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The Journal of general virology2010; 91(Pt 9); 2286-2301; doi: 10.1099/vir.0.019737-0

Molecular epidemiology and genetic characterization of equine arteritis virus isolates associated with the 2006-2007 multi-state disease occurrence in the USA.

Abstract: In 2006-2007, equine viral arteritis (EVA) was confirmed for the first time in Quarter Horses in multiple states in the USA. The entire genome of an equine arteritis virus (EAV) isolate from the index premises in New Mexico was 12 731 nt in length and possessed a previously unrecorded unique 15 nt insertion in the nsp2-coding region in ORF1a and a 12 nt insertion in ORF3. Sequence analysis of additional isolates made during this disease occurrence revealed that all isolates from New Mexico, Utah, Kansas, Oklahoma and Idaho had 98.6-100.0 % (nsp2) and 97.8-100 % (ORF3) nucleotide identity and contained the unique insertions in nsp2 and ORF3, indicating that the EVA outbreaks in these states probably originated from the same strain of EAV. Sequence and phylogenetic analysis of several EAV isolates made following an EVA outbreak on another Quarter Horse farm in New Mexico in 2005 provided evidence that this outbreak may well have been the source of virus for the 2006-2007 occurrence of the disease. A virus isolate from an aborted fetus in Utah was shown to have a distinct neutralization phenotype compared with other isolates associated with the 2006-2007 EVA occurrence. Full-length genomic sequence analysis of 18 sequential isolates of EAV made from eight carrier stallions established that the virus evolved genetically during persistent infection, and the rate of genetic change varied between individual animals and the period of virus shedding.
Publication Date: 2010-05-05 PubMed ID: 20444993DOI: 10.1099/vir.0.019737-0Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This research article investigates equine viral arteritis (EVA) outbreaks in the USA from 2006-2007, specifically focusing on the genetic characteristics of the equine arteritis virus (EAV) isolates from these outbreaks. The aim was to understand the origin and spread of the EVA illness during these periods and deduce how the virus changes over time in infected animals.

Study Context and Objectives

  • The study was aimed at understanding the genetic characteristics of the EAV isolates associated with the 2006-2007 outbreaks of EVA. This was the first time EVA was confirmed in Quarter Horses in multiple states.
  • The main objectives included identifying the origin of EAV strains causing the outbreaks, observing the genetic evolution of the virus in infected animals, and understanding the connection between different EVA outbreaks.

Research Methodology and Findings

  • The researchers captured and analyzed the full genome of an EAV isolate from New Mexico, which was the index (initial) premises. The genome was found to have unique genetic insertions that were previously unrecorded.
  • Further sequence analysis was performed on additional isolates from states including New Mexico, Utah, Kansas, Oklahoma and Idaho. The isolates contained similar unique insertions, suggesting that the multiple outbreaks likely originated from a same EAV strain.
  • Another significant finding was that an EAV isolate from a Utah aborted fetus exhibited a different neutralizing phenotype, implying a potential variation within the virus strain.
  • Finally, the researchers also mapped the genetic evolution of EAV in infected carrier stallions by sequencing 18 isolates made sequentially from these animals. It was observed that the virus’s genetic composition changed over time and varied depending on individual animals and the duration of virus shedding.

Implications and Significance of the Study

  • The study highlights the importance of genetic characterization in understanding disease transmission and management. By genetically mapping the EAV strain, the researchers demonstrated how a single strain could be the source of multiple outbreaks.
  • The work potentially contributes to effective EVA outbreak management strategies and could augment the development of improved viral countermeasures and therapies.
  • Knowledge about the genetic evolution of viruses during persistent infection, as shown in this study, might be useful in developing effective treatment strategies for not only EVA, but also other similar viral infections in general.

