Oncoviral Proteins as Cellular Antigens

The immunobiology of the feline leukemia virus

“…situation may precipitate immune-ruediated disorders including chronic glomerulonephritis and hypocornplementemia (Kobilinsky et al, 1979;3ones et al. 19g0;Snyder et al, 1982).…”

“…Early observations that FOCMA-S and FOCMA-L were antigenically cross-reactive have led to the hypothesis that FeLV induces a c-onc sequence in transformable cells and that the FOCMA-L thus induced was a tumor-specific antigen (Essex eta]., 1971a,b;Hardy et al, 1977Hardy et al, ,1980. This has been strengthened by the apparent dissociation between expression of FOCMA-L and of FeLV structural proteins: (1) FOCMA is not present on nontransformed, FeLV-infected fibroblasts or lymphocytes (Sliski eta]., 1977;Fleissner and Snyder, 1992), (2) FeLV proteins do not absorb FOCMA activity from naturally occurring viremic cat sera (Essex et al, 1971a,b;Stephenson eta]., 1977), (3) VN and anti-FOCMA (IMI or CDA) activity in cat sera are not correlated (Essex et al, 1971a,b) and (4) FOCMA is expressed on the surface of nonproducer (p27-negative) feline lymphoma cells . Furthermore~ a 707000 dalton protein immunoprecipitated from FeLV-negative lymphoma cells has been shown to have a tryptic peptide map analogous to a 70,000 dalton protein of FL74 (FeLV-positive Iymphoma)…”

“…Virus-negative leukemic cats have circulating immune complexes which contain viral p27, gp70 and reverse transcriptase (Day et al, 19g0;3ones et al, 1980;Snyder et al, 1982).…”

Evidence for a new form of retroviral env transcript in leukemic and normal mouse lymphoid cells

“…The expression of endogenous retroviruses in normal mice as well as in mouse lymphoid tumors has led many investigators to address the question of their role in leukemogenesis (6,21,34). T-cell lymphomas occurring spontaneously in AKR mice or after X-irradiation in C57BL and BALB/c are good models to study this problem.…”

“…In B-cell leukemogenesis by avian leukosis viruses, an exogenous provirus is integrated in the tumor cells next to a cellular onc gene (c-myc); the promoter or enhancer (or both) sequences present in the long terminal repeat (LTR) of the provirus increases the expression of this gene (9,20,22). A second line of evidence connects T-cell leukemogenesis in inbred mice to recombinant MuLV env expression, e.g., in the case of spontaneous leukemia in AKR mice (6,8). Although polytropic (mink cell focus-inducing [MCF] type) env recombinant MuLV has not been isolated from radiation leukemias of BALB/c mice, an ecotropic env recombinant virus with leukemogenic activity was isolated from one such leukemia (2; R. Ellis and E. Fleissner, unpublished data).…”