Résumé
T cell surface CD4 molecules act as co‐receptors that amplify the T cell receptor (TcR)/CD3‐induced signal transduction by a mechanism that requires the interaction of CD4 with p56lck tyrosine kinase (Veillette et al.; Nature 1989. 338: 257). Here, we demonstrate that in the absence of TcR signaling, heat‐inactivated HIV‐1 (HIV‐HI) also elicits a cascade of events generally considered to convey a positive signal, such as protein tyrosine phosphorylation, phosphatidylinositol 4‐kinase and mitogen‐activated protein kinase activation. These results contribute to understand better the control that HIV may exert on its own replication or on T cell apoptosis by modulating the activation status of its target cells through its interaction with T cell surface CD4 molecules.