Related Experiment Videos
Clinical and immunological findings in HTLV-III infection
Clinical, immunological, microbiological, virological, and lifestyle parameters were followed in 200 homosexual men living in Finland. The subjects were seen at 3- to 6-month intervals starting in summer 1983. Human T-cell lymphotropic virus III (HTLV-III) antibodies detected by enzyme immunoassay and confirmed by Western blotting were seen in 18 (9%) of the cases. Initially two cases had acquired immunodeficiency syndrome, three had acquired immunodeficiency syndrome-related complex, three had lymphadenopathy syndrome, and ten were asymptomatic. During the follow-up two asymptomatic cases developed lymphadenopathy syndrome and three developed enlarged lymph nodes. Immunological studies revealed decreased T-helper cell values and/or T-helper/suppressor ratios in all clinical categories, the findings being more severe and progressive in the symptomatic cases. The finding most clearly distinguishing HTLV-III antibody positive cases from the antibody negative ones was a decreased response to a specific recall antigen, purified protein derivative of tuberculoprotein. Responses to mitogens phytohemagglutinin and pokeweed mitogen were also decreased, but to a lesser extent. The primary immunological defect associated with helper T-cell infection by HTLV-III thus seems to be loss of antigen specific immune responses. It is suggested that this is the result of previous antigenic stimulation of HTLV-III infected T-helper cells and that the cellular destruction is associated with initial mitotic activity.
Clinical, immunological, microbiological, virological, and lifestyle parameters were followed in 200 homosexual men living in Finland. The subjects were seen at 3- to 6-month intervals starting in summer 1983. Human T-cell lymphotropic virus III (HTLV-III) antibodies detected by enzyme immunoassay and confirmed by Western blotting were seen in 18 (9%) of the cases. Initially two cases had acquired immunodeficiency syndrome, three had acquired immunodeficiency syndrome-related complex, three had lymphadenopathy syndrome, and ten were asymptomatic. During the follow-up two asymptomatic cases developed lymphadenopathy syndrome and three developed enlarged lymph nodes. Immunological studies revealed decreased T-helper cell values and/or T-helper/suppressor ratios in all clinical categories, the findings being more severe and progressive in the symptomatic cases. The finding most clearly distinguishing HTLV-III antibody positive cases from the antibody negative ones was a decreased response to a specific recall antigen, purified protein derivative of tuberculoprotein. Responses to mitogens phytohemagglutinin and pokeweed mitogen were also decreased, but to a lesser extent. The primary immunological defect associated with helper T-cell infection by HTLV-III thus seems to be loss of antigen specific immune responses. It is suggested that this is the result of previous antigenic stimulation of HTLV-III infected T-helper cells and that the cellular destruction is associated with initial mitotic activity.