Dahabieh Matthew S, Battivelli Emilie, Verdin Eric
Gladstone Institute of Virology and Immunology, University of California, San Francisco, California 94941; email:
Annu Rev Med. 2015;66:407-21. doi: 10.1146/annurev-med-092112-152941.
Treatment with antiretroviral therapy dramatically increases the survival of HIV-infected individuals. However, treatment has to be continued for life because it does not lead to the full eradication of infection. HIV persists in resting CD4(+) T cells, and possibly other cell types, and can reemerge from these cells when therapy is interrupted. Here, we review molecular mechanisms that have been proposed to contribute to HIV latency, as well as the relative roles of cis- and trans-acting mechanisms. We also discuss existing and future therapeutic opportunities regarding HIV latency that might lead to a future cure for HIV infection.
抗逆转录病毒疗法显著提高了HIV感染者的生存率。然而,治疗必须终身持续,因为它并不能完全根除感染。HIV潜伏于静息CD4(+) T细胞以及可能的其他细胞类型中,当治疗中断时可从这些细胞中重新出现。在此,我们综述了已提出的有助于HIV潜伏的分子机制,以及顺式和反式作用机制的相对作用。我们还讨论了关于HIV潜伏的现有和未来治疗机会,这些机会可能会带来未来治愈HIV感染的方法。