Cellular immune responses in AIDS virus controllers

为了阐明持续控制HIV复制的机制，本研究分析了在挑战后控制猴免疫缺陷病毒（SIV）复制超过2年的接种恒河猴。值得注意的是，这些SIV控制者中有一半在2岁时有多个前病毒gag和nef突变，而其余一半则没有。在1年时，前一组表现出更广泛的细胞毒性T淋巴细胞（CTL）反应，靶向病毒非Gag/Nef蛋白以及Gag/Nef，而Gag和Nef特异性CTL反应在后者中仍然占主导地位。后一组代表了Gag/Nef特异性CTL的极其稳定的SIV控制，提供了CTL功能性HIV治愈的可能机制。

To elucidate the mechanism for sustained control of HIV replication, this study analyzed vaccinated rhesus macaques that controlled simian immunodeficiency virus (SIV) replication for more than 2 years after challenge. Remarkably, half of these SIV controllers had multiple proviral gag and nef mutations at 2 years whereas the remaining half did not. At 1 year, the former group showed broader cytotoxic T lymphocyte (CTL) responses targeting viral non-Gag/Nef proteins as well as Gag/Nef, whereas Gag- and Nef-specific CTL responses were still dominant in the latter. The latter group represents an extremely stable SIV control by Gag/Nef-specific CTLs, providing a possible mechanism of functional HIV cure by CTLs.