促进潜伏艾滋病病毒库细胞死亡的药理方法。

Current opinion in HIV and AIDS Pub Date : 2024-03-01 Epub Date: 2023-12-20 DOI:10.1097/COH.0000000000000837
Marilia Rita Pinzone, Liang Shan
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引用次数: 0

摘要

审查目的:由于潜伏感染细胞库的持续存在,艾滋病病毒需要终生抗病毒治疗。为了促进感染细胞的死亡,人们采取了多种策略:最近的研究结果:一些研究小组致力于采用多管齐下的方法诱导感染细胞凋亡。其中一种方法是将潜伏期逆转剂与促凋亡化合物和细胞毒性 T 细胞结合起来,首先重新激活,然后清除感染细胞。其他策略包括使用自然杀伤细胞或嵌合抗原受体细胞来减少储库的规模。这种机制依赖于艾滋病毒蛋白酶激活含 Caspase 招募域蛋白 8 (CARD8) 的炎性体,非核苷类逆转录酶抑制剂可以增强这种机制。总结:要想在临床上显著减少病毒库的规模,很可能需要采取综合策略,因为迄今为止,没有一种方法能在临床试验中单独取得成功。体外研究结果很有希望,但体内研究结果却不尽如人意,这凸显了要找到一种普遍有效的策略所面临的障碍,因为艾滋病病毒储库在组织位置、逆转潜伏期的能力以及对细胞死亡的敏感性等方面存在很大的异质性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pharmacological approaches to promote cell death of latent HIV reservoirs.

Purpose of review: HIV requires lifelong antiviral treatment due to the persistence of a reservoir of latently infected cells. Multiple strategies have been pursued to promote the death of infected cells.

Recent findings: Several groups have focused on multipronged approaches to induce apoptosis of infected cells. One approach is to combine latency reversal agents with proapoptotic compounds and cytotoxic T cells to first reactivate and then clear infected cells. Other strategies include using natural killer cells or chimeric antigen receptor cells to decrease the size of the reservoir.A novel strategy is to promote cell death by pyroptosis. This mechanism relies on the activation of the caspase recruitment domain-containing protein 8 (CARD8) inflammasome by the HIV protease and can be potentiated by nonnucleoside reverse transcriptase inhibitors.

Summary: The achievement of a clinically significant reduction in the size of the reservoir will likely require a combination strategy since none of the approaches pursued so far has been successful on its own in clinical trials. This discrepancy between promising in vitro findings and modest in vivo results highlights the hurdles of identifying a universally effective strategy given the wide heterogeneity of the HIV reservoirs in terms of tissue location, capability to undergo latency reversal and susceptibility to cell death.

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