Inhibition of human lymphocyte mitogenesis by human and other retroviruses. Differential effect of interleukin-2 in restoration of responsiveness.

The addition of both live and ultraviolet-inactivated preparations of human T lymphotropic virus type I (HTLV-I) and HIV to cultures of human peripheral lymphocytes impeded the ability of these cells to respond to phytohaemagglutinin (PHA). This inhibition depended on the concentration of the virus and seemed due, in part at least, to interference with the generation of interleukin-2 (IL-2) activity in the PHA-stimulated cultures. However, the addition of exogenous IL-2 did not effectively restore the lymphocyte proliferative responsiveness of cells which had been co-incubated with these human retroviruses. Exposure to the viruses did not affect expression on co-incubated cells of the Tac antigen, an epitope of the IL-2 receptor, as determined by an indirect immunofluorescence assay. These results suggest that one mechanism through which human retroviruses may be able to impede cellular proliferative responsiveness is interference with the ability of target cells to respond to IL-2, even though IL-2 receptors continue to be expressed under the conditions tested.