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Infection with human immunodeficiency virus (HIV) induces potent cytotoxic T lymphocyte (CTL) response. Their level of activity is often extraordinary high, which in the presence of normal precursor levels suggests that effector CTL may be overstimulated and terminally differentiated. Late in HIV infection the CTL response declines. Possible mechanisms for this are discussed, including clonal exhaustion, lack of T cell help and virus escape by mutations involving epitope sequences. Evidence for the last is presented. Such escape potential implies that CTL are important in controlling the virus infection and that HLA type could have an effect on outcome. Escape mutation also has implications for vaccine design. © 1993 Academic Press. All rights reserved.

Original publication




Journal article


Seminars in Virology

Publication Date





83 - 94