Key result
Duck enteritis virus targets epithelial and B cells in the lymphoid organs of infected white Pekin ducklings, causing irreversible depletion of B cells from the bursa.
The study identifies epithelial and B cells as the primary target cells for duck enteritis virus replication, explaining the mechanism of lymphoid organ atrophy and immunosuppression in infected ducklings.
May guide DEV control in ducklings; leaves open translation to field conditions or other species.
Duck enteritis virus (DEV), a herpesvirus, has been shown to cause lymphoid organ atrophy and immunosuppression in white Pekin ducklings. The cells that support virus replication and could be important for immunosuppression were identified in this study. Lymphoid organs of white Pekin ducks infected at 2 weeks of age were collected at 3, 6, 8 and 10 days post-inoculation (d.p.i.). Frozen sections were double-stained for DEV-infected (DEV+) and epithelial cells, DEV+ and CD3+ cells or DEV+ and B cells. DEV antigen was detected in the spleen, thymus and bursa for 3, 6 and 8 d.p.i., respectively. DEV antigen was demonstrated in epithelial cells of all examined lymphoid organs. B cells were irreversibly depleted from bursa; however, the depletion in the spleen was only for 8 d.p.i. Depletion of CD3+ cells was only observed in the thymus. These data show that the target cells for DEV are epithelial and B cells.
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Samia A. Shawky (2000) studied Duck enteritis virus (DEV) infection. Duck enteritis virus (DEV) infection was evaluated on Identification of target cells for DEV replication and immunosuppression. Duck enteritis virus targets epithelial and B cells in the lymphoid organs of infected white Pekin ducklings, causing irreversible depletion of B cells from the bursa.
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