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Immunopathogenesis of equine infectious anemia lentivirus disease.

Virus replication and subsequent viremia are clearly correlated with clinical disease in EIAV infected horses. Termination of viremia is the result of specific immune responses. Recurrences of viremia are associated with antigenic variation of neutralization-sensitive epitopes. Immunosuppression experiments indicate that the eventual control of EIAV and development of carriers is mediated by the immune system. Even though the immune response to EIAV has a protective effect, immune responses also cause some of the lesions. At least one part of the anemia, erythrocyte destruction, is caused by the immune response. Not all of the mechanisms of decreased erythropoiesis are known, but EIAV infection of monocyte/macrophages results in altered iron metabolism and functional iron deficiency. Viral antigen-antibody-C3 complexes cause glomerulitis and the combination of antigen-antibody reactions results in significant reductions in plasma C3. Lesions in the liver and other organs are infiltrations of lymphocytes and monocytes/macrophages in the interstitial areas and it is assumed that these lesions are initiated by specific immune responses to viral antigens. The observations on kinetics of EIAV infection, immune control by the horse, and immunopathologic basis of most of the lesions lead to the conclusion that mechanisms of lentivirus control and disease can be determined by study of EIAV.