the variability of EAV types and identifying potential genetic factors that may contribute to the ongoing presence of EAV in horse populations.

Research Context and Objectives

  • The study focuses on elucidating how EAV, a virus that leads to respiratory disease and reproductive disorders in horses, spreads and is maintained in Polish Hucul horses, which are a distinct breed.
  • The researchers aimed to investigate how the virus evolves within and between individual hosts, and to unravel any genetic factors that may enhance its persistence.
  • The gene EqCXCL16 was specifically examined as previous studies suggested a strong link between its different forms (alleles) and the likelihood of long-term EAV persistence in stallions (male horses).

Methodology

  • Over a period of approximately two and a half years (December 2010 to May 2013), the team collected serum samples from 62 horses to screen for EAV antibodies, indicating exposure to the virus.
  • This group was comprised of 46 mares (female horses) and 16 stallions.
  • In addition to the serum samples, semen from 11 stallions was tested for EAV RNA to directly confirm the presence of the virus.
  • Next-generation sequencing was utilized to fully interpret the genetic material of EAV from selected breeding stallions.

Results and Analysis

  • The percentage of mares with EAV antibodies (seropositive) dramatically increased from 7% to 92%, while the percentage of stallions with antibodies remained relatively stable (64% to 71%) over the study period.
  • EAV genomes, the complete set of genetic material of the virus, from different stallions showed high similarity, ranging from 94.7% to 99.6% identical.
  • Despite this similarity, a considerable variation was present at single DNA base levels (single nucleotide variants) within EAV sequences from infected stallions.
  • Distinct genotypes (genetic types) of the EqCXCL16 gene were found to correlate with EAV persistence, with four stallions possessing the EqCXCL16S genotype, three of them were confirmed as persistent virus shedders. No EAV persistent shedders were found among 12 stallions with a different genotype, EqCXCL16R.

Interpretation

  • This research demonstrates that EAV can not only persist but spread rapidly within a horse population.
  • It also posits that certain genetic factors, specifically variants of the EqCXCL16 gene, might play a significant role in dictating whether a stallion becomes a long-term carrier and shedder of EAV.
  • The discovery of the EAV genetic diversity within individual horses gives a hint towards the potential of the virus to adapt and survive in different environments.

Cite This Article

APA
Socha W, Sztromwasser P, Dunowska M, Jaklinska B, Rola J. (2020). Spread of equine arteritis virus among Hucul horses with different EqCXCL16 genotypes and analysis of viral quasispecies from semen of selected stallions. Sci Rep, 10(1), 2909. https://doi.org/10.1038/s41598-020-59870-y

Publication

Scientific reports
ISSN: 2045-2322
NlmUniqueID: 101563288
Country: England
Language: English
Volume: 10
Issue: 1
Pages: 2909

Researcher Affiliations

Socha, Wojciech
  • National Veterinary Research Institute, Al. Partyzantow 57, 24-100, Pulawy, Poland.
Sztromwasser, Pawel
  • National Veterinary Research Institute, Al. Partyzantow 57, 24-100, Pulawy, Poland.
  • Medical University of Lodz, Al. Kosciuszki 4, 90-419, Lodz, Poland.
Dunowska, Magdalena
  • School of Veterinary Science, Massey University, Palmerston North, New Zealand.
Jaklinska, Barbara
  • Hucul Horse Stud Gladyszow, Regietow 28, 38-315, Uscie Gorlickie, Poland.
Rola, Jerzy
  • National Veterinary Research Institute, Al. Partyzantow 57, 24-100, Pulawy, Poland. jrola@piwet.pulawy.pl.

MeSH Terms

  • Alleles
  • Animals
  • Arterivirus Infections / blood
  • Arterivirus Infections / genetics
  • Arterivirus Infections / veterinary
  • Chemokine CXCL16 / genetics
  • Equartevirus / physiology
  • Female
  • Genome, Viral
  • Genotype
  • Horse Diseases / genetics
  • Horse Diseases / virology
  • Horses / blood
  • Horses / genetics
  • Horses / virology
  • Male
  • Phylogeny
  • Polymorphism, Single Nucleotide / genetics
  • Quasispecies / genetics
  • Semen / virology

Conflict of Interest Statement

The authors declare no competing interests.

