Previous Article | Next Article ![]()
Journal of Virology, March 2009, p. 2765-2769, Vol. 83, No. 6
0022-538X/09/$08.00+0 doi:10.1128/JVI.02088-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Department of Pediatrics,1 Center for Infectious Diseases and Microbiology Translational Research, University of Minnesota Medical School, Minneapolis, Minnesota 55455,2 Department of Laboratory Medicine,3 Department of Microbiology,4 Program in Molecular and Cellular Biology, University of Washington, Seattle, Washington 98195,5 Program in Infectious Diseases, Fred Hutchinson Cancer Research Center, Seattle, Washington 981096
Received 3 October 2008/ Accepted 22 December 2008
Herpes simplex virus (HSV) inhibits apoptosis induced by external stimuli in epithelial cells. In contrast, apoptosis is the primary outcome in HSV-infected lymphocytes. Here, we show that HSV type 2 (HSV-2) gene expression appears to be necessary for the induction of apoptosis in Jurkat cells, a T-cell leukemia line. HSV-2 ICP10 gene expression is sufficient to induce apoptosis in Jurkat cells, while its expression protects epithelial HEp-2 cells from apoptosis triggered by cycloheximide and tumor necrosis factor alpha. Thus, the effect of HSV-2 gene expression on the cellular apoptotic pathway appears to depend on the specific cell type.
Published ahead of print on 30 December 2008.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»