Normal DBA/2 mouse cells synthesize a glycoprotein which interferes with MCF virus infection

The mechanism of resistance to Friend leukemia virus-induced [mink cell focus-inducing, (MCF)-mediated] leukemogenesis in DBA/2 mice was investigated in cell culture systems. DBA/2 fibroblasts were found to be resistant to infection with MCF viruses but not to ecotropic or amphotropic murine leukemia viruses (MuLV's). Since this resistance has been correlated with the presence of an MCF virus-related gp70 constitutively present on the surface of DBA/2 cells, it seemed possible that the mechanism of resistance in this system involved the saturation of MCF-specific cell surface receptors with the gp70 in analogy to viral interference. Two inhibitors of glycoprotein synthesis, 2-deoxy- d-glucose and tunicamycin, which have been shown to reduce retrovirus-induced interference in productively infected cells, significantly decreased the resistance of DBA/2 cells to productive infection with MCF viruses. This decrease in resistance to MCF virus infection could be correlated with a decrease in the expression of MCF-related gp70 at the cell surface. Cells from several other mouse strains showed neither resistance to MCF virus infection nor enhancement of MCF infectivity following drug treatment. These data indicate that DBA/2 cells are resistant to MCF infection in vitro and, by implication, to MCF-mediated leukemogenesis in vivo by a process analogous to viral interference. Ecotropic pseudotypes of MCF virus were able to productively infect untreated DBA/2 cells, indicating that the cell surface interference-like process described here is the only restriction mechanism responsible for resistance to MCF infection in DBA/2 cells. The results are consistent with the idea that Friend leukemia virus actually causes disease via MCF intermediates.