Résumé : T cells are central players in the immune response to infectious disease, with the specificity of their responses controlled by the T-cell receptor (TCR)/CD3 complex on the cell surface. Impairment of TCR/CD3- directed CD4+ T-cell immune responses is frequently observed in individuals infected with human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2). Virus replication is also regulated by T-cell activation factors, with HIV-1 and HIV-2 responding to different TCR/CD3-directed cellular pathways. We previously demonstrated that HIV-1 infection of the human interleukin-2- dependent CD4+ T-cell line WE17/10 abrogates TCR/CD3 function and surface expression by a specific loss of CD3-γ gene transcripts. In this study, we show that HIV-2 provokes the same molecular defect in CD3-γ gene transcripts, resulting in a similar but delayed progressive loss of TCR/CD3 surface expression after infection.