Lassen Kara, Han Yefei, Zhou Yan, Siliciano Janet, Siliciano Robert F
Johns Hopkins University School of Medicine, 879 BRB, 733N, Baltimore, MD 21205, USA.
Trends Mol Med. 2004 Nov;10(11):525-31. doi: 10.1016/j.molmed.2004.09.006.
HIV-1 can avoid host immune responses and antiretroviral drugs through the latent infection of resting memory CD4(+) T cells. Recently, latent viral genomes have been shown to reside within the introns of active host genes. Therefore, latency is not simply due to an inaccessibility of the integrated proviruses to the transcriptional machinery. Rather, latency might result from insufficient nuclear levels of the crucial activation-dependent host transcription factors required to overcome the transcriptional interference that is an automatic consequence of the nature of HIV-1 integration sites. In addition, resting cells lack sufficient levels of HIV-1 Tat and Tat-associated activation-dependent host factors that are necessary for processive transcription. Defects at consecutive steps of transcriptional initiation and elongation enable HIV-1 to remain hidden within resting CD4(+) T cells.
人类免疫缺陷病毒1型（HIV-1）可通过静息记忆性CD4（+）T细胞的潜伏感染来逃避宿主免疫反应和抗逆转录病毒药物。最近研究表明，潜伏的病毒基因组存在于活跃宿主基因的内含子中。因此，潜伏期不只是由于整合的前病毒难以接触转录机制。相反，潜伏期可能是由于克服转录干扰所需的关键激活依赖性宿主转录因子的核水平不足，而转录干扰是HIV-1整合位点性质的必然结果。此外，静息细胞缺乏HIV-1反式激活因子（Tat）及Tat相关的激活依赖性宿主因子，而这些因子是持续转录所必需的。转录起始和延伸连续步骤中的缺陷使HIV-1能够隐藏在静息CD4（+）T细胞内。
