These findings implicate both the thymus-and bursa-dependent lymphoid systems in MD, and are consistent with the hypothesis that both systems responddirectly to the presence of MD virus. Pathologically MD is much more suggestive of an aberrant immunological response with failure of the cellular proliferation to be cut off than it is of a neoplasm arising as a result of virus-induced malignant transformation of a line of lymphoid cells. The majority of lymphoid cells in the tumours in fact appear to be free of virus infection as judged by their lack of infectivity in-tissue culture (Churchill & Biggs 1967) and lack of morphological evidence of virus under the electron microscope (Ahmed & Schidlovsky 1968). It may be that the immune deficiencies in MD arise from antigenic competition between MDV and other antigens. If this is so, it would appear that the antigenic challenge presented by MDV infection is of an unusual nature in view of the progressive cellular response leading to tumour formation. The abnormality could be in the nature of the antigen, its amount or the failure of some feedback mechanism responsible for control of cellular proliferation.