Infection of human diploid cells with Simian virus 40 (SV 40) leads to an abortive virus cycle characterized by little virus production, little or no cell destruction, no inhibition of cell replicating capacity, low efficiency of induction of tumour antigen (T-antigen) and eventual transformation of the morphological, chromosomal, and growth characteristics of the cells (Koprowski 1962; Shein & Enders, 1962; Rabson 1962; Weinstein & Moorhead, 1965). In marked contrast, in stationary-phase primary African green monkey kidney (GMK) cells, SV 40 infection leads to high yields of virus, highly efficient induction of T-antigen and extensive cell destruction (Carp & Gilden, 1966). The determination of the cause of these marked differences might clarify the mechanism of the transformation process. Previous results indicated that the virus adsorbed and entered into eclipse phase with equal efficiency for the two cell types (Carp & Gilden, 1966).


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