The aim of this study is to follow the gp production in IBDV-vaccinated and challenged
birds. The progress of IBDV infection was monitored using anti-VP2 immunocytochemistry,
light and transmission electron microscopy. In the medulla of the bursal follicle,
the Movat pentachrome staining discovered an extracellular glycoprotein (gp) produced
by bursal secretory dendritic cells (BSDCs). The secretory granules of BSDCs either
discharge resulting in extracellular gp or fuse together forming intracellular corpuscles.
The double fate of granules suggests a dual function of BSDCs: (a.) For the discharged
granules, gp contributes to the medullary microenvironment (ME). (b.) The intracellular
corpuscles may be the sign of BSDC transformation to a macrophage-like cell (Mal).
Infectious bursal disease virus (IBDV) infection accelerates the BSDC transformation
to Mal. The decreased number of BSDCs is feedback for the precursor cells of BSDCs
lodging in the cortico-medullary epithelial arches (CMEA), where they proliferate.
Opening the CMEA, the precursor cells enter the medulla, and differentiate to immature
BSDCs. The virus uptake in the corpuscles prevents the granular discharge resulting
in the absence of gp and alteration in ME. In vaccine-take birds, the mitotic rate
of BSDC precursor cells cannot restore the precursor pool; therefore, in the case
of IBDV challenge, the number of newly formed BSDCs is too low for outbreak of clinical
disease. The BSDCs, as a primary target of IBDV, may contribute to the long-lasting
immunosuppressive status of IBDV-infected chickens.
