This Article Full Text (PDF) Other Versions of this Article: JVI.00311-07v1 81/12/6316    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kalamvoki, M. Articles by Roizman, B. Search for Related Content PubMed PubMed Citation Articles by Kalamvoki, M. Articles by Roizman, B.

 Previous Article  |  Next Article 

J. Virol. doi:10.1128/JVI.00311-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Bcl-2 blocks accretion or depletion of stored calcium, but has no effect on the redistribution of the IP3R-I receptor mediated by glycoprotein E of herpes simplex virus 1

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

^* To whom correspondence should be addressed. Email: bernard.roizman{at}bsd.uchicago.edu.

	Abstract

We examined the status of stable, resting [Ca²⁺] 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 become depleted in wild-type and mutant virus infected cells late in infection, but increased significantly in ICP4 or 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 1 (IP3R-1) 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 wild-type and all mutant viruses, except that lacking glycoprotein E (gE). In transfected HEp-2 cells, gE and gI were more effective in augmenting the signal intensity and redistribution of IP3R-I than gE or gI alone. We conclude that (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 that the redistribution is not related to changes in stored calcium.

This article has been cited by other articles:

• Kalamvoki, M., Qu, J., Roizman, B. (2008). Translocation and Colocalization of ICP4 and ICP0 in Cells Infected with Herpes Simplex Virus 1 Mutants Lacking Glycoprotein E, Glycoprotein I, or the Virion Host Shutoff Product of the UL41 Gene. J. Virol. 82: 1701-1713 [Abstract] [Full Text]  
• Benetti, L., Roizman, B. (2007). In Transduced Cells, the US3 Protein Kinase of Herpes Simplex Virus 1 Precludes Activation and Induction of Apoptosis by Transfected Procaspase 3. J. Virol. 81: 10242-10248 [Abstract] [Full Text]