Laboratory of Virology, Department of Biological Chemistry, IQUIBICEN, School of Science, University of Buenos Aires, Ciudad Universitaria, Pabellón 2, 4to. Piso, Intendente Güiraldes 2160, C1428EGA Buenos Aires, Argentina.
Biomed Res Int. 2014;2014:989101. doi: 10.1155/2014/989101. Epub 2014 May 12.
Since antiretroviral therapy suppresses but does not eradicate HIV-1 infection, methods to purge viral reservoirs are required. Many strategies involve the reactivation of chronically HIV infected cells to induce the expression of integrated viral genome. In this study, five bioactive compounds, the plant derivatives 1-cinnamoyl-3,11-dihydroxymeliacarpin (CDM), nordihydroguaiaretic acid (NDGA), and curcumin (Cur) and the synthetic stigmasterol analogs (22S,23S)-22,23-dihydroxystigmast-4-en-3-one (compound 1) and (22S,23S)-3 β -bromo-5 α ,22,23-trihydroxystigmastan-6-one (compound 2), were evaluated for their ability to elicit HIV replication in promonocytic (U1) and lymphocytic (H9+) HIV-1 chronically infected cells. The results revealed that natural compounds CDM, NDGA, and Cur were able to increase HIV-1 p24 antigen, determined by ELISA, only in latently infected promonocytic cells. CDM would reactivate HIV from latency by modulating the release of IL-6 and TNF- α , since the amount of both cytokines measured through ELISA significantly increased in U1 treated cells. Besides, NDGA increased ROS production, which might be related to the increase on p24 level observed in NDGA treated U1. These findings suggest that CDM, NDGA, and Cur might be candidates for further studies on latency-reversing therapeutics to eliminate latently HIV-1 reservoirs.
由于抗逆转录病毒疗法抑制但不能消除 HIV-1 感染,因此需要清除病毒库的方法。许多策略涉及到慢性 HIV 感染细胞的激活,以诱导整合病毒基因组的表达。在这项研究中,五种生物活性化合物,植物衍生物 1-肉桂酰基-3,11-二羟基美拉卡宾(CDM)、去甲二氢愈创木酸(NDGA)和姜黄素(Cur)以及合成豆甾醇类似物(22S,23S)-22,23-二羟基豆甾-4-烯-3-酮(化合物 1)和(22S,23S)-3β-溴-5α,22,23-三羟基豆甾烷-6-酮(化合物 2),被评估其诱导促单核细胞(U1)和淋巴细胞(H9+)HIV-1 慢性感染细胞中 HIV 复制的能力。结果表明,天然化合物 CDM、NDGA 和 Cur 仅能通过 ELISA 测定,在潜伏感染的促单核细胞中增加 HIV-1 p24 抗原。CDM 通过调节白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的释放来重新激活 HIV 潜伏感染,因为通过 ELISA 测量的这两种细胞因子的量在 U1 处理的细胞中显著增加。此外,NDGA 增加了 ROS 的产生,这可能与 NDGA 处理的 U1 中观察到的 p24 水平增加有关。这些发现表明,CDM、NDGA 和 Cur 可能是进一步研究潜伏逆转治疗以消除潜伏 HIV-1 库的候选药物。