Cite This Article

APA
Zhang J, Timoney PJ, Shuck KM, Seoul G, Go YY, Lu Z, Powell DG, Meade BJ, Balasuriya UB. (2010). Molecular epidemiology and genetic characterization of equine arteritis virus isolates associated with the 2006-2007 multi-state disease occurrence in the USA. J Gen Virol, 91(Pt 9), 2286-2301. https://doi.org/10.1099/vir.0.019737-0

Publication

ISSN: 1465-2099
NlmUniqueID: 0077340
Country: England
Language: English
Volume: 91
Issue: Pt 9
Pages: 2286-2301

Researcher Affiliations

Zhang, Jianqiang
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, KY 40546, USA.
Timoney, Peter J
    Shuck, Kathleen M
      Seoul, Gong
        Go, Yun Young
          Lu, Zhengchun
            Powell, David G
              Meade, Barry J
                Balasuriya, Udeni B R

                  MeSH Terms

                  • Amino Acid Sequence
                  • Animals
                  • Arterivirus Infections / epidemiology
                  • Arterivirus Infections / veterinary
                  • Arterivirus Infections / virology
                  • Base Sequence
                  • DNA, Viral / genetics
                  • Disease Outbreaks / veterinary
                  • Equartevirus / genetics
                  • Equartevirus / immunology
                  • Equartevirus / isolation & purification
                  • Evolution, Molecular
                  • Female
                  • Horse Diseases / epidemiology
                  • Horse Diseases / virology
                  • Horses
                  • Male
                  • Molecular Epidemiology
                  • Molecular Sequence Data
                  • Neutralization Tests
                  • Phenotype
                  • Phylogeny
                  • Pregnancy
                  • Sequence Homology, Amino Acid
                  • Sequence Homology, Nucleic Acid
                  • Time Factors
                  • United States / epidemiology

                  Citations

                  This article has been cited 11 times.
                  1. Moyo NA, Westcott D, Simmonds R, Steinbach F. Equine Arteritis Virus in Monocytic Cells Suppresses Differentiation and Function of Dendritic Cells. Viruses 2023 Jan 16;15(1).
                    doi: 10.3390/v15010255pubmed: 36680295google scholar: lookup
                  2. Otzdorff C, Beckmann J, Goehring LS. Equine Arteritis Virus (EAV) Outbreak in a Show Stallion Population. Viruses 2021 Oct 24;13(11).
                    doi: 10.3390/v13112142pubmed: 34834949google scholar: lookup
                  3. 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
                  4. 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
                  5. 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
                  6. 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
                  7. 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
                  8. van Kasteren PB, Bailey-Elkin BA, James TW, Ninaber DK, Beugeling C, Khajehpour M, Snijder EJ, Mark BL, Kikkert M. Deubiquitinase function of arterivirus papain-like protease 2 suppresses the innate immune response in infected host cells. Proc Natl Acad Sci U S A 2013 Feb 26;110(9):E838-47.
                    doi: 10.1073/pnas.1218464110pubmed: 23401522google scholar: lookup
                  9. Zhang J, Go YY, Huang CM, Meade BJ, Lu Z, Snijder EJ, Timoney PJ, Balasuriya UB. Development and characterization of an infectious cDNA clone of the modified live virus vaccine strain of equine arteritis virus. Clin Vaccine Immunol 2012 Aug;19(8):1312-21.
                    doi: 10.1128/CVI.00302-12pubmed: 22739697google scholar: lookup
                  10. Firth AE, Zevenhoven-Dobbe JC, Wills NM, Go YY, Balasuriya UBR, Atkins JF, Snijder EJ, Posthuma CC. Discovery of a small arterivirus gene that overlaps the GP5 coding sequence and is important for virus production. J Gen Virol 2011 May;92(Pt 5):1097-1106.
                    doi: 10.1099/vir.0.029264-0pubmed: 21307223google scholar: lookup
                  11. Go YY, Snijder EJ, Timoney PJ, Balasuriya UB. Characterization of equine humoral antibody response to the nonstructural proteins of equine arteritis virus. Clin Vaccine Immunol 2011 Feb;18(2):268-79.
                    doi: 10.1128/CVI.00444-10pubmed: 21147938google scholar: lookup