Release of intracellular calcium stores facilitates coxsackievirus entry into polarized endothelial cells.

Journal Article (Journal Article)

Group B coxsackieviruses (CVB) are associated with viral-induced heart disease and are among the leading causes of aseptic meningitis worldwide. Here we show that CVB entry into polarized brain microvasculature and aortic endothelial cells triggers a depletion of intracellular calcium stores initiated through viral attachment to the apical attachment factor decay-accelerating factor. Calcium release was dependent upon a signaling cascade that required the activity of the Src family of tyrosine kinases, phospholipase C, and the inositol 1,4,5-trisphosphate receptor isoform 3. CVB-mediated calcium release was required for the activation of calpain-2, a calcium-dependent cysteine protease, which controlled the vesicular trafficking of internalized CVB particles. These data point to a specific role for calcium signaling in CVB entry into polarized endothelial monolayers and highlight the unique signaling mechanisms used by these viruses to cross endothelial barriers.

Full Text

Duke Authors

Cited Authors

  • Bozym, RA; Morosky, SA; Kim, KS; Cherry, S; Coyne, CB

Published Date

  • October 7, 2010

Published In

Volume / Issue

  • 6 / 10

Start / End Page

  • e1001135 -

PubMed ID

  • 20949071

Pubmed Central ID

  • PMC2951373

Electronic International Standard Serial Number (EISSN)

  • 1553-7374

Digital Object Identifier (DOI)

  • 10.1371/journal.ppat.1001135


  • eng

Conference Location

  • United States