China Animal Husbandry & Veterinary Medicine ›› 2026, Vol. 53 ›› Issue (2): 926-936.doi: 10.16431/j.cnki.1671-7236.2026.02.037

• Preventive Veterinary Medicine • Previous Articles     Next Articles

Effect of Transcription Factor STAT1 on Porcine Deltacoronavirus Replication

ZHANG Shuai1(), XIA Liangxing1, ZHANG Xueli1, CAO Yanan1, BAO Wenbin1,2()   

  1. 1.Key Laboratory for Animal Genetic,Breeding,Reproduction and Molecular Design of Jiangsu Province,College of Animal Science and Technology,Yangzhou University,Yangzhou 225009,China
    2.Joint International Research Laboratory of Agriculture & Agri-Product Safety,Yangzhou University,Yangzhou 225009,China
  • Received:2025-07-08 Online:2026-02-20 Published:2026-01-27
  • Contact: BAO Wenbin E-mail:shuai_zhang1990@163.com;wbbao@yzu.edu.cn

Abstract:

Objective This experiment aimed to investigate the impact of Porcine deltacoronavirus (PDCoV) infection on the innate immunity and the interference mechanism of immune signal transduction, with a focus on the roles of signal transducer and activator of transcription 1 (STAT1) and tripartite-motif protein 21 (TRIM21) in this process. Method Morphological changes in IPEC-J2 cells infected with PDCoV at a multiplicity of infection (MOI) of 1 were observed via an inverted microscope at 1, 12, 24 and 48 hours post-infection.Meanwhile, Real-time quantitative PCR and Western blotting were used to detect the expression of PDCoV-N gene and protein, respectively, for screening the optimal conditions of the PDCoV-infected IPEC-J2 cell model. At the peak of PDCoV infection, the mRNA and protein expression of STAT1, TRIM21, and interferon-stimulated genes (ISGs) were detected by Real-time quantitative PCR and Western blotting,respectively. The effects of overexpression or inhibition of STAT1 on the replication of PDCoV and the activity of the interferon-stimulated response element (ISRE) promoter were detected using the dual-luciferase reporter gene system. Additionally, eukaryotic expression vectors of TRIM21 and STAT1 were co-transfected into IPEC-J2 cells. Laser confocal microscopy, co-immunoprecipitation (Co-IP), and Western blotting were used to verify the interaction between TRIM21 and STAT1 as well as the regulatory effect of TRIM21 on STAT1. Result PDCoV reached replication peak at 24 hour post-infection in IPEC-J2 cells. At the same time, the protein expression of STAT1 and TRIM21, as well as the transcription level of ISGs in experiment group, were extremely significantly higher than those in control group (P<0.01). Compared with control group, the activity of ISRE promoter was extremely significantly enhanced after overexpression of STAT1, and the expression of PDCoV-N gene and its protein were extremely significantly reduced (P<0.01) , while inhibition of STAT1 by fludarabine extremely significantly promoted viral replication (P<0.01). Laser confocal microscopy and Co-IP confirmed the co-localization and interaction between STAT1 and TRIM21. Moreover, compared with control group, the expression of STAT1 protein was extremely significantly reduced after overexpression of TRIM21 (P<0.01). Conclusion This study illuminated the intricate interplay between PDCoV and the innate immune response of host IPEC-J2 cells. As a key antiviral factor, STAT1 enhanced innate immunity via the ISRE pathway to inhibit viral replication. In contrast, TRIM21 participated in viral immune evasion by interacting with STAT1 and downregulating its expression. These findings provided novel insights into the molecular pathogenesis of PDCoV, and laid a foundation for formulating PDCoV prevention and control strategies.

Key words: Porcine deltacoronavirus (PDCoV); STAT1; TRIM21; innate immunity; immune escape

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