The cytolytic interaction of Polyoma virus with mouse embryo cellshas been studied by radiobiological methods known to distinguish temperate from virulent bacteriophage. No evidence for "temperate" propertiesof Polyoma was found. During the course of these studies, it wasobserved that the curve of inactivation of Polyoma virus by ultravioletlight had two components - a more sensitive one at low doses, and aless sensitive one at higher doses. Virus which survives a low dosehas an eclipse period similar to that of unirradiated virus, whilevirus surviving higher doses shows a significantly longer eclipse period.If Puromycin is present during the early part of the eclipse period,the survival curve becomes a single exponential with the sensitivityof the less sensitive component. These results suggest a repair mechanismin mouse cells which operates more effectively if virus developmentis delayed.
A comparison of the rates of inactivation of the cytolytic andtransforming abilities of Polyoma by ultraviolet light, X-rays, nitrousacid treatment, or the decay of incorporated P32, showed that the transforming ability has a target size roughly 60% of that of the plaque-formingability. It is thus concluded that only a fraction of the viralgenes are necessary for causing transformation.
The appearance of virus-specific RNA in productively infectedmouse kidney cells has been followed by means of hybridization betweenpulse-labelled RNA from the infected cells and the purified virus DNA.The results show a sharp increase in the amount of virus-specific RNAaround the time of virus DNA synthesis. The presence of a small amountof virus-specific RNA in virus-free transformed cells has also beenshown. This result offers strong evidence for the persistence of atleast part of the viral genome in transformed cells.
