The C-promoter binding factor-1 (CBF-1) is a potent and specific inhibitor of the human immunodeficiency virus (HIV)-1 LTR promoter. Here, we demonstrate that the knockdown of endogenous CBF-1 in latently infected primary CD4+ T cells, using specific small hairpin RNAs (shRNA), resulted in the reactivation of latent HIV proviruses. Chromatin immunoprecipitation (ChIP) assays using latently infected primary T cells and Jurkat T-cell lines demonstrated that CBF-1 induces the establishment and maintenance of HIV latency by recruiting polycomb group (PcG/PRC) corepressor complexes or polycomb repressive complexes 1 and 2 (PRC1 and PRC2). Knockdown of CBF-1 resulted in the dissociation of PRCs corepressor complexes enhancing the recruitment of RNA polymerase II (RNAP II) at HIV LTR. Knockdown of certain components of PRC1 and PRC2 also led to the reactivation of latent proviruses. Similarly, the treatment of latently infected primary CD4+ T cells with the PRC2/EZH2 inhibitor, 3-deazaneplanocin A (DZNep), led to their reactivation.

中文翻译：

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CBF-1通过在HIV LTR招募多梳抑制复合物PRC1和PRC2来促进建立和维持HIV潜伏期。

C启动子结合因子1（CBF-1）是一种有效且特异性的人类免疫缺陷病毒（HIV）-1 LTR启动子抑制剂。在这里，我们证明了使用特定的小发夹RNA（shRNA）在潜在感染的原代CD4 + T细胞中内源性CBF-1的敲低导致了潜在HIV原病毒的重新激活。使用潜在感染的原代T细胞和Jurkat T细胞系的染色质免疫沉淀（ChIP）分析表明，CBF-1通过募集多梳子组（PcG / PRC）核心加压复合物或多梳子抑制复合物1和2诱导了HIV潜伏期的建立和维持（ PRC1和PRC2）。击倒CBF-1导致PRCs核心加压因子复合物解离，从而增强了HIV LTR上RNA聚合酶II（RNAP II）的募集。敲低PRC1和PRC2的某些组件也导致潜在的前病毒重新激活。同样，用PRC2 / EZH2抑制剂3-deazaneplanocin A（DZNep）处理潜伏感染的原代CD4 + T细胞导致其重新激活。