Evans D T, O'Connor D H, Jing P, Dzuris J L, Sidney J, da Silva J, Allen T M, Horton H, Venham J E, Rudersdorf R A, Vogel T, Pauza C D, Bontrop R E, DeMars R, Sette A, Hughes A L, Watkins D I
Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Court, Madison, Wisconsin 53715, USA.
Nat Med. 1999 Nov;5(11):1270-6. doi: 10.1038/15224.
Cytotoxic T-lymphocyte (CTL) responses to human immunodeficiency virus arise early after infection, but ultimately fail to prevent progression to AIDS. Human immunodeficiency virus may evade the CTL response by accumulating amino-acid replacements within CTL epitopes. We studied 10 CTL epitopes during the course of simian immunodeficiency virus disease progression in three related macaques. All 10 of these CTL epitopes accumulated amino-acid replacements and showed evidence of positive selection by the time the macaques died. Many of the amino-acid replacements in these epitopes reduced or eliminated major histocompatibility complex class I binding and/or CTL recognition. These findings strongly support the CTL 'escape' hypothesis.
细胞毒性T淋巴细胞（CTL）对人类免疫缺陷病毒的反应在感染后早期就会出现，但最终无法阻止病情发展为艾滋病。人类免疫缺陷病毒可能通过在CTL表位内积累氨基酸置换来逃避CTL反应。我们在三只相关猕猴的猿猴免疫缺陷病毒疾病进展过程中研究了10个CTL表位。在猕猴死亡时，所有这10个CTL表位都积累了氨基酸置换，并显示出正选择的证据。这些表位中的许多氨基酸置换减少或消除了主要组织相容性复合体I类结合和/或CTL识别。这些发现有力地支持了CTL“逃逸”假说。
