Release of Intracellular Calcium Stores Facilitates Coxsackievirus Entry into Polarized Endothelial Cells e1001135

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 initiat...

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Bibliographic Details
Published inPLoS pathogens Vol. 6; no. 10
Main Authors Bozym, Rebecca A, Morosky, Stefanie A, Kim, Kwang S, Cherry, Sara, Coyne, Carolyn B
Format Journal Article
LanguageEnglish
Published San Francisco Public Library of Science 01.10.2010
Subjects
Calcium
Cells
Cellular biology
Proteins
Rodents
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Summary: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.
ISSN:1553-7366
1553-7374
DOI:10.1371/journal.ppat.1001135