本文第一作者、CRCHUM 博士后研究人员Jonathan Richard 解释说：“病毒已经摆脱了CD4蛋白来保护自己。添加小分子可迫使病毒包膜打开，就像一朵花。然后，感染后自然存在的抗体，可以靶定感染的细胞，所以它们会被免疫系统杀死。”JP-III-48分子是由哈佛大学和宾夕法尼亚大学的研究人员开发；然而，这是第一次在HIV感染者中测试成功。
几十年来，科学家们一直试图设计一种疫苗，阻止HIV的感染，HIV可导致艾滋病。抗逆转录病毒药物可以减缓病毒的传播，但病毒仍然隐藏潜伏在细胞中，当治疗停止时它们就会恢复。这就是所谓的HIV“病毒库”。 Finzi认为：“解决这个问题的办法是，开发一种‘引蛇出洞（shock and kill）’的治疗方法。我们必须重新激活HIV病毒库，以迫使病毒从它藏身的地方出来，然后用这种分子和已经存在的抗体杀死受感染的细胞。”
原文：CD4 mimetics sensitize HIV-1-infected cells to ADCC
Abstract: HIV-1-infected cells presenting envelope glycoproteins (Env) in the CD4-bound conformation on their surface are preferentially targeted by antibody-dependent cell-mediated cytotoxicity (ADCC). HIV-1 has evolved a sophisticated mechanism to avoid exposure of ADCC-mediating Env epitopes by down-regulating CD4 and by limiting the overall amount of Env at the cell surface. Here we report that small-molecule CD4-mimetic compounds induce the CD4-bound conformation of Env, and thereby sensitize cells infected with primary HIV-1 isolates to ADCC mediated by antibodies present in sera, cervicovaginal lavages, and breast milk from HIV-1-infected individuals. Importantly, we identified one CD4 mimetic with the capacity to sensitize endogenously infected ex vivo-amplified primary CD4 T cells to ADCC killing mediated by autologous sera and effector cells. Thus, CD4 mimetics hold the promise of therapeutic utility in preventing and controlling HIV-1 infection.