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The pericentriolar recycling endosome plays a key role in Vpu-mediated enhancement of HIV-1 particle release

机译：中心粒回收内体在Vpu介导的HIV-1颗粒释放增强中起关键作用

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摘要

The HIV-1 accessory gene product Vpu is required for efficient viral particle release from infected human cells. The mechanism by which Vpu enhances particle assembly or release is not yet defined. Here, we identify an intracellular site that is critical for Vpu-mediated enhancement of particle release. Vpu was found to co-localize with markers for the pericentriolar recycling endosome. Expression of dominant negative mutants of Rab11a and myosin Vb that disrupt protein sorting through the recycling endosome abrogated the ability of Vpu to augment particle release. Remarkably, the effects of blocking recycling endosome function on HIV particle release were demonstrable only in human cell lines known to be responsive to Vpu, while no effect on particle release was seen in African green monkey cells. Inhibition of recycling endosome function in human cells also blocked the ability of HIV-2 envelope to enhance particle release. These studies indicate that Vpu and HIV-2 envelope glycoprotein enhance particle release via a common mechanism that requires the activity of the pericentriolar recycling endosome.
机译：HIV-1辅助基因产物Vpu是从受感染的人类细胞中有效释放病毒颗粒所必需的。 Vpu增强颗粒组装或释放的机制尚未确定。在这里，我们确定了对Vpu介导的颗粒释放增强至关重要的细胞内位点。已发现Vpu与中心粒周再循环内体的标记共定位。 Rab11a和肌球蛋白Vb的显性负突变体的表达通过循环内体破坏了蛋白质的分选，从而废除了Vpu增加颗粒释放的能力。值得注意的是，阻断循环内体功能对HIV颗粒释放的作用仅在已知对Vpu有反应的人类细胞系中可见，而在非洲绿猴细胞中未见对颗粒释放的影响。抑制人类细胞中的内体循环功能也阻止了HIV-2包膜增强颗粒释放的能力。这些研究表明，Vpu和HIV-2包膜糖蛋白通过共同的机制来增强颗粒的释放，该机制需要中心粒周再循环内体的活性。

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