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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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
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spelling doaj-1eff1db7f5cb4436b22e9ffd6f899efd2020-11-24T22:16:24ZengBMCVirology Journal1743-422X2006-08-01316210.1186/1743-422X-3-62Involvement of intracellular free Ca<sup>2+ </sup>in enhanced release of herpes simplex virus by hydrogen peroxideOgawa YuzoSumi TetsuroIwai SoichiArimoto EmikoYura Yoshiaki<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> http://www.virologyj.com/content/3/1/62
collection DOAJ
language English
format Article
sources DOAJ
author Ogawa Yuzo
Sumi Tetsuro
Iwai Soichi
Arimoto Emiko
Yura Yoshiaki
spellingShingle Ogawa Yuzo
Sumi Tetsuro
Iwai Soichi
Arimoto Emiko
Yura Yoshiaki
Involvement of intracellular free Ca<sup>2+ </sup>in enhanced release of herpes simplex virus by hydrogen peroxide
Virology Journal
author_facet Ogawa Yuzo
Sumi Tetsuro
Iwai Soichi
Arimoto Emiko
Yura Yoshiaki
author_sort Ogawa Yuzo
title Involvement of intracellular free Ca<sup>2+ </sup>in enhanced release of herpes simplex virus by hydrogen peroxide
title_short Involvement of intracellular free Ca<sup>2+ </sup>in enhanced release of herpes simplex virus by hydrogen peroxide
title_full Involvement of intracellular free Ca<sup>2+ </sup>in enhanced release of herpes simplex virus by hydrogen peroxide
title_fullStr Involvement of intracellular free Ca<sup>2+ </sup>in enhanced release of herpes simplex virus by hydrogen peroxide
title_full_unstemmed Involvement of intracellular free Ca<sup>2+ </sup>in enhanced release of herpes simplex virus by hydrogen peroxide
title_sort involvement of intracellular free ca<sup>2+ </sup>in enhanced release of herpes simplex virus by hydrogen peroxide
publisher BMC
series Virology Journal
issn 1743-422X
publishDate 2006-08-01
description <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>
url http://www.virologyj.com/content/3/1/62
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