References

This article includes 47 references
  1. Balasuriya UBR, Go YY, MacLachlan NJ. Equine arteritis virus. Vet. Microbiol. 2013;167:93–122.
    doi: 10.1016/j.vetmic.2013.06.015pmc: PMC7126873pubmed: 23891306google scholar: lookup
  2. King AM. Changes to taxonomy and the International Code of Virus Classification and Nomenclature ratified by the International Committee on Taxonomy of Viruses (2018). Arch. Virol. 2018;163:2601–2631.
    doi: 10.1007/s00705-018-3847-1pubmed: 29754305google scholar: lookup
  3. McFadden AM. Evidence for absence of equine arteritis virus in the horse population of New Zealand. New Zeal. Vet. J. 2013;61:300–304.
    doi: 10.1080/00480169.2012.755664pubmed: 23611669google scholar: lookup
  4. Golnik W, Michalak T. Causes of equine viral arteritis (arteritis quorum) in Poland. Med. Weter. 1978;35:605–606.
  5. Golnik W. The results of serological examinations of stallions for equine arteritis virus antibodies. Med. Weter. 2000;56:573–575.
  6. Rola J, Larska M, Rola JG, Belák S, Autorino GL. Epizotiology and phylogeny of equine arteritis virus in hucul horses. Vet. Microbiol. 2011;148:402–407.
    doi: 10.1016/j.vetmic.2010.09.008pubmed: 20956062google scholar: lookup
  7. Bażanów BA, Frącka AB, Jackulak NA, Staroniewicz ZM, Ploch SM. A 34-year retrospective study of equine viral abortion in Poland. Pol. J. Vet. Sci. 2014;17:607–612.
    doi: 10.2478/pjvs-2014-0091pubmed: 25638974google scholar: lookup
  8. Holyoak GR, Balasuriya UBR, Broaddus CC, Timoney PJ. Equine viral arteritis: current status and prevention. Theriogenology 2008;70:403–414.
    doi: 10.1016/j.theriogenology.2008.04.020pubmed: 18502495google scholar: lookup
  9. de Vries AAF. The Molecular Biology of Equine Arteritis Virus. Doctoral Thesis, University of Utrecht, Utrecht, the Netherlands (1994).
  10. Guthrie AJ. Lateral transmission of equine arteritis virus among Lipizzaner stallions in South Africa. Equine. Vet. J. 2003;35:596–600.
    doi: 10.2746/042516403775467162pubmed: 14515961google scholar: lookup
  11. Sarkar S. 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 Genetics 2016;12:e1006467.
    doi: 10.1371/journal.pgen.1006467pmc: PMC5145142pubmed: 27930647google scholar: lookup
  12. Balasuriya UBR. Genetic characterization of equine arteritis virus during persistent infection of stallions. J. Gen. Virol. 2004;85:379–390.
    doi: 10.1099/vir.0.19545-0pubmed: 14769895google scholar: lookup
  13. Van den Hoecke S, Verhelst J, Vuylsteke M, Saelens X. Analysis of the genetic diversity of influenza A viruses using next-generation DNA sequencing. BMC Genomics 2015;16:79.
    doi: 10.1186/s12864-015-1284-zpmc: PMC4342091pubmed: 25758772google scholar: lookup
  14. Andino R, Domingo E. Viral quasispecies. Virology 2015;479:46–51.
    doi: 10.1016/j.virol.2015.03.022pmc: PMC4826558pubmed: 25824477google scholar: lookup
  15. Miszczak F. Emergence of novel equine arteritis virus (EAV) variants during persistent infection in the stallion: origin of the 2007 French EAV outbreak was linked to an EAV strain present in the semen of a persistently infected carrier stallion. Virology 2012;423:165–174.
    doi: 10.1016/j.virol.2011.11.028pubmed: 22209234google scholar: lookup
  16. Hedges JF, Balasuriya UBR, Timoney PJ, McCollum WH, MacLachlan NJ. Genetic divergence with emergence of novel phenotypic variants of equ ine arteritis virus during persistent infection of stallions. J. Virol. 1999;73:3672–3681.
    doi: 10.1128/JVI.73.5.3672-3681.1999pmc: PMC104142pubmed: 10196259google scholar: lookup
  17. Liu L. Analysis of ORFs 2b, 3, 4, and partial ORF5 of sequential isolates of equine arteritis virus shows genetic variation following experimental infection of horses. Vet. Microbiol. 2008;129:262–268.
