SEVERAL classes of murine leukaemia viruses (MuLV) are recognised according to their ability to induce XC plaque formation with high or low efficiency after infection of various mouse cell lines1,2. N- and B-tropic MuLVs, for example, can be distinguished on the basis of their relative ability to infect N-type or B-type mouse cells, the cells themselves differing at a single genetic locus, Fv-1 (ref. 3). Fv-1 restriction is not absolute1, is dominant over susceptibility in F1 hybrids4, and may be mediated by a specific intracellular inhibitor5,6. Studies using vesicular stomatitis virus (VSV) pseudotypes made with N- or B-tropic MuLV have shown that Fv-1 restriction occurs after virus penetration7,8, although the mechanism of inhibition is not known. A clear difference exists between Fv-1 restriction of MuLV and the host range restriction of avian leukaemia virus subgroups, in which host range restriction occurs at the cell surface9,10. Another class of MuLVs, NB-tropic, does not seem to be sensitive to Fv-1-mediated restriction1.