Abstract
Discussion and Summary
By producing an inapparent infection in adult hamsters or C57 mice with a single dose of diluted polyoma virus these animals subsequently manifest a relative resistance to transplantation of isologous polyoma fibrosarcomas. These sarcomas, although originally induced by virus inoculated into newborn animals, no longer contain any demonstrable virus or viral antigens. This resistance can be overcome if a large enough number of tumor cells are given in the challenge transplant; it is apparently specific for tumors of polyoma origin and would appear to be cell mediated since hyperimmune polyoma antiserum is not capable of transferring such resistance to normal mice.
The most logical explanation of this phenomenon is based on the hypothesis that polyoma induced tumors contain a cell antigen which is not present in normal isologous cells and the degree of this antigenic difference must be small. This new antigen would be produced by the normal cell after it has been transformed as the result of polyoma virus infection, both in the infected newborn and adult animal. The newborn being immunologically non-reactive would tolerate the foreign antigen and allow the transformed cells to multiply and produce a tumor. The adult animal being immunologically mature would reject the transformed cell with its foreign antigen and in so doing become hyper-reactive or resistant to the tumor when challenged with the transplant. This hypothesis is consistent with the findings of Law and Dawe(3) that adult mice given polyoma virus after whole body X-radiation do develop tumors.
If this hypothesis can be proven by immunological experiments, it would suggest that the genome of the virus-transformed cell either now contains viral genome or has been genetically altered by a non-lytic virus infection.
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