The Journal of Experimental Medicine, Vol 119, 71-81,
Copyright © 1964, by The Rockefeller Institute
POSSIBLE ROLE OF INTERFERON IN DETERMINING THE ONCOGENIC EFFECT OF POLYOMA VIRUS VARIANTS
Robert M. Friedman M.D.1 and
Alan S. Rabson M.D.1
1 From the United States Department of Health, Education, and Welfare, Public Health Service, National Institutes of Health, National Cancer Institute, Pathology Section, Bethesda
1. Infection of newborn C3Hf/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 C3Hf/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 C3Hf/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.
Submitted on September 4, 1963
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