Department of Microbiology and Molecular Genetics and Department of Medicine, Division of Infectious Diseases, School of Medicine, University of California, Irvine, Irvine, CA 92697, USA.
Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Cell Rep Med. 2020 Dec 22;1(9):100162. doi: 10.1016/j.xcrm.2020.100162.
HIV latency prevents cure of infection with antiretroviral therapy (ART) alone. One strategy for eliminating latently infected cells involves the induction of viral protein expression via latency-reversing agents (LRAs), allowing killing of host cells by viral cytopathic effects or immune effector mechanisms. Here, we combine a barcoded HIV approach and a humanized mouse model to study the effects of a designed, synthetic protein kinase C modulating LRA on HIV rebound. We show that administration of this compound during ART results in a delay in rebound once ART is stopped. Furthermore, the rebounding virus appears composed of a smaller number of unique barcoded viruses than occurs in control-treated animals, suggesting that some reservoir cells that would have contributed virus to the rebound process are eliminated by LRA administration. These data support the use of barcoded virus to study rebound and suggest that LRAs may be useful in HIV cure efforts.
HIV 潜伏期阻止了仅通过抗逆转录病毒疗法 (ART) 治愈感染。消除潜伏感染细胞的一种策略涉及通过潜伏逆转剂 (LRA) 诱导病毒蛋白表达,从而允许通过病毒细胞病变效应或免疫效应机制杀死宿主细胞。在这里,我们结合了带有条码的 HIV 方法和人源化小鼠模型来研究一种设计的、合成的蛋白激酶 C 调节 LRA 对 HIV 反弹的影响。我们表明,ART 期间给予该化合物可导致 ART 停止后反弹延迟。此外,与对照处理的动物相比,反弹病毒似乎由较少数量的独特条码病毒组成,这表明一些原本会为反弹过程提供病毒的储存细胞被 LRA 给药消除。这些数据支持使用带有条码的病毒来研究反弹,并表明 LRA 可能对 HIV 治愈努力有用。