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Decreased, Deformed, Defective—How HIV-1 Vpu Targets Peroxisomes

机译:减少,变形,有缺陷 - HIV-1 VPU如何靶向过氧化物

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摘要

Peroxisomes are found in essentially all eukaryotic cells and have been described as important hubs in innate sensing and the induction of type III interferons upon viral infection. Nevertheless, it remains poorly investigated how viral pathogens modulate biogenesis or function of peroxisomes to evade innate sensing and restriction. In a recent study, Hobman and colleagues found that the accessory viral protein u (Vpu) of HIV-1 inhibits peroxisome activity by depleting cellular peroxisome pools. This depletion could be ascribed to a Vpu-dependent induction of four microRNAs (miRNAs) that suppress the expression of peroxisomal biogenesis factors PEX2, PEX7, PEX11B, and PEX13. Although the downstream effects on antiretroviral gene expression and HIV-1 replication remain to be determined, these findings provide important insights into peroxisome biogenesis and the modulation of cell organelles by HIV-1 Vpu.
机译:过氧化血剂在基本上发现所有真核细胞,并且已被描述为先天感测的重要中心,并且在病毒感染时III型干扰素的诱导。尽管如此,它仍然仍然难以调节病毒病原体如何调节过氧化物的生物发生或功能,以逃避先天传感和限制。在最近的一项研究中,Hobman和同事发现,HIV-1的辅助病毒蛋白U(VPU)通过耗尽细胞过氧缺血池来抑制过氧缺血性活性。该耗竭可以归因于抑制过氧化体生物发生因子Pex2,Pex7,Pex11b和Pex13的表达的VPU依赖性诱导诱导的四个microRNAs(miRNA)。虽然仍有待确定对抗逆转录病毒基因表达和HIV-1复制的下游效应,但这些发现提供了对过氧化物体生物发生的重要见解和HIV-1 VPU的细胞器的调节。

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