Cellular immune responses in AIDS virus controllers

为了阐明持续控制HIV复制的机制，本研究分析了免疫恒河猴在攻击后控制SIV复制超过2年的情况。值得注意的是，这些SIV控制者中有一半在2年内有多个前病毒GAG和nef突变，而其余一半没有。1年后，前者表现出针对病毒非Gag/Nef蛋白和Gag/Nef蛋白的更广泛的细胞毒性T淋巴细胞(CTL)反应，而后者仍以GAG和Nef特异性CTL反应为主。后者代表了由Gag/Nef特异性CTL控制的非常稳定的SIV，提供了一种可能的CTL治愈HIV的机制。

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.