Journal
JOURNAL OF VIROLOGY
Volume 81, Issue 23, Pages 12985-12995Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01485-07
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Funding
- NCI NIH HHS [P01 CA016038, CA088796, T32 CA088796, CA16038] Funding Source: Medline
- NIAID NIH HHS [AI07647, R01 AI048582, AI48582, T32 AI007647] Funding Source: Medline
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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.
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