Parental and clonal lines of SV40-transformed human embryonic lung (WI38 Va13A) cells spontaneously produce infectious virus which is temperature-resistant (), i.e. replicates in monkey kidney cells at either 38.7 °C or 33.5 °C. Superinfection of WI38 Va13A cells lines with DNA from a temperature-sensitive () SV40 mutant at the permissive temperature (33.5 °C) did not enhance the yield of SV40 as would be expected if the superinfecting SV40 DNA neutralized an SV40-specific repressor, or if the SV40 DNA supplied a virus-specific excision function and/or post-excision functions for the maturation of the resident SV40. The failure of superinfecting SV40 to enhance replication of the resident SV40 of WI38 Va13A cells is not due merely to a competitive advantage of the replicating superinfecting SV40 over the endogenous SV40. Experiments were carried out with 1-β--arabinofuranosylcytosine (ara-C) treated and SV40 DNA-infected WI38 Va13A cells to permit expression of early SV40 functions and to synchronize replication of SV40 DNA and the newly excised endogenous SV40 DNA. Ara-C treatment did not enhance formation of the endogenous virus. In further competition experiments, CV-1 cells were preinfected with SV40 particles and superinfected 6 to 24 h later with SV40 DNA recovered from SV40 spontaneously produced by WI38 Va13A cells. Even when the interval between the first and second infection was 24 h, very significant amounts of SV40 synthesis occurred and 28% of doubly infected cells still produced temperature-resistant infectious centres. The experiments suggest that rescue of the resident SV40 is determined primarily by cellular rather than superinfecting SV40 gene functions.


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