Chickens vaccinated with infectious bursal disease virus (IBDV) early in life and revaccinated with an inactivated, oil-adjuvant IBDV vaccine at 18 weeks of age produced and maintained high levels of virus-neutralizing (VN) antibody through 10 months of lay. VN-antibody titers of chicks hatched from eggs laid during the same period closely matched the average VN-antibody titers of the dams. A sequential study of the decline rates of IBDV maternal antibody (MAB) in unvaccinated and IBDV-vaccinated chicks showed that the vaccine virus did not accelerate the antibody depletion rate in vaccinated chicks. Chicks carrying high IBDV MAB showed no active immune response to vaccination with commercial IBDV vaccines. They were also refractory to a pathogenic field isolate of IBDV (FV). However, chicks with low levels of MAB responded to both vaccine virus and the FV, although their response to vaccine virus was milder and delayed.
Previously untreated chicks and those treated neonatally with either cyclophosphamide (CY) or infectious bursal disease virus (IBDV) were subcutaneously inoculated with viral arthritis virus ( VAV ) to determine whether suppression of humoral immunity would affect VAV pathogenicity. No difference was apparent in the disease process that occurred in the immunosuppressed versus the nonimmunosuppressed chickens. However, in the immunosuppressed birds, VAV was recovered from the heart and tendon tissues earlier in the postinoculation (PI) period. Also, VAV inoculated immunosuppressed birds carried higher levels of serum gamma globulins at certain PI intervals than the VAV inoculated positive controls or the untreated negative control chickens. It is suggested that the suppression of the bursa of Fabricius (BF) by CY or IBDV did not interfere in the antibody production to VAV , but the antibody produced was qualitatively defective.
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