Aleutian disease of mink. Prevention of lesions by immunosuppression.
Mink that were homozygous recessive for the Aleutian gene (aa) were inoculated with Aleutian disease virus (ADV) and simultaneously treated with cyclophosphamide (Cy). Control mink were inoculated with ADV. All mink were injected with bovine serum albumin (BSA) and their anti-BSA antibody response was measured to monitor the influence of drug therapy on the humoral antibody response. Formation of anti-BSA antibody was markedly suppressed and the hypergammaglobulinemia and development of AD lesions was inhibited in the Cy-treated mink. The non-Cy-treated control mink developed characteristic signs and lesions including glomerulonephritis and arteritis. The nontreated ADV-infected mink, but not the Cy-treated ADV-infected mink, had glomerular deposition of C3 and gamma globulin. Both groups had high titers of virus in their blood. These results indicate that the development of ADV lesions can be prevented by immunosuppressive treatment and further implicate host immune mechanisms in the pathogenesis of Aleutian disease.
D000453:Aleutian Mink Disease / Q000209:etiology / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D003520:Cyclophosphamide / Q000627:therapeutic use*; D005260:Female; D005455:Fluorescent Antibody Technique; D006720:Homozygote; D006942:Hypergammaglobulinemia / Q000517:prevention & control; D007165:Immunosuppression Therapy; D007668:Kidney / Q000473:pathology; D007678:Kidney Glomerulus / Q000473:pathology; D008099:Liver / Q000473:pathology; D008297:Male; D008856:Microscopy, Fluorescence; D012710:Serum Albumin, Bovine / Q000037:antagonists & inhibitors
D012710:Serum Albumin, Bovine; D003520:Cyclophosphamide