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PLoS Pathog. 2010 Oct 7;6(10):e1001135. doi: 10.1371/journal.ppat.1001135.

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

Author information

1
Department of Microbiology and Molecular Genetics, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.

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 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.

PMID:
20949071
PMCID:
PMC2951373
DOI:
10.1371/journal.ppat.1001135
[Indexed for MEDLINE]
Free PMC Article

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