SUMMARYA virus designated bovine leukaemia virus (BLV), associated with leukaemia in cattle and previously demonstrated to induce the disease in sheep, was purified from chronically infected sheep cell cultures. Electrophoretic analysis showed a major protein of mol. wt. about 24ooo (p24) which reacted in gel diffusion and complement-fixation tests with sera from naturally infected cattle, experimentally infected sheep, and guinea pigs immunized with p24. BLV p24 has an isoelectric point of 8-6. Interspecies antigenic reactivities characteristic of mammalian Type C virus p3os were not detected in disrupted BLV or on p24. Sheep and guinea pig antisera to BLV, reactive with p24, also did not precipitate several Type C virus p3os in radioimmunoassays. BLV is also distinguished from Type C viruses and resembles mouse mammary turnout virus and Mason-Pfizer virus in having an RNA-dependent DNA polymerase which is preferentially active in the presence of Mg ++ when synthetic templates are used. Along with previously published morphological data, the above indicates that BLV is not a Type C virus as classically defined. Four hundred and forty one human sera from cancer patients and matched controls were non-reactive with disrupted BLV, BLV infected cells, and BLV p24 in complement-fixation tests.

The major internal protein of the RD-114 virus that appeared in a human tumor cell line, RD, after passage through fetal cats was purified by isoelectric focusing and used to prepare antibody in guinea pigs.

Abstract. Hamster sarcomas induced by the Gross pseudotype of Moloney sarcoma virus yielded a virus sarcomagenic for hamsters but not mice. This virus was able to produce foci on hamster embryo cells, but not on mouse embryo cells. A hamster-tropic nonfocus-forming helper virus was also found in the viral stocks. These hamster-tropic viruses are not immunologically related to the murine viruses in the original inoculum but appear to represent indigenous C-type RNA viruses of the hamster.Three strains of murine sarcoma viruses, Harvey (H-1VSV), Kirsten (Ki-MSV), and M\loloney (M-MSV), have been shown to induce sarcomas in hamsters which yield virus oncogenic for hamsters but not for mice. Electron microscopic examination of these hamster tumors reveals characteristic C-type particles.2-6 The "hamster-tropic" Ki-MSV was also shown to induce foci on hamster cells and not on mouse cells and to be antigenically distinct from its murine precursor virus.3' 4 Cocultivation of cell lines derived from these virus-induced hamster tumors with mouse embryo fibroblasts and appropriate murine leukemia viruses yielded pseudotype sarcoma viruses with host range and pathologic characteristics indistinguishable from the three murine precursor sarcoma viruses; and in the case of the Ki-1\iSV gave a virus that again had the murine envelope and group-specific antigens.This paper describes studies of another "hamster-tropic" sarcoma virus. This virus was isolated from hamster tumors induced originally by the Gross pseudotype of murine sarcoma virus, M1SV(GLV), and is designated for the purposes of this report MSV(GLV) (0-H).7

AKR/J mice, 80-90% of which ordinarily die of spontaneous lymphocytic leukemias by 12 months of age, were significantly protected from developing leukemia in the initial experiment by a single course of treatment with AKR serotype-specific antibodies made in goats and processed as immune gamma globulin (IgG). In experiment 1, IgG was given on the day of birth and on four additional days, and finished on day 14. This schedule resulted in suppression of over 4 logarithms of normal virogene expressions up to 25 days of age and led to partial viral suppression for over 200 days of age. At 365 days of age, 20 of 24 (83.3%) control animals were dead of leukemia whereas six of 30 (20%) treated animals had died of leukemia. In a second experiment, only four inoculations of IgG were given from birth to 20 days, after which they were given three inoculations of radiation-killed vaccine specific for AKR-Gross leukemia virus and one injection of murine sarcoma virus-Gross leukemia virus 10 days later. This combined immunization procedure provided significant virus suppression up to 288 days of age. At 300 days of age, 30 of the 50 (60%) controls had died of leukemia while only 1 of 24 (4.2%) of the immunized mice developed fatal leukemia; the significance of protection for each of the experiments was P << 0.001. We conclude that these data establish in classical fashion with type-specific immunosuppression the determining role of type-C endogenous virogenes in leukemogenesis and, at the same time, also establish the feasibility of nearly total prevention of leukemia in AKR mice.In this communication we report two experiments, both resulting in highly significant prevention of spontaneous leukemia in AKR/J mice. In the first experiment, several injections of virus-specific antisera prepared as immune gamma globulin (IgG) were given shortly after birth and continued to the 14th and 20th days of age, after which the control and immunized mice (starting at 170 days of age) were observed twice daily for development of the leukemia and/or thymic lymphomas which normally account for nearly all deaths in AKR mice by 12 months of age.