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Home / Equine Research Bank / Arch Virol / Complement-mediated hemolysis of horse erythrocytes treated ...
Archives of virology1987; 95(1-2); 53-66; doi: 10.1007/BF01311334

Complement-mediated hemolysis of horse erythrocytes treated with equine infectious anemia virus.

Abstract: Horse erythrocytes treated with equine infectious anemia virus hemagglutinin were found to be lysed after incubation with fresh horse serum at 37 degrees C. Fresh guinea pig serum induced more efficient hemolysis than horse serum. Direct immunofluorescence test revealed the adsorption of complement factors on the surface of the erythrocytes. Calcium and magnesium ions were necessary for the hemolysis to take place. Antibody against equine infectious anemia virus enhanced the virus-induced complement-mediated hemolysis. These observations indicated that the classical pathway of complement activation was responsible for this virus-induced hemolysis and suggest the possibility that virus antigen, anti-viral antibody and complement may play an important role in the genesis of the anemia of horses infected with the equine infectious anemia virus.
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Publication Date: 1987-01-01 PubMed ID: 3036045DOI: 10.1007/BF01311334Google Scholar: Lookup
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  • Journal Article

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 discusses how the equine infectious anemia virus causes hemolysis, or destruction of red blood cells, in horses. The study further suggests that the immune response generated by the horse’s body may play a crucial role in this process.

Methodology and Key Findings

  • The researchers treated horse red blood cells, also known as erythrocytes, with equine infectious anemia virus hemagglutinin – a substance that causes clumping of the cells. They found that these cells were destroyed after being incubated with fresh horse serum at 37 degrees Celsius.
  • Interestingly, fresh guinea pig serum was found to induce hemolysis more effectively than horse serum. This suggests that there may be differences in the immune response across different species.
  • The process of hemolysis, in this case, required calcium and magnesium ions. These ions are often required for various body processes and it was found that they were necessary for this virus-induced red blood cell destruction.

    • Role of the Immune Response

    • The researchers observed the accumulation of complement factors – proteins that contribute to the body’s immune response – on the surface of the erythrocytes. They used a test called direct immunofluorescence to confirm this.
    • The presence of antibodies (immune proteins that recognize and neutralize foreign substances) against the equine infectious anemia virus seemed to enhance the process of hemolysis. This implies that the body’s immune response may actually contribute to the destruction of red blood cells.
    • These findings led the researchers to conclude that a conventional (classical) pathway of immune response activation was primarily responsible for this virus-induced destruction of red blood cells.

      • Implications of the Research

      • This research sheds light on how horses suffering from equine infectious anemia experience red blood cell destruction. The study suggests that the disease is not just the result of the virus’ direct action on the cells, but also due to the body’s immune response against the virus.
      • The findings of this study could influence the development of new treatments for equine infectious anemia. By targeting both the virus and the body’s immune response, it might be possible to reduce the hemolysis and alleviate the symptoms of the disease.

Cite This Article

APA
Sentsui H, Kono Y. (1987). Complement-mediated hemolysis of horse erythrocytes treated with equine infectious anemia virus. Arch Virol, 95(1-2), 53-66. https://doi.org/10.1007/BF01311334

Publication

Archives of virology
ISSN: 0304-8608
NlmUniqueID: 7506870
Country: Austria
Language: English
Volume: 95
Issue: 1-2
Pages: 53-66

Researcher Affiliations

Sentsui, H
    Kono, Y

      MeSH Terms

      • Adsorption
      • Animals
      • Antibodies, Viral / immunology
      • Calcium / pharmacology
      • Complement System Proteins / immunology
      • Guinea Pigs
      • Hemagglutination
      • Hemolysis
      • Horses
      • Immune Sera / immunology
      • Infectious Anemia Virus, Equine / immunology
      • Infectious Anemia Virus, Equine / pathogenicity

      References

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      Citations

      This article has been cited 6 times.
      1. Du C, Ma J, Liu Q, Li YF, He XJ, Lin YZ, Wang XF, Meng QW, Wang X, Zhou JH. Mice transgenic for equine cyclin T1 and ELR1 are susceptible to equine infectious anemia virus infection. Retrovirology 2015 Apr 28;12:36.
        doi: 10.1186/s12977-015-0163-7pubmed: 25928027google scholar: lookup
      2. Crawford TB, Wardrop KJ, Tornquist SJ, Reilich E, Meyers KM, McGuire TC. A primary production deficit in the thrombocytopenia of equine infectious anemia. J Virol 1996 Nov;70(11):7842-50.
        doi: 10.1128/JVI.70.11.7842-7850.1996pubmed: 8892906google scholar: lookup
      3. Sellon DC. Equine infectious anemia. Vet Clin North Am Equine Pract 1993 Aug;9(2):321-36.
        doi: 10.1016/s0749-0739(17)30399-1pubmed: 8395326google scholar: lookup
      4. Sellon DC, Fuller FJ, McGuire TC. The immunopathogenesis of equine infectious anemia virus. Virus Res 1994 May;32(2):111-38.
        doi: 10.1016/0168-1702(94)90038-8pubmed: 8067050google scholar: lookup
      5. Sentsui H, Kono Y. Phagocytosis of horse erythrocytes treated with equine infectious anemia virus by cultivated horse leukocytes. Arch Virol 1987;95(1-2):67-77.
        doi: 10.1007/BF01311335pubmed: 3036046google scholar: lookup
      6. Clabough DL, Gebhard D, Flaherty MT, Whetter LE, Perry ST, Coggins L, Fuller FJ. Immune-mediated thrombocytopenia in horses infected with equine infectious anemia virus. J Virol 1991 Nov;65(11):6242-51.
        doi: 10.1128/JVI.65.11.6242-6251.1991pubmed: 1717720google scholar: lookup
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