INFECTION of cells with murine leukaemia virus (MuLV) strains involves an initial interaction between the major viral glycoprotein (gp71) and specific cell surface receptors1. Virus adsorption and penetration occur only in cells having specific receptors2. Other cellular factors such as virogene integration sites may also be required for productive infections. There are three major classes of MuLV: ecotropic viruses which replicate preferentially in murine cells; xenotropic viruses which do not replicate in mouse cells but can replicate in cells from other species; and amphotropic viruses which replicate in mouse cells as well as in ells from other species. None of the three classes of virus infect hamster cells3,4. Previous studies with hamster × mouse somatic cell hybrid clones segregating mouse chromosomes showed that replication of ecotropic and amphotropic viruses required a cell function(s) coded by genes assigned to mouse chromosomes 5 and 8, respectively3. However, the function(s) of these genes was not determined. The third class of MuLV, the xenotropic viruses, could not be tested in this system since both parent cells were resistant5. In the present study, the replication patterns of ecotropic and amphotropic strains were correlated with the ability of hamster x mouse hybrid clones to bind gp71 of Rauscher leukaemia virus (RLV), an ecotropic strain of MuLV. By comparing the mouse chromosome segregation patterns of hybrid clones which retained the gp71 binding ability with those clones which had lost it, we have been able to assign the gene(s) coding for RLV cell surface receptor to mouse chromosome 5.
ASJC Scopus subject areas