Abstract
1. Infection of newborn C(3)Hf/Bi mice with both the highly oncogenic S variant and the poorly oncogenic M variant of polyoma virus caused significantly fewer tumors than infection with the S variant alone 2. Infection of newborn C(3)Hf/Bi mice at birth with either M or S variant caused resistance to infection with a heterologous agent, encephalomyocarditis virus, but the M variant caused a somewhat greater degree of resistance. 3. Extracts of tissues of animals infected at birth with the M variant had measurable levels of interferon, reaching a peak on the 5th day after infection with the virus. Extracts of animals infected with the S variant showed no such activity. 4. The growth curves of the two variants in newborn C(3)Hf/Bi mice showed that the S variant grew to a 1000-fold greater titer than did the M variant at 5 days after infection. Samples tested at 10 days showed a 10-fold difference. 5. These findings suggested that the difference between the variants in oncogenic potential might have been due to the greater interferon production induced by infection with the M variant than by infection with the S variant.