Ultraviolet irradiation of polyoma virus inactivates different functions of the virus genome. This inactivation is related to the radiation dose.

It has been shown that the ultraviolet radiation target size of the nuclear T antigen is one-half that of the ability to form plaques, and that the radiation target size of the homograft rejection antigen is one-sixth that of the latter. In the present experiments, ultraviolet irradiation has been applied in a similar manner in order to study the cell surface antigen. Quantitative analysis shows that the radiation target size for this antigen is one-half that of the ability to form plaques (infectivity).

The difference in responses of the cell surface antigen and in the homograft rejection antigen observed after irradiation of the virus can be due either to differences in sensitivities of the techniques used or to a difference in antigenicity. Experiments with defective polyoma strains favour a difference in antigenicity.


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