Journal
FUTURE VIROLOGY
Volume 6, Issue 7, Pages 813-830Publisher
FUTURE MEDICINE LTD
DOI: 10.2217/FVL.11.55
Keywords
DNA tumor virus; EBV; Epstein-Barr virus; genomic instability; HBV; hepatitis B virus; HPV; human papillomavirus; human polyomavirus; Kaposi's sarcoma-associated herpesvirus; KSHV; oncogenic; stress; tumor suppression
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Funding
- NIAID [P30-AI064518]
- Duke Center for AIDS Research
- Golfers Against Cancer
- American Cancer Society
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Human DNA tumor viruses induce host cell proliferation in order to establish the necessary cellular milieu to replicate viral DNA. The consequence of such viral-programmed induction of proliferation coupled with the introduction of foreign replicating DNA structures makes these viruses particularly sensitive to the host DNA damage response machinery. In fact, sensors of DNA damage are often activated and modulated by DNA tumor viruses in both latent and lytic infection. This article focuses on the role of the DNA damage response during the life cycle of human DNA tumor viruses, with a particular emphasis on recent advances in our understanding of the role of the DNA damage response in EBV, Kaposi's sarcoma-associated herpesvirus and human papillomavirus infection.
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