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

Rebecca A. Bozym, Stefanie A. Morosky, Kwang S. Kim, Sara Cherry, Carolyn B. Coyne

Research output: Contribution to journalArticlepeer-review

Abstract

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 decayaccelerating 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.

Original languageEnglish (US)
Article numbere1001135
JournalPLoS pathogens
Volume6
Issue number10
DOIs
StatePublished - Oct 2010

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Molecular Biology
  • Genetics
  • Virology

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