**3. HPV, cervical dysplasia and HIV**

232 Cancer Prevention – From Mechanisms to Translational Benefits

has accumulated to more clearly define the mechanisms and processes that chronic, persistent infections induce cancer development, see Figure 1. Replication of DNA and RNA tumor viruses involve incorporation of the viral genome into the host cell chromosomes inducing several mutations that disrupt the homeostatic balance between proliferation and cell death; in the case of oncogenic HPV, the expression of viral E2, E6, and E7 genes lead to the production of proteins that initiate cell cycle and disable control of growth, allowing the proliferation of genetic damage to accumulate in HPV infected cells. (Georgakilas et al. 2010). Oxidative stress negatively impacting genetic and cellular processes can be brought about by reactive oxygen species (ROS) or free radicals induced by chronic infection (Kryston et al. 2011; Georgakilas et al. 2010). Although additional researches are needed to accurately define the relationship, oxidative stress is linked in

Schematic pathway of viral infection leading to cancer adapted from Figure1 Viral pathogens role(s) in human carcinogenesis based on current status of knowledge and

Alexandros Georgakilas, William Mosley, Stavroula Georgakila, Dominick Ziech, and Mihalis Panayiotidis. Viral-induced human carcinogenesis: an oxidative stress perspective.

In the 1990s a combination of large-scale epidemiologic studies and the application of new molecular techniques clearly established human papillomavirus (HPV) as the etiologic cause of cervical cancer (Clifford 2003; Walboomers 1999). Using the most sensitive assays, over

several studies with some tumor virus but not HPV (Kryston, et al. 2011)

Fig. 1. Role of Viral Infection in Carcinogenesis.

Molecular BioSystems Vol 6, pp 1162 – 1172, (2010).

clinical evidence.
