This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nguyen, M. L.
Right arrow Articles by Blaho, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nguyen, M. L.
Right arrow Articles by Blaho, J. A.

 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.

p53 and hTERT Determine Sensitivity to Viral Apoptosis{triangledown}

Marie L. Nguyen,1 Rachel M. Kraft,1 Martine Aubert,1 Edward Goodwin,2 Daniel DiMaio,2 and John A. Blaho1*

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.


* Corresponding author. Mailing address: Department of Microbiology, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029-6574. Phone: (212) 241-7319. Fax: (212) 534-1684. E-mail: john.blaho{at}mssm.edu

{triangledown} Published ahead of print on 12 September 2007.


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.