Entry of dengue virus serotype 2 into ECV304 cells depends on clathrin-dependent endocytosis, but not on caveolae-dependent endocytosis.
Entry of dengue virus serotype 2 into ECV304 cells depends on clathrin-dependent endocytosis, but not on caveolae-dependent endocytosis.
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DOI：
10.1139/w08-107
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发表时间：
2009-03
影响因子：
2.8
通讯作者：
T. Peng;Jia-li Wang;Wei Chen;Jun-lei Zhang;Na Gao;Zong-tao Chen;Xiaofeng Xu;Dong-ying Fan;J. An
中科院分区：
文献类型：
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作者：
T. Peng;Jia-li Wang;Wei Chen;Jun-lei Zhang;Na Gao;Zong-tao Chen;Xiaofeng Xu;Dong-ying Fan;J. An
小窝和网格蛋白介导的内吞作用是几种病原体使用的主要内化途径;然而，它们在登革病毒（DV）进入中的独特作用尚未得到解决。在这项研究中，我们比较了小窝和网格蛋白介导的内吞作用在感染性进入DV血清型2（DV 2）到人内皮样ECV 304细胞的参与。对DV 2感染细胞的共聚焦显微镜研究表明，病毒抗原与网格蛋白重链、表皮生长因子途径底物克隆15（Eps 15）和adaptin-α共定位，但不与小窝蛋白-1共定位。氯丙嗪，抑制网格蛋白依赖的内吞作用，治疗导致减少病毒进入细胞，而用制霉菌素，小窝抑制剂，治疗没有。此外，Eps 15的基因沉默导致DV 2对ECV 304细胞的感染平均减少75%。我们的研究结果表明，DV 2进入ECV 304细胞网格蛋白依赖的内吞作用，而不是小窝依赖的内吞作用。
Caveolae- and clathrin-mediated endocytosis are major internalization pathways used by several pathogens; however, their distinctive roles in dengue virus (DV) entry have not been addressed. In this study, we compared the involvement of caveolae- and clathrin-mediated endocytosis in the infectious entry of DV serotype 2 (DV2) into human endothelial-like ECV304 cells. Confocal microscopy study on DV2-infected cells showed that viral antigens were co-localized with clathrin heavy chains, epidermal growth factor pathway substrate clone 15 (Eps15), and adaptin-alpha, but not with caveolin-1. Treatment with chlorpromazine, which inhibits clathrin-dependent endocytosis, led to reduced virus entry into cells, whereas treatment with nystatin, a caveolae inhibitory agent, did not. Furthermore, gene silencing of Eps15 resulted in an average of 75% reduced infection of ECV304 cells by DV2. Our results demonstrated that DV2 enters ECV304 cells by clathrin-dependent endocytosis, not by caveolae-dependent endocytosis.