Involvement of intracellular free Ca<sup>2+ </sup>in enhanced release of herpes simplex virus by hydrogen peroxide

<p>Abstract</p> <p>Background</p> <p>It was reported that elevation of the intracellular concentration of free Ca<sup>2+ </sup>([Ca<sup>2+</sup>]i) by a calcium ionophore increased the release of herpes simplex virus type 1 (HSV-1). Freely diffus...

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Bibliographic Details
Main Authors: Ogawa Yuzo, Sumi Tetsuro, Iwai Soichi, Arimoto Emiko, Yura Yoshiaki
Format: Article
Language:English
Published: BMC 2006-08-01
Series:Virology Journal
Online Access:http://www.virologyj.com/content/3/1/62
Description
Summary:<p>Abstract</p> <p>Background</p> <p>It was reported that elevation of the intracellular concentration of free Ca<sup>2+ </sup>([Ca<sup>2+</sup>]i) by a calcium ionophore increased the release of herpes simplex virus type 1 (HSV-1). Freely diffusible hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) is implied to alter Ca<sup>2+ </sup>homeostasis, which further enhances abnormal cellular activity, causing changes in signal transduction, and cellular dysfunction. Whether H<sub>2</sub>O<sub>2 </sub>could affect [Ca<sup>2+</sup>]i in HSV-1-infected cells had not been investigated.</p> <p>Results</p> <p>H<sub>2</sub>O<sub>2 </sub>treatment increased the amount of cell-free virus and decreased the proportion of viable cells. After the treatment, an elevation in [Ca<sup>2+</sup>]i was observed and the increase in [Ca<sup>2+</sup>]i was suppressed when intracellular and cytosolic Ca<sup>2+ </sup>were buffered by Ca<sup>2+ </sup>chelators. In the presence of Ca<sup>2+ </sup>chelators, H<sub>2</sub>O<sub>2</sub>-mediated increases of cell-free virus and cell death were also diminished. Electron microscopic analysis revealed enlarged cell junctions and a focal disintegration of the plasma membrane in H<sub>2</sub>O<sub>2</sub>-treated cells.</p> <p>Conclusion</p> <p>These results indicate that H<sub>2</sub>O<sub>2 </sub>can elevate [Ca<sup>2+</sup>]i and induces non-apoptotic cell death with membrane lesions, which is responsible for the increased release of HSV-1 from epithelial cells.</p>
ISSN:1743-422X