    doi: 10.1016/j.vetmic.2007.11.021pubmed: 18191505google scholar: lookup
  18. Nam B. Intra-host Selection Pressure Drives Equine Arteritis Virus Evolution during Persistent Infection in the Stallion Reproductive Tract. J. Virol. JVI-00045 (2019).
    pmc: PMC6613756pubmed: 30918077
  19. Balasuriya UBR, MacLachlan NJ, De Vries AA, Rossitto PV, Rottier PJ. Identification of a neutralization site in the major envelope glycoprotein (GL) of equine arteritis virus. Virology 1995;207:518–527.
    doi: 10.1006/viro.1995.1112pubmed: 7533965google scholar: lookup
  20. Balasuriya UBR. Neutralization determinants of laboratory strains and field isolates of equine arteritis virus: identification of four neutralization sites in the amino-terminal ectodomain of the GL envelope glycoprotein. Virology 1997;232:114–128.
    doi: 10.1006/viro.1997.8551pubmed: 9185595google scholar: lookup
  21. Veit M, Matczuk AK, Sinhadri BC, Krause E, Thaa B. Membrane proteins of arterivirus particles: structure, topology, processing and function. Virus Res. 2014;194:16–36.
    doi: 10.1016/j.virusres.2014.09.010pmc: PMC7172906pubmed: 25278143google scholar: lookup
  22. Rola J, Socha W, Żmudziński JF. Sequence analysis of minor protein genes of equine arteritis virus during persistent infection. Bull. Vet. Inst. Pulawy. 2015;59:179–184.
    doi: 10.1515/bvip-2015-0027google scholar: lookup
  23. Wieringa R, de Vries AA, Post SM, Rottier PJ. Intra-and intermolecular disulfide bonds of the GP2b glycoprotein of equine arteritis virus: relevance for virus assembly and infectivity. J. Virol. 2003;77:12996–13004.
    doi: 10.1128/JVI.77.24.12996-13004.2003pmc: PMC296049pubmed: 14645556google scholar: lookup
  24. Archambault D, Laganiere G, Carman S, St-Laurent G. Comparison of nucleic and amino acid sequences and phylogenetic analysis of open reading frames 3 and 4 of various equine arteritis virus isolates. Vet. Res. 1997;28:505–516.
    pubmed: 9428144
  25. Zhang M, Veit M. Differences in signal peptide processing between GP3 glycoproteins of Arteriviridae. Virology 2018;517:69–76.
    doi: 10.1016/j.virol.2017.11.026pubmed: 29229370google scholar: lookup
  26. Matczuk AK, Veit M. Signal peptide cleavage from GP3 enabled by removal of adjacent glycosylation sites does not impair replication of equine arteritis virus in cell culture, but the hydrophobic C-terminus is essential. Virus. Res. 2014;183:107–111.
    doi: 10.1016/j.virusres.2014.02.005pubmed: 24556360google scholar: lookup
  27. Zhang J. Amino acid substitutions in the structural or nonstructural proteins of a vaccine strain of equine arteritis virus are associated with its attenuation. Virology 2008;378:355–362.
    doi: 10.1016/j.virol.2008.06.003pubmed: 18619638google scholar: lookup
  28. Balasuriya UBR. Genetic stability of equine arteritis virus during horizontal and vertical transmission in an outbreak of equine viral arteritis. J. Gen. Virol. 1999;80:1949–1958.
    doi: 10.1099/0022-1317-80-8-1949pubmed: 10466790google scholar: lookup
  29. Go YY, Snijder EJ, Timoney PJ, Balasuriya UBR. Characterization of equine humoral antibody response to the nonstructural proteins of equine arteritis virus. Clin. Vaccine Immunol. 2011;18:268–279.
    doi: 10.1128/CVI.00444-10pmc: PMC3067362pubmed: 21147938google scholar: lookup
  30. Snijder EJ, Kikkert M, Fang Y. Arterivirus molecular biology and pathogenesis. J. Gen. Virol. 2013;94:2141–2163.
    doi: 10.1099/vir.0.056341-0pubmed: 23939974google scholar: lookup
  31. De Coster W, van Broeckhoven C. Newest methods for detecting structural variations. Trends in biotechnology (2019).
