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Journal of Virology, June 2007, p. 6316-6325, Vol. 81, No. 12
0022-538X/07/$08.00+0     doi:10.1128/JVI.00311-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Bcl-2 Blocks Accretion or Depletion of Stored Calcium but Has No Effect on the Redistribution of IP3 Receptor I Mediated by Glycoprotein E of Herpes Simplex Virus 1{triangledown}

Maria Kalamvoki and Bernard Roizman*

The Marjorie B. Kovler Viral Oncology Laboratories, The University of Chicago, Chicago Illinois 606037

Received 12 February 2007/ Accepted 26 March 2007

We examined the status of stable, resting intracellular Ca2+ ([Ca2+]i) and the calcium that can be released from intracellular stores in HEp-2 or VAX-3 cells overexpressing Bcl-2 after infection with wild-type or mutant herpes simplex viruses. The mutants included viruses lacking ICP4 or ICP27 and known to induce apoptosis. We report the following. Stable Ca2+ levels decrease after infection with wild-type or mutant viruses in both HEp-2 and VAX-3 cells. The histamine-sensitive calcium stores became depleted in wild-type and mutant virus-infected cells late in infection but increased significantly in {Delta}ICP4- or {Delta}ICP27-infected cells prior to depletion. In VAX-3 cells, the depletion in calcium stores did not take place as late as 24 h after infection, concomitant with lack of visually detectable cytopathic effects. Concurrent analyses showed that the amounts of IP3 Ca2+-receptor type I (IP3R-I) remained stable throughout infection, but the intensity of the signal increased and intracellular distribution changed dramatically in both HEp-2 and VAX-3 cells infected with the wild-type and all mutant viruses, except for the mutant lacking glycoprotein E ({Delta}gE). In transfected HEp-2 cells, gE and gI were more effective at augmenting the signal intensity and redistribution of IP3R-I than gE or gI alone. We conclude the following. (i) Depleted histamine-sensitive calcium stores correlate with appearance of cytopathic effects. (ii) Apoptosis, the calcium stores, and cytopathic effects are regulated by Bcl-2. (iii) The changes in the distribution of IP3R-I are mediated by the viral Fc receptor complex, but the redistribution is not related to changes in stored calcium.

* Corresponding author. Mailing address: The Marjorie B. Kovler Viral Oncology Laboratories, The University of Chicago, 910 East 58th Street, Chicago, IL 60637. Phone: (773) 702-1898. Fax: (773) 702-1631. E-mail: bernard.roizman{at}bsd.uchicago.edu

{triangledown} Published ahead of print on 4 April 2007.

Journal of Virology, June 2007, p. 6316-6325, Vol. 81, No. 12
0022-538X/07/$08.00+0     doi:10.1128/JVI.00311-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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