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The cytotoxic T-cell (CTL) response to human immunodeficiency virus Type 1 (HIV-1) is vigorous and sustained, but despite this, the virus persists. Natural variation arising within CTL epitopes may affect CTL recognition of infected targets and allow viral escape. Some of these variant epitopes appear to engage T-cell receptors but fail to activate the CTL normally. This can interfere with recognition of the unmutated epitope - a phenomenon known as T-cell antagonism. We discuss the evidence for this in HIV-1 using CTL and epitope variants derived from infected donors, and discuss its possible relevance in vivo.

Original publication




Journal article


Seminars in Virology

Publication Date





31 - 39