Internalization and trafficking mechanisms of coxsackievirus B3 in HeLa cells

Sun Ku Chung, Joo Young Kim, In Beom Kim, Sang Ick Park, Kyung Hee Paek, Jae Hwan Nam

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

Coxsackievirus B3 (CVB3) is nonenveloped and has a single-stranded positive-sense RNA genome. CVB3 induces myocarditis and ultimately dilated cardiomyopathy. Although there are mounting evidences of an interaction between CVB3 particles and the cellular receptors, coxsackievirus and adenovirus receptor (CAR) and decay-accelerating factor (DAF), very little is known about the mechanisms of internalization and trafficking. In the present study, we used the CVB3 H3 strain, which is CAR-dependent but DAF-independent Woodruff variant and found that during entry, CVB3 particles were colocalized in clathrin, after interacting primarily with CAR, which was not recycled to the plasma membrane. We also found that CVB3 internalization was dependent on the function of dynamin, a large GTPase that has an essential role in endocytosis. Heat-shock cognate protein, Hsc70, which acts as a chaperone in the release of coat proteins from clathrin-coated vesicles (CCV), played a role in CVB3 trafficking processes. Moreover, endosomal acidification was crucial for CVB3 endocytosis. Finally, CVB3 was colocalized in early endosome autoantigen 1 (EEA1) molecules, which are involved in endosome-endosome tethering and fusion. In conclusion, these data together indicate that CVB3 uses clathrin-mediated endocytosis and is transcytosed to early endosomes.

Original languageEnglish
Pages (from-to)31-40
Number of pages10
JournalVirology
Volume333
Issue number1
DOIs
Publication statusPublished - 2005 Mar 1

    Fingerprint

Keywords

  • CAR
  • Clathrin
  • CVB3
  • Dynamin
  • EEA1
  • Endosomal acidification
  • Hsc70

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases

Cite this