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Updated: Jun 21, 2026

An Ex Vivo Chicken Primary Bursal-cell Culture Model to Study Infectious Bursal Disease Virus Pathogenesis
Published on: October 4, 2018
Impaired intestinal mucosal immunity in specific-pathogen-free chickens after infection with very virulent infectious
1College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China. wdc268@yahoo.com.cn
Abstract:
Diarrhea is one of the most important clinical side effects that occurs in chickens after infection with bursal disease virus. However, the kinetics of the intestinal mucosal immune parameters in infectious bursal disease virus (IBDV)-infected birds remains unclear. Forty-five specific-pathogen-free chickens were randomly divided into 2 groups [30 chickens in the very virulent IBDV (vvIBDV)-infected group and 15 chickens in the control group] to determine the effect of vvIBDV infection on intestinal mucosal immunity. All chickens were raised in negative-pressure isolators and fed the same diet. Results indicate that severe histologic lesions were observed in the intestinal tract in the vvIBDV-infected group, and the villus heights of the duodenum, jejunum, and ileum were decreased after vvIBDV infection (P < 0.01 or P < 0.05). The number of intestinal intraepithelial lymphocytes, mast cells, and goblet cells decreased significantly in the vvIBDV-infected group compared with the control (P < 0.01 or P < 0.05) on d 1, 2, and 3 postchallenge with vvIBDV. Very virulent IBDV infection reduced the expression of each fragment of intestinal secretory IgA at all 3 time points. Intestinal alkaline phosphatase decreased dramatically on d 2 and 3 postchallenge with vvIBDV. Taken together, these results indicate that vvIBDV infection contributes to considerable damage to the normal structure of the intestine and intestinal mucosal immune parameters of specific-pathogen-free chickens. Our research helps to increase an understanding of the pathogenesis of diarrhea induced by vvIBDV infection. These findings provide new insights into the pathogenesis and pathophysiology of vvIBDV infection.
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