The pathogenesis of Marek's disease (MD) in chicks with maternal antibody (AP) or without antibody (AN) was studied up to 35 days after infection. MD virus antigens, detected by fluorescent antibody tests, and lymphoid proliferation were more frequent in the tissues of AN chicks than in those of AP chicks. In AN chicks, lymphoid proliferation was preceded by a phase of reticulum cell hyperplasia in the bursa, thymus', and spleen, 5–7 days after infection and showing abundant viral antigen, cytolysis, intranuclear inclusion bodies, and infiltration by granulocytes, macrophages, and lymphocytes. This phase appeared to represent an Inflammatory response to viral antigen and cellular degeneration and was accompanied by lymphoid regression in the bursa and thymus. These changes were absent or markedly suppressed in AP chicks. The acute phase was followed by a recovery phase from 7–21 days after infection, in which viral antigen disappeared from the lymphoid organs, lymphocyte populations in the bursa and thymus tended to return to normal, and areas of reticulum cell hyperplasia disappeared or were replaced by lymphoid tissue. Lymphoid proliferation leading to lymphoma formation and nerve infiltration commenced during the recovery phase; at the end of the experimental period, a second phase of viral antigen production occurred in the bursa and, less regul,arly, in the thymus and spleen; it was accompanied by lymphoid regression in the bursa and thymus.