Department of Medicine, University of California San Francisco, Box 1270, 513, Parnassus Avenue, San Francisco, CA, 94143-1270, USA.
AIDS Res Ther. 2012 May 20;9(1):16. doi: 10.1186/1742-6405-9-16.
Autophagy, the major mechanism for degrading long-lived intracellular proteins and organelles, is essential for eukaryotic cell homeostasis. Autophagy also defends the cell against invasion by microorganisms and has important roles in innate and adaptive immunity. Increasingly evident is that HIV-1 replication is dependent on select components of autophagy. Fittingly, HIV-1 proteins are able to modulate autophagy to maximize virus production. At the same time, HIV-1 proteins appear to disrupt autophagy in uninfected cells, thereby contributing to CD4+ cell death and HIV-1 pathogenesis. These observations allow for new approaches for the treatment and possibly the prevention of HIV-1 infection. This review focuses on the relationship between autophagy and HIV-1 infection. Discussed is how autophagy plays dual roles in HIV-1 replication and HIV-1 disease progression.
自噬是降解长寿细胞内蛋白质和细胞器的主要机制,对真核细胞的内稳态至关重要。自噬还能抵御微生物的入侵,并在先天和适应性免疫中发挥重要作用。越来越明显的是,HIV-1 的复制依赖于自噬的选择成分。恰当地说,HIV-1 蛋白能够调节自噬以最大限度地提高病毒产量。与此同时,HIV-1 蛋白似乎会破坏未感染细胞中的自噬,从而导致 CD4+细胞死亡和 HIV-1 发病机制。这些观察结果为 HIV-1 感染的治疗和可能的预防提供了新的方法。这篇综述重点介绍了自噬与 HIV-1 感染之间的关系。讨论了自噬如何在 HIV-1 复制和 HIV-1 疾病进展中发挥双重作用。