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Virology2002; 298(1); 39-44; doi: 10.1006/viro.2002.1466

Growth characteristics of a highly virulent, a moderately virulent, and an avirulent strain of equine arteritis virus in primary equine endothelial cells are predictive of their virulence to horses.

Abstract: Equine viral arteritis (EVA) is an endotheliotropic viral disease of horses caused by equine arteritis virus (EAV). Although there is only one serotype of EAV, there is marked variation in the virulence of different strains of the virus. The replication and cytopathogenicity of three well-characterized strains of EAV of different virulence to horses were compared in rabbit kidney (RK-13) and primary equine pulmonary artery endothelial cells (ECs). Viral protein expression, plaque size, and cytopathogenicity of all three viruses were similar in RK-13 cells, whereas two virulent strains of EAV were readily distinguished from an avirulent strain by their plaque morphology and cytopathogenicity in primary equine ECs. Furthermore, EAV nucleocapsid protein was detected by flow cytometric analysis significantly later in ECs infected with the avirulent than those infected with the virulent strains of EAV. Primary equine ECs provide a convenient and relevant model for in vitro characterization of the pathogenesis of EVA and the virulence determinants of EAV.
(c) 2002 Elsevier Science (USA).
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Publication Date: 2002-07-03 PubMed ID: 12093171DOI: 10.1006/viro.2002.1466Google Scholar: Lookup
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  • Comparative Study
  • Journal Article
  • Research Support
  • Non-U.S. Gov't
  • Research Support
  • U.S. Gov't
  • Non-P.H.S.

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 investigates the growth characteristics of three different strains of Equine Arteritis Virus (EAV) with varied levels of virulence. The study underscores the predictive value of growth characteristics on virulence, and extends the potential of primary equine endothelial cells as a model for studying EVA pathogenesis.

Research Background and Purpose

  • The paper focuses on Equine Arteritis Virus (EAV), which can cause a disease in horses known as Equine Viral Arteritis (EVA). EAV is unique in the sense that it has only one serotype but differs largely in virulence across different strains.
  • The purpose of this study is to compare the replication and cytopathogenicity (ability to cause disease at the cellular level) of three strains of EAV with different virulence in rabbit kidney cells and primary equine pulmonary artery endothelial cells.

Research Process and Findings

  • The researchers used both rabbit kidney (RK-13) cells and primary equine pulmonary artery endothelial cells for the study.
  • The results show that viral protein expression, plaque size, and cytopathogenicity of all the three EAV strains were similar when observed in RK-13 cells.
  • Contrastingly, in the primary equine endothelial cells (ECs), the two virulent EAV strains could be easily distinguished from the avirulent strain based on their plaque morphology and cytopathogenicity.
  • Additionally, it was noted that the nucleocapsid protein of the EAV was detected significantly later in ECs infected with the avirulent strain as compared to those infected with the virulent strains.

Conclusion and Implications

  • Based on these findings, the paper implies that the growth characteristics of EAV in primary equine endothelial cells are predictive of their level of virulence to horses, thus laying foundation for predictive models.
  • The study also suggests that primary equine ECs can be useful for in vitro (lab-grown) characterization of EVA pathogenesis (development of the disease) and for studying the virulence determinants of EAV, potentially helping in development of future treatment methods.

Cite This Article

APA
Moore BD, Balasuriya UB, Hedges JF, MacLachlan NJ. (2002). Growth characteristics of a highly virulent, a moderately virulent, and an avirulent strain of equine arteritis virus in primary equine endothelial cells are predictive of their virulence to horses. Virology, 298(1), 39-44. https://doi.org/10.1006/viro.2002.1466

Publication

Virology
ISSN: 0042-6822
NlmUniqueID: 0110674
Country: United States
Language: English
Volume: 298
Issue: 1
Pages: 39-44

Researcher Affiliations

Moore, Brian D
  • Bernard and Gloria Salick Equine Viral Disease Laboratory, Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, Davis, California 95616, USA.
Balasuriya, Udeni B R
    Hedges, Jodi F
      MacLachlan, N James

        MeSH Terms

        • Animals
        • Cells, Cultured
        • Cytopathogenic Effect, Viral
        • Endothelium / virology
        • Equartevirus / growth & development
        • Equartevirus / pathogenicity
        • Horses / virology
        • Rabbits
        • Viral Plaque Assay
        • Virulence
        • Virus Replication

        Citations

        This article has been cited 14 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. 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
        3. Zhu Z, Yang F, Cao W, Liu H, Zhang K, Tian H, Dang W, He J, Guo J, Liu X, Zheng H. The Pseudoknot Region of the 5' Untranslated Region Is a Determinant of Viral Tropism and Virulence of Foot-and-Mouth Disease Virus. J Virol 2019 Apr 15;93(8).
          doi: 10.1128/JVI.02039-18pubmed: 30728251google scholar: lookup
        4. 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
        5. Sarkar S, Chelvarajan L, Go YY, Cook F, Artiushin S, Mondal S, Anderson K, Eberth J, Timoney PJ, Kalbfleisch TS, Bailey E, Balasuriya UB. Equine Arteritis Virus Uses Equine CXCL16 as an Entry Receptor. J Virol 2016 Jan 13;90(7):3366-84.
          doi: 10.1128/JVI.02455-15pubmed: 26764004google scholar: lookup
        6. Go YY, Li Y, Chen Z, Han M, Yoo D, Fang Y, Balasuriya UB. Equine arteritis virus does not induce interferon production in equine endothelial cells: identification of nonstructural protein 1 as a main interferon antagonist. Biomed Res Int 2014;2014:420658.
          doi: 10.1155/2014/420658pubmed: 24967365google scholar: lookup
        7. Mottahedin A, Paidikondala M, Cholleti H, Baule C. NF-κB activation by equine arteritis virus is MyD88 dependent and promotes viral replication. Arch Virol 2013 Mar;158(3):701-5.
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          doi: 10.1128/CVI.00302-12pubmed: 22739697google scholar: lookup
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        10. Go YY, Zhang J, Timoney PJ, Cook RF, Horohov DW, Balasuriya UB. 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 2010 May;84(10):4898-911.
          doi: 10.1128/JVI.02743-09pubmed: 20219931google scholar: lookup
        11. 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.
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        13. Burnouf T, Griffiths E, Padilla A, Seddik S, Stephano MA, Gutiérrez JM. Assessment of the viral safety of antivenoms fractionated from equine plasma. Biologicals 2004 Sep;32(3):115-28.
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        14. Artiushin S, Timoney JF, Nally J, Verma A. Host-inducible immunogenic sphingomyelinase-like protein, Lk73.5, of Leptospira interrogans. Infect Immun 2004 Feb;72(2):742-9.
          doi: 10.1128/IAI.72.2.742-749.2004pubmed: 14742516google scholar: lookup
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