Schematic representation of main pathways involved in processing of genotoxic DNA damage including base damages (BDs), DNA single-strand breaks (SSBs) and double-strand breaks (DSBs). BDs and SSBs are efficiently repaired by base-excision (BER) and SSBR mechanisms. DSBs are repaired by non-homologous end joining (NHEJ) and homologous recombination (HR). These activate panoply of interacting proteins in tissues, cells and mitochondria that lead to the expression and inhibition of multiple genes. These normally results in cell cycle arrest to allow for accurate DNA healing to prevent the cells from entering DNA synthesis with damaged DNA. The aim is to maintain genomic integrity which enables recovery or otherwise triggers cell death. The E6 and E7 oncoproteins produced by high risk HPV infections will respectively interact with TP53 and RB tumor suppressor proteins and inhibit their functions leading to genomic instability. Lines represent interactions. Arrows indicate activation and blunt ends indicate inhibition. Thickness represents the strength of the actions. Underlined text designates encoding genes selected for polymorphic variations predisposing to cervical cancer (See text for details).