Inherited resistance to N- and B-tropic murine leukemia viruses in vitro. Effect of the Fv-1 locus on the rescue of a replication-defective and transformation-defective murine sarcoma virus in the Fv-1 congenic strains SIM.S and SIM.R.

An in vitro assay for MuLV (murine leukemia virus) using mouse embryo cultures derived from the congeneic strains SIM.S and SIM.R differing at the Fv-1 locus and containing the genome of a replication- and transformation-defective (R^?T^?) MuSV (murine sarcoma virus) isolate is described. Studies on the interrelationship of MuLV and MuLV using this focus induction assay indicated that rescue of the defective MuSV was subject to Fv-1 restriction of the superinfecting MuLV helper. Titration patterns of N-, B-, and NB-tropic MuLV on these SIM.S and SIM.R “R^?T^?” cells were all linear and parallel over the range of dilutions used. The kinetics of MuLV infection appeared to be single hit using both focus and XC-plaque assays in both permissive and nonpermissive host cells. MuSV rescued by N-, B-, or NB-tropic MuLV showed no strict host range specificity. Host range of these rescued MuSV was determined by the degree of restriction of coinfecting MuLV. Results of these studies using both normal and MuSV(R^?T^?)-infected SIM.S(Fv-1^n/n) and SIM.R(Fv-l^b/b) cell lines suggest that Fv-1-mediated restriction acts solely by restricting MuLV replication and thereby inhibiting focus formation by the defective MuSV genome in Fv-1 nonpermissive cells.