HIV-1 infection is efficiently controlled by combination anti-retroviral therapy (cART). However, despite preventing disease progression, cART does not eradicate virus infection which persists in a latent form for an individual's lifetime. The latent reservoir comprises memory CD4+ T lymphocytes, macrophages, and dendritic cells; however, for the most part, the reservoir is generated by virus entry into activated CD4+ T lymphocytes committed to return to a resting state, even though resting CD4+ T lymphocytes can be latently infected as well. The HIV-1 reservoir is not recognized by the immune system, is quite stable, and has the potential to re-seed systemic viremia upon cART interruption. Viral rebound can occur even after a long period of cART interruption. This event is most likely a consequence of the extended half-life of the HIV-1 reservoir, the maintenance of which is not clearly understood. Several recent studies have identified extracellular vesicles (EVs) as a driving force contributing to HIV-1 reservoir preservation. In this review, we discuss recent findings in the field of EV/HIV-1 interplay, and then propose a mechanism through which EVs may contribute to HIV-1 persistence despite cART. Understanding the basis of the HIV-1 reservoir maintenance continues to be a matter of great relevance in view of the limitations of current strategies aimed at HIV-1 eradication.

中文翻译：

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HIV-1感染中的细胞外囊泡介导的细胞间通讯及其在水库维护中的作用。

通过联合抗逆转录病毒疗法（cART）可有效控制HIV-1感染。但是，尽管可以预防疾病的发展，但cART并不能消除病毒潜伏的病毒感染，这种病毒以潜伏的形式持续存在。潜在的储库包括记忆CD4 + T淋巴细胞，巨噬细胞和树突状细胞。然而，在大多数情况下，即使病毒也可以潜伏地感染静止的CD4 + T淋巴细胞，病毒还是通过病毒进入活化的CD4 + T淋巴细胞而产生，从而使病毒库恢复为静止状态。HIV-1储库未被免疫系统识别，非常稳定，并有可能在cART中断后重新接种系统性病毒血症。即使长时间中断cART，也可能发生病毒反弹。该事件很可能是由于HIV-1储存库的半衰期延长所致，其维护尚不清楚。最近的几项研究已将细胞外囊泡（EVs）识别为有助于保存HIV-1的驱动力。在这篇综述中，我们讨论了EV / HIV-1相互作用领域的最新发现，然后提出了一种机制，尽管cART，EV仍可通过该机制促进HIV-1的持久性。鉴于目前旨在消灭HIV-1的策略的局限性，了解HIV-1储库维护的基础仍然是非常重要的问题。我们讨论了EV / HIV-1相互作用领域的最新发现，然后提出了一种机制，尽管cART，EV仍可通过该机制促进HIV-1的持久性。鉴于目前旨在消灭HIV-1的策略的局限性，了解HIV-1储库维护的基础仍然是非常重要的问题。我们讨论了EV / HIV-1相互作用领域的最新发现，然后提出了一种机制，尽管cART，EV仍可通过该机制促进HIV-1的持久性。鉴于目前旨在消灭HIV-1的策略的局限性，了解HIV-1储库维护的基础仍然是非常重要的问题。