Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2011 Jan 1;6(1):45-57.
doi: 10.2217/fvl.10.73.

HPV-DNA integration and carcinogenesis: putative roles for inflammation and oxidative stress

Vonetta M Williams  1 , Maria Filippova, Ubaldo Soto, Penelope J Duerksen-Hughes
Affiliations

HPV-DNA integration and carcinogenesis: putative roles for inflammation and oxidative stress

Vonetta M Williams et al. Future Virol. .

Abstract

HPV-DNA integration into cellular chromatin is usually a necessary event in the pathogenesis of HPV-related cancer; however, the mechanism of integration has not been clearly defined. Breaks must be created in both the host DNA and in the circular viral episome for integration to occur, and studies have shown that viral integration is indeed increased by the induction of DNA double strand breaks. Inflammation generates reactive oxygen species, which in turn have the potential to create such DNA strand breaks. It is plausible that these breaks enable a greater frequency of HPV-DNA integration, and in this way contribute to carcinogenesis. Consistent with this idea, co-infections with certain sexually transmitted diseases cause cervical inflammation, and have also been identified as cofactors in the progression to cervical cancer. This article examines the idea that inflammation facilitates HPV-DNA integration into cellular chromatin through the generation of reactive oxygen species, thereby contributing to carcinogenesis.

PubMed Disclaimer

Figures

Figure 1
Figure 1. Inflammation-induced HPV integration
CIN: Cervical intraepithelial neoplasia; HPV: Human papillomavirus; RNS: Reactive nitrogen species; ROS: Reactive oxygen species.
See this image and copyright information in PMC

References

    1. Flores E, Lambert P. Evidence for a switch in the mode of human papillomavirus type 16 DNA replication during the viral life cycle. J. Virol. 1997;71(10):7167–7179. - PMC - PubMed
    1. Calleja-Macias IE, Kalantari M, Allan B, et al. Papillomavirus subtypes are natural and old taxa: phylogeny of human papillomavirus types 44 and 55 and 68a and -b. J. Virol. 2005;79(10):6565–6569. - PMC - PubMed
    1. Ault KA. Human papillomavirus vaccines and the potential for cross-protection between related HPV types. Gynecol. Oncol. 2007;107(2 Suppl. 1):S31–S33. - PubMed
    1. Guccione E, Pim D, Banks L. HPV-18 E6*I modulates HPV-18 full-length E6 functions in a cell cycle dependent manner. Int. J. Cancer. 2004;110(6):928–933. - PubMed
    1. Weaver BA. Epidemiology and natural history of genital human papillomavirus infection. J. Am. Osteopath. Assoc. 2006;106(Suppl. 1):S2–S8. - PubMed

LinkOut - more resources