Institute of Research in Infectious disease of Montpellier (IRIM), University of Montpellier, UMR9004 CNRS, Montpellier, France.
Institute for Glycomics, Griffith University, Brisbane, Australia.
Nat Commun. 2023 Oct 31;14(1):6945. doi: 10.1038/s41467-023-41940-0.
Enveloped viruses assemble and bud from the host cell membranes. Any role of cortical actin in these processes have often been a source of debate. Here, we assessed if cortical actin was involved in HIV-1 assembly in infected CD4 T lymphocytes. Our results show that preventing actin branching not only increases HIV-1 particle release but also the number of individual HIV-1 Gag assembly clusters at the T cell plasma membrane. Indeed, in infected T lymphocytes and in in vitro quantitative model systems, we show that HIV-1 Gag protein prefers areas deficient in F-actin for assembling. Finally, we found that the host factor Arpin, an inhibitor of Arp2/3 branched actin, is recruited at the membrane of infected T cells and it can associate with the viral Gag protein. Altogether, our data show that, for virus assembly and particle release, HIV-1 prefers low density of cortical actin and may favor local actin debranching by subverting Arpin.
包膜病毒从宿主细胞膜组装和出芽。皮质肌动蛋白在这些过程中的任何作用常常引起争议。在这里，我们评估了皮质肌动蛋白是否参与感染的 CD4 T 淋巴细胞中的 HIV-1 组装。我们的结果表明，阻止肌动蛋白分支不仅会增加 HIV-1 颗粒的释放，还会增加 T 细胞膜上单个 HIV-1 Gag 组装簇的数量。实际上，在感染的 T 淋巴细胞和体外定量模型系统中，我们表明 HIV-1 Gag 蛋白更喜欢缺乏 F-肌动蛋白的区域来组装。最后，我们发现宿主因子 Arpin（Arp2/3 分支肌动蛋白的抑制剂）被募集到感染 T 细胞的膜上，并且可以与病毒 Gag 蛋白结合。总而言之，我们的数据表明，对于病毒组装和颗粒释放，HIV-1 偏爱低皮质肌动蛋白密度，并可能通过颠覆 Arpin 来促进局部肌动蛋白去分支。
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