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Updated: Aug 15, 2025

An Ex Vivo Chicken Primary Bursal-cell Culture Model to Study Infectious Bursal Disease Virus Pathogenesis
Published on: October 4, 2018
Chicken PRMT1 promotes infectious bursal disease virus replication via suppressing IFN-β production
Xifeng Hu1, Xiangdong Wu1, Zheng Chen1
1Department of Veterinary Preventive Medicine, College of Animal Science and Technology, Jiangxi Agricultural University, Zhimin Street, Qingshan Lake, Nanchang, 330045, PR China; Jiangxi Provincial Key Laboratory for Animal Science and Technology, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, PR China.
Abstract:
The protein arginine methyltransferase (PRMT) family, such as PRMT1, regulates the arginine methylation of various substrates. Many studies have examined the role of PRMT1 in mammals, however, it is still unknown how PRMT1 works in chickens. To investigate the effect of chicken PRMT1 (chPRMT1) on regulating IFN-β production and IBDV replication, chPRMT1 knock out DF-1 cells were constructed in this study. First, we found that chPRMT1 was widely expressed in a variety of chicken tissues and that it was distributed in the cytoplasm and nucleus of DF-1 cells. Additionally, IFN-β activation was inhibited by chPRMT1 at the step of chMAVS. In addition, chPRMT1 knock out DF-1 cells were constructed using CRISPR-Cas9 technique. The morphology and viability of chPRMT1 knock out DF-1 cells were similar with the wild-type cells. In addition, the IFN-β as well as interferon stimulate genes activation induced by chMAVS in PRMT1 knock out DF-1 cells were significantly higher than that in WT cells. Furthermore, ectopic expression of chPRMT1 significantly supports IBDV replication. We also found that the ability of IBDV replication in PRMT1 knock out DF-1 cells was remarkably lower than that of in WT cells, suggesting that PRMT1 negatively regulate IBDV replication via suppressing IFN-β production. In conclusion, the PRMT1 knock out DF-1 cells were constructed, which was further used to demonstrate an inhibitory role of chPRMT1 in IFN-β production, and a contributor of chPRMT1 in IBDV replication.

