HIV-1转录延伸调控潜伏感染的分子机制  

The molecular mechanism of HIV-1 transcriptional elongation regulating latent infection

作　　者：胡淑婧 邓凯 HU Shujing;DENG Kai(Zhongshan School of Medicine Sun Yat-sen University,Guangzhou 510080,China)

机构地区：[1]中山大学中山医学院,广州510080

出　　处：《广西医科大学学报》2024年第10期1331-1337,共7页Journal of Guangxi Medical University

摘　　要：人类免疫缺陷病毒1型(HIV-1)作为获得性免疫缺陷综合征(AIDS)的主要致病病原体,目前尚无有效治愈方法。现有的抗逆转录病毒疗法(ART)虽然可以有效抑制病毒复制,但却无法清除潜伏感染的细胞。因此,当前面临的主要挑战是找到安全、有效的方法清除HIV-1潜伏储存库。HIV-1潜伏维持和再激活分子机制的研究已经揭示了HIV-1转录延伸过程在其中所起的核心作用。本综述主要概述HIV-1转录延伸的具体分子过程以及对潜伏感染的调控作用,为进一步探究HIV-1如何实现潜伏和活跃转录之间的平衡提供理论支持,为实现AIDS治愈提供新方向。Human immunodeficiency virus type 1(HIV-1)is the main causative agent of acquired immunodeficiency syndrome(AIDS),and there is currently no effective cure.Although the existing antiretroviral therapy(ART)can effectively suppress virus replication,it cannot clear the latently infected cells.Therefore,the main challenge in this field is to find safe and effective methods to clear HIV-1 latent reservoirs.The current research on the molecular mechanisms of HIV-1 latency maintenance and reactivation has revealed that the transcriptional elongation process of HIV-1 plays a central role in this process.This review summarizes and provides an overview of the specific molecular processes of HIV-1 transcription elongation and its role in regulating latent infection,providing theoretical support for further exploring how HIV-1 achieves a balance between latent and active transcription,with the aim of providing new directions for achieving AIDS cure.

关 键 词：人类免疫缺陷病毒1型 潜伏感染 转录延伸 反式激活蛋白(Tat) 正转录延伸因子b(P-TEFb) 

分 类 号：R512.91[医药卫生—内科学]