Previous Article | Next Article ![]()
Journal of Virology, December 2007, p. 12985-12995, Vol. 81, No. 23
0022-538X/07/$08.00+0 doi:10.1128/JVI.01485-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Microbiology, One Gustave L. Levy Place, Mount Sinai School of Medicine, New York, New York 10029,1 Department of Genetics, Yale University School of Medicine, New Haven, Connecticut 065102
Received 6 July 2007/ Accepted 5 September 2007
Apoptosis is a potent host defense against microbes. Most viruses have adapted strategies to counteract this response. Herpes simplex virus (HSV) produces a balance between pro- and antiapoptotic processes during infection. When antiapoptotic signals become limiting, infected cells die through HSV-dependent apoptosis (HDAP). Oncogenic pathways were previously implicated in HDAP susceptibility. Here, we exploited our ability to selectively express all, one, or no oncogenes in the well-defined HeLa cell system to dissect the requirements for HDAP. Human papillomavirus E6 and E7 oncogene expression was inhibited by the E2 viral repressor. Sole expression of E6 mediated HDAP sensitization. Next, two known cellular targets of E6 were independently modulated. This demonstrated that E6 sensitizes HeLa cells to HDAP through hTERT and p53. Given the universality of the apoptotic antiviral response, p53 and telomerase regulation will likely be important for counteracting host defenses in many other viral infections.
Published ahead of print on 12 September 2007.
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»