Skip to main content

Entry of dengue virus serotype 2 into ECV304 cells depends on clathrin-dependent endocytosis, but not on caveolae-dependent endocytosis

Buy Article:

$50.00 plus tax (Refund Policy)


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.

L’endocytose par cavéoles et l’endocytose par clathrine constituent les deux voies d’internalisation principales utilisées par plusieurs pathogènes, mais leurs rôles distinctifs dans l’entrée du virus de la dengue (VD) n’ont jamais été examinés. Dans cette étude, nous avons comparé l’implication des voies d’endocytose par cavéoles et par clathrine dans l’entrée infectieuse du VD de sérotype 2 (VD2) dans les cellules de type endothélial ECV304. Une étude réalisée en microscopie électronique confocale sur des cellules infectées par le VD2 a démontré que les antigènes viraux sont co-localisés avec les chaînes lourdes de la clathrine, l’Eps15 (« epidermal growth factor pathway substrate clone 15 ») et l’adaptine-α, mais pas avec la cavéoline-1. Un traitement à la chlorpromazine, qui inhibe l’endocytose par clathrine, a diminué l’entrée du virus dans les cellules, alors qu’un traitement à la nystatine, un agent inhibiteur des cavéoles, est resté sans effet. Qui plus est, le silençage de Eps15 a réduit de 75 % en moyenne l’infection des cellules ECV304 par le VD2. Nos résultats démontrent que le VD2 entre dans les cellules ECV304 par endocytose par clathrine, mais pas par endocytose par cavéoles.

Document Type: Research Article

Publication date: 2009-02-01

More about this publication?
  • Published since 1954, this monthly journal contains new research in the field of microbiology including applied microbiology and biotechnology; microbial structure and function; fungi and other eucaryotic protists; infection and immunity; microbial ecology; physiology, metabolism and enzymology; and virology, genetics, and molecular biology. It also publishes review articles and notes on an occasional basis, contributed by recognized scientists worldwide.
  • Information for Authors
  • Submit a Paper
  • Subscribe to this Title
  • Terms & Conditions
  • Sample Issue
  • Reprints & Permissions
  • Ingenta Connect is not responsible for the content or availability of external websites
  • Access Key
  • Free ContentFree content
  • Partial Free ContentPartial Free content
  • New ContentNew content
  • Open Access ContentOpen access content
  • Partial Open Access ContentPartial Open access content
  • Subscribed ContentSubscribed content
  • Partial Subscribed ContentPartial Subscribed content
  • Free Trial ContentFree trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more