Autographa Californica Multiple Nucleopolyhedrovirus Enters Host Cells via Clathrin-Mediated Endocytosis and Direct Fusion with the Plasma Membrane.
Autographa Californica Multiple Nucleopolyhedrovirus Enters Host Cells via Clathrin-Mediated Endocytosis and Direct Fusion with the Plasma Membrane.
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苜蓿银纹夜蛾多核多角体病毒通过网格蛋白介导的内吞作用并与质膜直接融合进入宿主细胞
DOI：
10.3390/v10110632
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发表时间：
2018-11-14
期刊：
影响因子：
--
通讯作者：
Sun X
中科院分区：
文献类型：
--
作者：
Qin F;Xu C;Lei C;Hu J;Sun X
苜蓿银纹夜蛾多重核多角体病毒 (AcMNPV) 的细胞进入机制尚不完全清楚。先前的研究表明，AcMNPV 主要通过网格蛋白介导的内吞作用进入宿主细胞，并且在低 pH 触发后可以通过与质膜融合来有效感染细胞。然而，AcMNPV是否同时通过这两种途径进入细胞，以及AcMNPV颗粒内化到细胞中的确切方式仍不清楚。在这项研究中，使用单病毒追踪，我们观察到 AcMNPV 颗粒首先被预先存在的网格蛋白包被的小坑 (CCP) 捕获，然后被递送到早期内体。基于群体的单病毒追踪分析和定量电子显微镜表明，大多数颗粒被 CCP 捕获并通过内陷内化。相比之下，少数病毒颗粒没有被递送到CCP，而是通过与质膜直接融合而不内陷而被内化。定量电子显微镜还表明，虽然抑制 CCP 组装会显着损害病毒内化，但抑制内体酸化会阻止病毒颗粒脱离囊泡。总的来说，这些发现表明，大约 90% 的 AcMNPV 颗粒通过网格蛋白介导的内吞作用进入细胞，10% 通过与质膜直接融合进入细胞。这项研究将有助于更好地了解 AcMNPV 感染。
The cell entry mechanism of Autographa californica multiple nucleopolyhedrovirus (AcMNPV) is not fully understood. Previous studies showed that AcMNPV entered host cells primarily through clathrin-mediated endocytosis, and could efficiently infect cells via fusion with the plasma membrane after a low-pH trigger. However, whether AcMNPV enters cells via these two pathways simultaneously, and the exact manner in which AcMNPV particles are internalized into cells remains unclear. In this study, using single-virus tracking, we observed that AcMNPV particles were first captured by pre-existing clathrin-coated pits (CCP), and were then delivered to early endosomes. Population-based analysis of single-virus tracking and quantitative electron microscopy demonstrated that the majority of particles were captured by CCPs and internalized via invagination. In contrast, a minority of virus particles were not delivered to CCPs, and were internalized through direct fusion with the plasma membrane without invagination. Quantitative electron microscopy also showed that, while inhibition of CCP assembly significantly impaired viral internalization, inhibition of endosomal acidification blocked virus particles out of vesicles. Collectively, these findings demonstrated that approximately 90% of AcMNPV particles entered cells through clathrin-mediated endocytosis and 10% entered via direct fusion with the plasma membrane. This study will lead toward a better understanding of AcMNPV infection.
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