And only the objections of an informed public can quash them. However, evidence is building that the X protein of HBV may cause cancer by interfering with the cellular repair mechanisms under the control of the crucial p53 tumor suppressor protein, much as the E6 protein of human papillomavirus is known to do. The unphosphorylated Rb keeps the cell arrested at the G1 stage. When the DNA has been repaired, p53 levels decline, which lowers the WAF1 levels and releases the cdks, which phosphorylate the Rb so the cell is free to progress from the G1 to the S stage. The activity of p53 is blocked, however, if cells contain the polyoma virus large T antigen, human papillomavirus E6 protein, or adenovirus E1B 55KD protein.
Mutations occur during practically every cell division.
High levels of p53 occur after widespread cell damage such as caused by ultraviolet light. So, these viruses can cause cancer by interfering with the normal protective mechanisms that guard against mutations. Hepatitis B virus X protein and p53 tumor suppressor interactions in the modulation of apoptosis. LW Elmore, AR Hancock, S-F Chang, XW Wang, S Chang, CP Callahan, DA Geller, H Will, CC Harris. SA Becker, T-H Lee, JS Butel, BL Slagle.