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A chicken lymphoblastoid cell line (TLT)-6855 originally established from an avian oncornavirus-induced lymphoma (Siegfried and Olson, 1972) was studied for the presence and expression of Marek's disease virus (MDV) genome. By nucleic acid hybridization a significant amount of MDV DNA was found in this cell line. This virus DNA, however, was not expressed in either virus-specific intracellular or membrane antigens or the MD-associated tumour-specific surface antigen (MATSA). Moreover, MDV-specific antigens could not be activated in this cell line by treatment with 5-IdUrd. In several experiments, when chickens were inoculated with the cell line a herpesvirus was repeatedly isolated from the kidneys. This herpesvirus was antigenically similar to MDV but was low in oncogenicity for chickens.

Chickens inoculated as embyros or at hatching with the chick syncytial strain of reticuloendotheliosis virus developed a high incidence of lymphoid neoplasms between the 17th and 43rd weeks of age, involving principally the liver and bursa of Fabricius. On the basis of organ distribution, latent period, pathology and surface IgM production, the lymphomas closely resembled those of lymphoid leukosis. One inoculated chicken developed a myxosarcoma. No tumors were observed in uninoculated controls. The tumor-bearing chickens were free of infection with Marek's disease virus and exogenous avian leukosis virus (ALV) of subgroups A, B, C or D. However, the chickens were known to express endogenous ALV genes to varying degrees.

Chickens of lines 6(3) and 151(5) X 7(1) were inoculated with the chick syncytial strain of reticuloendotheliosis virus (REV) or with the Rous-associated virus-I of avian leukosis virus (ALV) at hatching. At 4, 10, 16, and 36 weeks post inoculation (PI), chickens were tested for REV- and ALV-induced viremia and antibody. The incidence of REV- or ALV-induced bursa-associated lymphomas in line 6(3) chickens was compared with that in line 151(5) X 7(1) chickens. Inoculation of REV at hatching resulted in immunological tolerance to the virus in line 6(3) but not in line 151(5) X 7(1) chickens. Between 70% and 100% of line 6(3) chickens remained viremic and lacked REV antibody throughout the experimental period of 36 weeks. In contrast, ALV-inoculated chickens of both lines had antibody by 16 weeks PI. The frequencies of REV- and ALV-induced bursa-associated lymphomas in line 6(3) chickens were significantly lower than in line 151(5) X 7(1) chickens. Further, the incidence of bursa-associated lymphomas induced by REV in line 151(5) X 7(1) chickens was significantly lower than that induced by ALV. These results suggest that: (1) the genetic constitution of the host may influence the immunological response to REV infection; (2) chickens resistant to ALV-induced bursa-associated lymphomas are equally resistant to such lymphomas induced by another unrelated avian retrovirus, REV; and (3) ALV is a more potent inducer of bursa-associated lymphomas than REV.