In:
Canadian Journal of Microbiology, Canadian Science Publishing, Vol. 55, No. 2 ( 2009-02), p. 139-145
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-α, 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.
Type of Medium:
Online Resource
ISSN:
0008-4166
,
1480-3275
Language:
English
Publisher:
Canadian Science Publishing
Publication Date:
2009
detail.hit.zdb_id:
280534-0
detail.hit.zdb_id:
1481972-7
SSG:
12
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