Abstract

THE infection of confluent cultures of “permissive” cells by polyoma virus promotes a sharp increase in the rate of cellular DNA synthesis1–3 in the cells in which the production of virus eventually takes place4. It is also known from investigations carried out with viral mutants that the induction of DNA synthesis in the host cells does not require viral DNA replication5,6. Nevertheless it is known from inactivation experiments that the stimulation of cellular DNA synthesis is a function of the viral genome, although the processes involved at the molecular level remain rather obscure4,7,8. In systems of cells where multiplication is controlled by population density, viral infection with either polyoma or SV40 releases cells from contact inhibition. DNA synthesis does not shift to an uncontrolled level; only the block between the G1 and the S phases in resting cells seems to be removed8. Several other physiological or artificial states, notably that resulting from differentiation in which cell DNA synthesis is suppressed, can be overcome by infection with such viruses8,9. In any case the extent of stimulation seems to reach an absolute limit in the normal rate of cellular DNA replication during exponential growth.

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