Abstract

In an effort to clarify the effect of human T cell leukaemia virus type I (HTLV-I) infection on virus-specific CD8+ cytotoxic T cells, a herpes simplex virus-specific CD8+ cytotoxic T cell clone was infected with HTLV-I in vitro. The cytotoxic activity of the clone was found to have declined early after HTLV-I infection when the expression of T cell receptor-CD3 complex on the cell surface still showed no difference in comparison with that of uninfected parent cells. After 16 weeks of HTLV-I infection, expression of T cell receptor-CD3 complex on HTLV-I-infected clone cells became decreased. This phenomenon is similar to the effect of HTLV-I infection on CD4+ cytotoxic T cells as we previously reported, and suggests that there are common mechanisms of declined cytotoxic activity mediated by both CD4+ and CD8+ cytotoxic T cells following infection with HTLV-I. Such functional alterations of cytotoxic effector cells might be one of the mechanisms underlying immunodeficiency caused by HTLV-I infection.

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