Some Aspects of the Interaction Between Polyoma Virus and Cell DNA

Abstract

Publisher Summary Polyoma virus is widely used for in vitro studies on the mechanism of viral carcinogenesis. Polyoma virus infection can overcome the blocks in cell DNA synthesis imposed by contact inhibition, elevated temperature, X-rays, mustard gas, mitomycin C, 5-fluorodeoxyuridine, 5-fluorouracil, and possibly, the state of cell differentiation. The mode of action of some of these eight inhibitory agents and conditions may overlap. Nevertheless, it is striking that the virus can overcome the blocks imposed by such widely varying conditions, and this feature supports the assumption that a primary switch in the cells' regulation of DNA synthesis is triggered by the virus infection. A variety of experiments have supplied evidence that the cell DNA, made both before and after the time of infection, is incorporated into some polyoma particles. The technique of growing the virus on cells labeled with radioactive thymidine before infection has the advantage that the cell DNA-containing particles can be differentially labeled. The main limiting factor is the amount of homology to normal cell DNA, which is displayed by the virus DNA preparation. Only a relatively large number of viral genomes per transformed cell can be detected by techniques operating at the current level of sensitivity. The experimental results suggest that, in the case of Polyoma transformed cells, the number of possible viral genomes is less than 10-20 per cell; with SV40-transformed cells, where the evidence for the presence of viral genomes is stronger, the results suggest that the number must be greater than 30 copies per cell.