ExtractIntramuscular inoculation of 19-day old chickens with heterologous erythrocytes elicited significantly lower levels of agglutinins in embryonically infected birds when compared with control birds (reciprocal ha titer 10 vs. 100, respectively,P<0.01). The IgG component of this antibody was substantially less in experimental chickens, 25% vs. 70% in controls. Subsequent anamnestic antibody response in experimental birds was also significantly less than control chickens (reciprocal ha titers 25 vs. 512, respectively,P<0.02), with continued predominance of IgM antibody in experimental chickens (70% IgM-ha) vs. controls (60% IgG-ha).Induction of cell-mediated immunity by footpad inoculation of 46-day-old birds with diphtheria-tetanus toxoid in complete Freund's adjuvant failed to discern suppression of T cell function in previously infected chicks.Before hatch, the bursae of experimental and control embryos possessed a few IgM-producing lymphoid cells in equivalent numbers. There was also no difference in the relative population of IgM-producing cells in the medullary area of bursal follicles of 7-day-old hatchling chickens, approximately 70%. However, the mean density of IgG-producing cells in the bursae of experimental chickens was less than that of control chickens, 10% vs. 19%, respectively. Consistent with persistent embryonic viral infection and altered bursal function, only IgM-producing cells were detected in the spleens of 7-day-old experimental birds.These observations suggest that persistent embryonic viral infection disturbs the function of bursal-dependent immunopoiesis in the avian host.SpeculationEarly and persistent embryonic mumps virus infection in the avian host results in abnormal immunoglobulin maturation and antibody production. The following mechanisms may influence the immune response in this experimental model: viral replication may directly suppress the transition of IgM-producing cells within the embryonic and hatchling bursa at the stem cell level by altering genetic expression; infection may induce the production of a bursal repressor which disturbs the transition of immunoglobulin synthesis from IgM to IgG; growth retardation may be associated with generalized diminution of immunocellular replication and function.