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Qualitative analyses of cellular immune functions in equine infectious anemia show homology with AIDS

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Summary

Equine infectious anemia (EIA) is a disease caused by a lymphocytotropic lentivirus which belongs to the same subfamily as HIV. Because of the very close relationship of their predictedgag andpol gene products and similarities in clinical manifestations of the disease, EIA served as a model to study immunological events involved in the host defence against lymphocytotropic viral infections. The existence of antibody dependent cell-mediated cytotoxicity against autologous EIA virus infected lymphoblasts was demonstrated in vitro at the beginning of an acute attack of the disease. Cytotoxic activity was not found or was very low during chronic infection. Reactivity of peripheral blood lymphocytes to Protein A and allogeneic cells in vitro was significantly suppressed in the presence of an acute serum, while the reactivity to PHA was at the normal level. These results suggest that cellular immune mechanism(s) are also involved in removal of EIA virus infected cells as has been reported recently in HIV-1 infected individuals and that EIAV and HIV immunopathogenesis show similarities in affecting the immune response of the host.

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Author notes

  1. M. Gerenčer

    Present address: Immuno AG, Biomedical Research Center, A-2304, Orth/D., Austria

Authors and Affiliations

  1. Tissue Typing Center, KBC Rebro, University Hospital, Zagreb, Yugoslavia

    M. Gerenčer & Marija Tomaškovic

  2. EIA Disease Center, Veterinary Faculty, University of Zagreb, Zagreb, Yugoslavia

    Ivica Valpotić & B. Jukić

  3. Department of Animal Physiology, Faculty of Science, University of Zagreb, Zagreb, Yugoslavia

    I. Bašić

Authors
  1. M. Gerenčer
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  2. Ivica Valpotić
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  3. B. Jukić
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  4. Marija Tomaškovic
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  5. I. Bašić
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Gerenčer, M., Valpotić, I., Jukić, B. et al. Qualitative analyses of cellular immune functions in equine infectious anemia show homology with AIDS. Archives of Virology 104, 249–257 (1989). https://doi.org/10.1007/BF01315547

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  • DOI: https://doi.org/10.1007/BF01315547

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