Abstract
Mutants of Simian virus 40 which have suffered deletions in one of the two early viral gene products, the small-t protein (dl 54 59 mutants), induce tumors following subcutaneous injection into newborn LHC inbred Syrian hamsters. The tumors, mainly fibrosarcomas, are histologically identical to those induced by WT (strain 776) SV40 and are indistinguishable by a number of criteria once explanted to culture. However, the dl 54 59 SV40 mutants induce tumors with only 50% the efficiency of WT virus and with tumor latencies twice as long. The viral large-T protein is primarily responsible for SV40 oncogenicity while the small-t protein may function as a tumor promoter.
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