    pubmed: 30902345doi: 10.1016/j.tibtech.2019.02.003google scholar: lookup
  32. Balasuriya UBR. Host factors that contribute to equine arteritis virus persistence in the stallion: An update. J. Equine Vet. Sci. 2016;43(Suppl):11–17.
    doi: 10.1016/j.jevs.2016.05.017google scholar: lookup
  33. Balasuriya UB, Zhang J, Go YY, MacLachlan NJ. Experiences with infectious cDNA clones of equine arteritis virus: lessons learned and insights gained. Virology 2014;462:388–403.
    doi: 10.1016/j.virol.2014.04.029pmc: PMC7172799pubmed: 24913633google scholar: lookup
  34. Balasuriya UBR, Carossino M, Timoney PJ. Equine viral arteritis: A respiratory and reproductive disease of significant economic importance to the equine industry. Equine Vet. Educ. 2018;30:497–512.
    doi: 10.1111/eve.12672google scholar: lookup
  35. McCollum WH, Timoney PJ, Roberts AW, Willard JE, Carswell GD. Response of vaccinated and non-vaccinated mares to artificial insemination with semen from stallions persistently infected with equine arteritis virus. Proceedings of the 5th International Conference on Equine Infectious Diseases The University Press of Kentucky, Lexington, Ky pp 13–18 (1988).
  36. Anonymous. Equine viral arteritis. OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animals (2013) Chapter 2.5.10.
  37. Balasuriya UBR. Detection of equine arteritis virus by real-time TaqMan® reverse transcription-PCR assay. J. Virol. Methods. 2002;101:21–28.
    doi: 10.1016/S0166-0934(01)00416-5pubmed: 11849680google scholar: lookup
  38. Bushnell B. BBTools. https://jgi.doe.gov/data-and-tools/bbtools/ (2018).
  39. Bolger AM, Lohse M, Usadel B. Trimmomatic: a flexible trimmer for Illumina sequence data. Bioinformatics 2014;30:2114–2120.
    doi: 10.1093/bioinformatics/btu170pmc: PMC4103590pubmed: 24695404google scholar: lookup
  40. Quast C. The SILVA ribosomal RNA gene database project: improved data processing and web-based tools. Nucleic Acids Res. 2013;41(D1):D590–D596.
    doi: 10.1093/nar/gks1219pmc: PMC3531112pubmed: 23193283google scholar: lookup
  41. Li H. Aligning sequence reads, clone sequences and assembly contigs with BWA-MEM. arXiv preprint arXiv:1303.3997 (2013).
  42. Bankevich A. SPAdes: a new genome assembly algorithm and its applications to single-cell sequencing. J. Comput. Biol. 2012;19:455–477.
    doi: 10.1089/cmb.2012.0021pmc: PMC3342519pubmed: 22506599google scholar: lookup
  43. Johnson M. NCBI BLAST: a better web interface. Nucleic. Acids Res. 2008;36(suppl_2):W5–W9.
    doi: 10.1093/nar/gkn201pmc: PMC2447716pubmed: 18440982google scholar: lookup
  44. Wilm A. LoFreq: A sequence-quality aware, ultra-sensitive variant caller for uncovering cell-population heterogeneity from high-throughput sequencing datasets. Nucleic Acids Research 2012;40(22):11189–201.
    doi: 10.1093/nar/gks918pmc: PMC3526318pubmed: 23066108google scholar: lookup
  45. R Core Team. R: a language and environment for statistical computing. Foundation for Statistical Computing, Vienna, Austria. https://www.r-project.org (2015).
  46. Hasing ME, Hazes B, Lee BE, Preiksaitis JK, Pang XL. A next generation sequencing-based method to study the intra-host genetic diversity of norovirus in patients with acute and chronic infection. BMC Genomics 2016;17:480.
    doi: 10.1186/s12864-016-2831-ypmc: PMC4929757pubmed: 27363999google scholar: lookup
  47. Tamura K. MEGA5: Molecular Evolutionary Genetics Analysis using Maximum Likelihood, Evolutionary Distance, and Maximum Parsimony Methods. Mol. Biol. Evol. 2011;28:2731–2739.
    doi: 10.1093/molbev/msr121pmc: PMC3203626pubmed: 21546353google scholar: lookup
Subscribe to our newsletter
Join 99,344 horse owners like you who receive our email updates on horse health and nutrition.