Immune activation is the hallmark of HIV infection and plays a role in the pathogenesis of the disease. In the context of suppressed HIV RNA replication by combination antiretroviral therapy (cART), there remains immune activation which is associated to the HIV reservoirs. Persistent virus contributes to a sustained inflammatory environment promoting accumulation of “activated/exhausted” T cells with diminished effector function. These T cells show increased expression of immunomodulatory receptors including Programmed cell death protein (PD1), Cytotoxic T Lymphocyte Associated Protein 4 (CTLA4), Lymphocyte activation gene 3 (LAG3), T cell immunoglobulin and ITIM domain (TIGIT), T cell immunoglobulin and mucin domain containing 3 (TIM3) among others. More importantly, recent reports had demonstrated that, HIV infected T cells express checkpoint receptors, contributing to their survival and promoting maintenance of the viral reservoir. Therapeutic strategies are focused on viral reservoir elimination and/or those to achieve sustained cART-free virologic remission. In this review, we will discuss the immunological basis and the latest advances of the use of checkpoint inhibitors to treat HIV infection.

免疫激活是HIV感染的标志，并在疾病的发病机理中起作用。在通过联合抗逆转录病毒疗法（cART）抑制HIV RNA复制的情况下，仍然存在与HIV储库相关的免疫激活。持久性病毒有助于持续的炎症环境，促进“激活/耗尽”的T细胞积累，效应功能减弱。这些T细胞显示出免疫调节受体的表达增加，包括程序性细胞死亡蛋白（PD1），细胞毒性T淋巴细胞相关蛋白4（CTLA4），淋巴细胞激活基因3（LAG3），T细胞免疫球蛋白和ITIM结构域（TIGIT），T细胞免疫球蛋白和包含3（TIM3）的粘蛋白域。更重要的是，最近的报告表明，被HIV感染的T细胞表达检查点受体，有助于其存活并促进病毒库的维持。治疗策略集中在消除病毒库和/或实现持续无cART病毒学缓解的策略上。在这篇综述中，我们将讨论使用检查点抑制剂治疗HIV感染的免疫学基础和最新进展。