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首页> 外文期刊>AIDS Research and Human Retroviruses >Activation of P-TEFb at Sites of Dual HIV/TB Infection, and Inhibition of MTB-Induced HIV Transcriptional Activation by the Inhibitor of CDK9, lndirubin-3'-Monoxime
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Activation of P-TEFb at Sites of Dual HIV/TB Infection, and Inhibition of MTB-Induced HIV Transcriptional Activation by the Inhibitor of CDK9, lndirubin-3'-Monoxime

机译：在双重HIV / TB感染部位激活P-TEFb，并通过CDK9抑制剂Indirubin-3'-Monoxime抑制MTB诱导的HIV转录激活。

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At sites of Mycobacterium tuberculosis (MTB) infection, HIV-1 replication is increased during tuberculosis (TB). Here we investigated the role of positive transcription elongation factor (P-TEFb), comprised of CycT1 and CDK9, as the cellular cofactor of HIV-1 Tat protein in transcriptional activation of HIV-1 in mononuclear cells from HIV-1-infected patients with pleural TB. Expression of CycT1 in response to MTB was assessed in mononuclear cells from pleural fluid (PFMC) and blood (PBMC) from HIV/TB patients with pleural TB, and in blood monocytes (MN) from singly infected HIV-1-seropositive subjects. We then examined whether the CDK9 inhibitor, Indirubin 3'-monoxime (IM), was effective in inhibition of MTB-induced HIV-1 mRNA expression. We found higher expression of CycT1 mRNA in PFMCs as compared to PBMCs from HIV/TB-coinfected subjects. MTB induced the expression of CycT1 and HIV-1 gag/pol mRNA in both PFMCs from HIV/TB subjects and MN from HIV-1-infected subjects. CycT1 protein was also induced by MTB stimulation in PFMCs from HIV/TB patients, and both MN and in vitro-derived macrophages. Inhibition of CDK9 by IM in both PFMCs from HIV/TB and MN from HIV-1-infected subjects in response to MTB led to inhibition of HIV-1 mRNA expression. These data imply that IM may be useful as an adjunctive therapy in control of HIV-1 replication in HIV/TB dually infected subjects.
机译：在结核分枝杆菌（MTB）感染部位，HIV-1复制在结核病（TB）期间增加。在这里，我们研究了由CycT1和CDK9组成的正转录延伸因子（P-TEFb）作为HIV-1 Tat蛋白的细胞辅因子在HIV-1感染患者单核细胞中HIV-1转录激活中的作用。胸膜结核。在来自患有胸膜结核的HIV / TB患者的胸膜液（PFMC）和血液（PBMC）的单核细胞中，以及来自单独感染HIV-1血清阳性受试者的血液单核细胞（MN）中，对CycT1响应MTB的表达进行了评估。然后，我们检查了CDK9抑制剂靛玉红3'-一肟（IM）是否有效抑制MTB诱导的HIV-1 mRNA表达。我们发现，与来自HIV / TB合并感染受试者的PBMC相比，PFMC中CycT1 mRNA的表达更高。 MTB诱导了来自HIV / TB受试者的PFMC和来自HIV-1感染受试者的MN中CycT1和HIV-1 gag / pol mRNA的表达。 CycT1蛋白也被MTB刺激在来自HIV / TB患者，MN和体外巨噬细胞的PFMC中诱导。 IM对来自HIV / TB的PFMC和来自HIV-1感染的受试者的MN响应MTB的IM抑制CDK9导致HIV-1 mRNA表达的抑制。这些数据表明，IM可用作控制HIV / TB双重感染受试者中HIV-1复制的辅助治疗。

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