Lack of reactivity of anti-human immunodeficiency virus (HIV) P17/18 antibodies against alpha 1 thymosin and of anti-alpha 1 thymosin monoclonal antibody against P17/18 protein.

The blood rate of alpha 1 thymosin is increased during HIV infection, despite the thymus involution. Anti-alpha 1 thymosin antibodies inhibit HIV replication in vitro. A homology between alpha 1 thymosin and the HIV P17/18 core protein exists and would explain a cross-antigenicity. We have studied the interaction between anti P17/18 antibodies from HIV patients and alpha 1 thymosin and between an anti-alpha 1 thymosin monoclonal antibody and the P17/18 protein. We were unable to confirm any cross-reactivity. During acquired immune deficiency syndrome, a major involution of the thymus appears with a severe depletion of thymocytes and epithelial cells. Certain thymic functions are missing, as corroborated by the reduction of the hormone thymulin in the blood. At the same time, the blood rate of the 2 other hormones (partly of thymic origin), alpha 1 thymosin and beta 4 thymosin is increased. One of the theories explaining this discordance is that patients with acquired immunodeficiency syndrome produce molecules which have a cross antigenicity with these thymic hormones. Sarin et al. have recorded a 50% homology between the C-terminal part (last 18 aminoacids) of alpha 1 thymosin and the part between the 92nd and the 109th aminoacids of the HIV P17/18 protein. The cross reactivity between this P17/18 protein and alpha 1 thymosin would explain the high rates of alpha 1 thymosin found in the radio-immunoassay of sera from patients infected with HIV. Another result of this cross-reactivity is the ability of alpha 1 thymosin antibodies to inhibit HIV replication in the H9 permissive cell line.(ABSTRACT TRUNCATED AT 250 WORDS)