Permanent cell lines have been established in vitro from lymphoid tumors induced in C57BH/Ka mice by fractionated X-irradiation or by inoculation of the radiation leukemia virus (RadOV). The cultured cells are lymphoblastic, replicate rapidly in vitro, and are tumorigenic in vivo. The cell surface markers Thy 1, Ly 1, Ly 2,3 and GIX are expressed by the lymphoid tumor cells in the mouse and persist in the corresponding cell lines; expression of the H-2 and TL antigens is greatly reduced during in vitro passage, but is restored on in vivo transplantation. The cell lines derived from RadLV-induced tumors (BL/VL lines) produce a virus population (RadLV/LTC) with the thymotropic and leukemogenic attributes of RadLV. Those derived from radiation-induced, virus-negative lymphomas (BL/RL lines) are initially devoid of MuLV expression, but frequently become spontaneous virus producers during in vitro cultivation.

Radiation leukemia virus, isolated from radiation-induced lymphomas in C57BL/Ka mice and propagated in that strain, is thymotropic and leukemogenic in vivo but replicates poorly, if at all, in mouse and mink fibroblast cultures in vitro. Comparative studies indicate that this naturally occurring virus is distinct from the previously recognized classes of endogenous murine ecotropic and xenotropic C-ype viruses which are capable of replication on fibroblasts (fibrotropic) but are neither thymotropic nor leukemogenic. These studies also demonstrate that a differentiation-specific restriction system governing the replication of the murine ecotropic C-type viruses operates in addition to the previously defined Fv-1 and SRV gene restriction systems. Radiation leukemia virus (RadLV), a naturally occurring murine leukemogenic virus, is recovered from thymic lymphomas induced by x-irradiation in strain C57BL/Ka mice (1, 2). This virus replicates selectively in the host thymus (3, 4). Mice of strain C57BL have also been shown to harbor three classes of endogenous C-type viruses, all of which can be propagated on fibroblastic cells in vitro but differ in host range. They include B-tropic (5, 6), N-tropic (6, 7), and X-tropic viruses (8,9). It is now reported that the thymotropic, leukemogenic particles in RadLV differ at the molecular level, as revealed by their antigenic determinants, from the B, N, and X endogenous viruses and from any combination thereof, and must therefore be recognized as a distinctive subclass of murine ecotropic viruses. MATERIALS AND METHODSMice. C57BL/Ka mice of both sexes, 3-5 weeks of age, were obtained from our own colony. NIH/Swiss mice were kindly provided by Dr.

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The serological properties of the gag gene products p15 and p12 of N-and B-tropic viruses of C57BL mice have been examined. Although these viruses were serologically identical by competition assays for proteins gp7l and p30, they were readily distinguishable in competition assays for proteins p15 and p12. Two isolates of N-tropic viruses had pi2s serologically indistinguishable from AKR murine leukemia virus p12, while two Btropic isolates had distinctly different p12s. The latter pi2s were serologically indistinguishable from the p12 purified from the Btropic radiation leukemia virus (RadLV)-/VL-3. Moreover, this p12 was indistinguishable from the p12 of the endogenous C57BL/Ka xenotropic virus. Similarly, the piSs of the B-tropic viruses were serologically distinct from the AKR murine leukemia virus type of p15, as was the p15 of one C57BL N-tropic virus, while another N-tropic isolate had a p15 identical to the AKR murine leukemia virus p15. These results are interpreted to suggest that the endogenous N-tropic virus of C57BL mice undergoes recombination with the endogenous, xenotropic virus and that this mechanism is involved in the generation of B-tropic viruses in C57BL mice.

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