Redox-dependent mechanisms of carcinogenesis in human papillomavirus infection

Abstract Infection with human papillomavirus (HPV) has been implicated as an important etiological factor in the causation of cervical cancer that still plagues many women all over the world and remains to be one of the major focuses of researchers. A large body of knowledge supports the view that high-risk HPV types have the ability to transform normal cells into a malignant phenotype. However, the frequent spontaneous clearance of HPV infection and the long delay between the onset of persistent infection and the emergence of the malignancy suggest that viral oncogenes expression, although necessary, is not per se sufficient to induce cancer. Increasing evidence supports that oxidative stress may play relevant roles in HPV-dependent carcinogenesis. In this chapter, we discuss the role of oxidative stress as a concurrent agent in the malignant transformation of HPV-infected cells, as well as the viral infection itself, may determine a complex adaptive metabolic profile allowing cell survival in an increasing oxidant environment.