Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Methods Mol Biol. 2022;2407:31-43. doi: 10.1007/978-1-0716-1871-4_3.
HIV-1 establishes latency primarily by infecting activated CD4+ T cells that later return to quiescence as memory cells. Latency allows HIV-1 to evade immune responses and to persist during antiretroviral therapy, which represents an important problem in clinical practice. Here we describe both the original and a simplified version of HIV-1 latency models that mimics this process using replication competent viruses. Our model allows generation of large numbers of latently infected CD4+ T cell to dissect molecular mechanisms of HIV latency and reactivation.
HIV-1 主要通过感染激活的 CD4+T 细胞建立潜伏感染,这些细胞随后作为记忆细胞进入静止状态。潜伏感染使 HIV-1 能够逃避免疫反应,并在抗逆转录病毒治疗期间持续存在,这是临床实践中的一个重要问题。在这里,我们描述了 HIV-1 潜伏感染模型的原始版本和简化版本,该模型使用复制型病毒模拟了这一过程。我们的模型允许大量潜伏感染的 CD4+T 细胞的产生,从而剖析 HIV 潜伏和激活的分子机制。