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  • Title: Entry of dengue virus serotype 2 into ECV304 cells depends on clathrin-dependent endocytosis, but not on caveolae-dependent endocytosis.
    Author: Peng T, Wang JL, Chen W, Zhang JL, Gao N, Chen ZT, Xu XF, Fan DY, An J.
    Journal: Can J Microbiol; 2009 Feb; 55(2):139-45. PubMed ID: 19295646.
    Abstract:
    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.
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