Chickens were bursectomized by cyclophosphamide treatment at hatching. At 8 or 9 weeks of age, bursectomized and unbursectomized hatchmates, free from prior infection, were challenged with pathogenic Marek's disease virus. Oncogenicity of the virus inoculum was confirmed by inoculating 1-day-old susceptible chickens. At the time of virus challenge, blood cells from the cyclophosphamide-treated chickens were able to mount a vigorous graft-versus-host reaction in allogeneic embryos. This ability indicated that the thymus function was intact. There were no significant differences in Marek's disease response of bursectomized and unbursectomized chickens, in spite of a severe defect in the bursa-dependent functions in the bursectomized chickens. Some bursa-deficient chickens had non-proliferating, presumably regressing lesions in peripheral nerves. Because these lesions lacked plasma cells, it was concluded that the plasma cell may not play a functional role in recovery from Marek's disease.