蛋白激酶R的抑制作用可抑制HIV在CD4 T细胞中的复制和整合。
Inhibition of protein kinase R suppresses HIV replication and integration in CD4 T cells.
作者信息
Pyburn Jaeden, Zhao Juan, Wang Ling, Schank Madison, Hill Addison C, Banik Puja, Zhang Yi, Wu Xiao Y, Lightner Janet W, Orfield Holly K, Leshaodo Tabitha O, El Gazzar Mohamed, Ning Shunbin, Moorman Jonathan P, Yao Zhi Q
机构信息
Center of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Department of Internal Medicine, Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
出版信息
J Virus Erad. 2025 Aug 7;11(3):100605. doi: 10.1016/j.jve.2025.100605. eCollection 2025 Sep.
Evaluation of CD4 T cell status in early HIV infection is critical for developing strategies targeting HIV replication. In this study, we infected CD4 T cells with HIV-1 and investigated the cell survival mechanisms in HIV-infected versus uninfected cells during early HIV infection. Notably, HIV-infected CD4 T cells exhibited elevated levels of phosphorylated eukaryotic translation initiation factor 2-alpha (p-eIF2α) compared to uninfected cells. Importantly, inhibition of protein kinase R (PKR) in HIV-infected cells significantly suppressed HIV p24 protein expression by disrupting HIV reverse transcription and integration. These results suggest that targeting PKR could be a promising therapeutic approach against HIV infection.
评估早期HIV感染中CD4 T细胞状态对于制定针对HIV复制的策略至关重要。在本研究中，我们用HIV-1感染CD4 T细胞，并研究了早期HIV感染期间HIV感染细胞与未感染细胞的细胞存活机制。值得注意的是，与未感染细胞相比，HIV感染的CD4 T细胞中磷酸化真核翻译起始因子2-α（p-eIF2α）水平升高。重要的是，抑制HIV感染细胞中的蛋白激酶R（PKR）可通过破坏HIV逆转录和整合来显著抑制HIV p24蛋白表达。这些结果表明，靶向PKR可能是一种有前景的抗HIV感染治疗方法。
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