Abstract
A model is presented that attempts to explain how SV40 or polyoma maintains the transformed state or phenotype. It is proposed that SV40 or polyoma codes for a protein involved in the initiation of cellular DNA synthesis (positive control element). This viral directed cellular DNA synthesis is different in some way from normal cellular DNA synthesis. This difference, in addition to other factors (possibly a second viral coded protein), results in a permanent cell surface alteration. This same cell surface alteration is observed transiently (only during mitosis) in the normal cell cycle. The permanent cell surface change permits the synthesis or activation of the viral positive control element for cellular DNA replication by-passing the normal cellular control for the initiation of DNA synthesis and allowing the cell to enter a new S period. This results in loss of density growth and expression of the transformed phenotype. The model is presented as a working hypothesis that makes specific predictions for new experiments.
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