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Rous sarcoma virus (RSV) appears to contain ribonucleic acid (RNA), but not deoxyribonucleic acid (DNA) ( 1 ,2 ) . Recently, Temin(3) showed that Actinomycin D inhibits production of RSV, a finding which suggested that the growth of the RNA-virus is somehow associated with the synthesis of DNA. The present work indicates that 5iodo-2'-deoxyuridine ( IUdR) , an antagonist of DNA synthesis, not only inhibits RSV multiplication in primary cultures of chick embryo fibroblasts, but also appears to suppress the malignant transformation of the infected cells.Materials and methods. Compound. IUdR was obtained from the California Corporation for Biochemical Research.Tissue culture. The trunks of 10-day-old White Leghorn chick embryos, from RSVsusceptible flocks, were minced, washed with Scherer's solution and trypsinized with 0.25% trypsin (Difco, 1:250) for 5 minutes at room temperature. Tissue culture flasks (30 ml; Falcon Plastics) were seeded with 15 X lo6 cells contained in 5 ml of growth medium, which consisted of 30% medium 199, 60% Scherer's solution, 10% horse serum (heat-inactivated at 56°C for 40 minutes), pH 7.2, and 100 units of penicillin G and 1001 pg of streptomycin sulfate per ml. After incubation for 48 hours at 36"C, the cells were washed and refed for use with 5 ml of Scherer's solution (pH 7.2) containing 2.5% horse serum plus antibiotics (S-1).Virus. Standard stock Rous sarcoma virus, lot CT-929, was kindy supplied by Dr.

Viruses with 1059 and HGP serotype and with human and monkey host range characteristics, respectively, were employed. Adsorption kinetics of the 1059 and HGP strains to WI-26 cells, and HGP to Green African monkey kidney cells (MKC), were similar. Fifty per cent of the virus was adsorbed to ceU monolayers within 10 min; adsorption was essentially complete by 2 hr. The 1059 strain failed to adsorb to MKC, at least to an appreciable extent. Lack of receptors for adsorption of 1059 accounts for the inability of this cell to support multiplication of the virus. It is probable that MKC are refractory to infection with other H strains of rhinovirus for the same reason. Single-step multiplication cycles have been described for the HGP strain in WI-26 and MKC cultures and for the 1059 strain in WI-26 cells. In both cells, HGP exhibited a latent period of 7 hr. Increase of intracellular and cell-associated virus appeared somewhat prior to that of extracellular virus. Maximal titers were attained by 9 to 10 hr. In contrast, initial increase of 1059 in WI-26 cells occurred after 10 hr. Titer rose to peak level 15 hr after infection. Yield of 1059 in WI-26 cells was also fivefold lower than that of HGP in either cell system.