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Biomedical subjects

J B Henson

Publications and source records attributed to J B Henson.

At least 37 records · Page 2Linked to original sources

Study of the one-step growth curve of equine infectious anemia virus by immunofluorescence.

Primary horse leukocyte cultures were inoculated with 2 or 10 50% tissue culture infective doses (TCID(50)) of equine infectious anemia (EIA) virus per cell, and the titer of cell-associated and fluid-phase virus was determined from 1 to 72 hr postinoculation (PI). Cover slips were collected from 4 to 72 hr PI and stained for EIA viral antigen by the indirect immunofluorescent (FA) technique. Viral replication was detected after a latent period of approximately 18 to 24 hr and reached peak titers of approximately 10(4.5) to 10(6) TCID(50)/0.5 ml from 48 to 72 hr PI. The fluid phase contained 10(1) to 10(2) TCID(50)/0.5 ml more virus than the cells. Viral antigen was first detected by FA from 18 to 24 hr PI. Approximately 75% of the cells contained antigen in their cytoplasm 72 hr PI. The FA technique is a sensitive method for detecting EIA virus in horse leukocyte cultures.

Animals↗

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.

Aleutian Mink Disease↗