Murine models of Vpr-mediated pathogenesis.
Murine models of Vpr-mediated pathogenesis.
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DOI：
10.2174/157016209787581526
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发表时间：
2009-02
影响因子：
1
通讯作者：
Alexandra Snyder;M. Ross
中科院分区：
文献类型：
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作者：
Alexandra Snyder;M. Ross
HIV病毒蛋白r（Vpr）发挥多种细胞效应，包括调节转录和细胞因子产生、凋亡和细胞周期停滞。Vpr通过包括抑制NF-κ B活化、诱导线粒体损伤和促进导致细胞周期停滞的细胞因子的蛋白酶体降解的机制诱导这些作用。小鼠模型为我们理解HIV发病机制提供了宝贵的贡献，然而许多HIV-1蛋白（包括Vpr）的细胞效应取决于细胞类型和物种特异性因素。由于大多数阐明Vpr在疾病发病机制中的作用的体内研究都使用了小鼠模型，因此了解可能影响Vpr功能的种属特异性因素至关重要。在这篇手稿中，我们回顾了细胞通路和终末器官的影响，Vpr已在小鼠细胞系和小鼠模型中进行了研究，并讨论了这些研究的相关性Vpr在艾滋病毒/艾滋病患者的疾病中的作用。
HIV viral protein r (Vpr) exerts a variety of cellular effects, including modulation of transcription and cytokine production, apoptosis, and cell cycle arrest. Vpr induces these affects by mechanisms that include inhibition of NF-kappaB activation, inducing mitochondrial injury, and promoting proteasomal degradation of cellular factor(s) leading to cell cycle arrest. Murine models have provided invaluable contributions to our understanding of HIV pathogenesis, however many of the HIV-1 proteins, including Vpr, differ in their cellular effects depending upon cell type and species-specific factors. Since the majority of in vivo studies elucidating the role of Vpr in disease pathogenesis have utilized murine models, it is critical to understand the species-specific factors that may affect Vpr function. In this manuscript, we review the cellular pathways and end organ effects of Vpr that have been studied in murine cell lines and mouse models, and discuss the relevance of these studies to the role of Vpr in disease in persons living with HIV/AIDS.