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

doi:10.1016/0042-6822(82)90301-4

Virology

Volume 123, Issue 1, November 1982, Pages 139-151

https://doi.org/10.1016/0042-6822(82)90301-4 Get rights and content

Abstract

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.

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

Abstract

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Arch. Biochem. Biophys.

Rapid cell culture assay technique for murine leukaemia viruses

Nature (London)

Mechanism of restriction of murine leukemia viruses varies between different strains of Fv-1n mice

Int. J. Cancer

A film detection method for tritium-labeled proteins and nucleic acids in polyacrylamide gels

Eur. J. Biochem.

Cellular origin and role of mink cell focus-forming viruses in murine thymic lymphomas

Nature (London)

Host genetic control of recovery from Friend leukemia virus-induced splenomegaly. Mapping of a gene within the major histocompatibility complex

J. Exp. Med.

Rfv-1 and Rfv-2, two H-2-associated genes that influence recovery from Friend leukemia virus-induced splenomegaly

J. Immunol.

Antibody-induced modulation of Friend virus cell surface antigens decreases virus production by persistent erythroleukemia cells: Influence of the Rfv-3 gene

Heteroduplex analysis of the sequence relations between the RNAs of mink focus-inducing and murine leukemia viruses

J. Virol.

Lymphomagenicity of recombinant mink cell focus-inducing murine leukemia viruses

J. Exp. Med.

Biochemical evidence that MCF murine leukemia viruses are envelope gene recombinants

Genomic masking of nondefective recombinant murine leukemia virus in Moloney virus stocks

Science

Detection of a recombinant murine leukemia virus-related glycoprotein on virus-negative thymoma cells

Akvr-1, a dominant murine leukemia virus restriction gene is polymorphic in leukemia-prone wild mice

Mechanism of restriction of murine leukemia viruses varies between different strains of Fv-1ⁿ mice