2. Academic Validation
  3. TRIM7 suppresses transmissible gastroenteritis virus replication by targeting the degradation of N protein and activating RIG-I-mediated type I IFN antiviral response

TRIM7 suppresses transmissible gastroenteritis virus replication by targeting the degradation of N protein and activating RIG-I-mediated type I IFN antiviral response

  • Vet Res. 2025 Nov 5;56(1):210. doi: 10.1186/s13567-025-01610-z.
Weiyun Qin 1,  Yunxiao Xie 2,  Haijiang Liang 1,  Zuolin Wu 1,  Songbai Yang 1,  Xiaolong Zhou 1,  Ayong Zhao 3
Affiliations

Affiliations

  • 1 Key Laboratory of Applied Technology On Green-Eco-Healthy Animal Husbandry of Zhejiang Province, College of Animal Science and Technology, College of Veterinary Medicine, Zhejiang A&F University, Hangzhou, 310000, China.
  • 2 College of Animal Science and Technology, Yangzhou University, Yangzhou, 225009, China.
  • 3 Key Laboratory of Applied Technology On Green-Eco-Healthy Animal Husbandry of Zhejiang Province, College of Animal Science and Technology, College of Veterinary Medicine, Zhejiang A&F University, Hangzhou, 310000, China. [email protected].
PMID: 41194212 DOI: 10.1186/s13567-025-01610-z
Abstract

Transmissible gastroenteritis virus (TGEV) is a major enteric pathogen causing severe diarrhea in swine, with substantial implications for the biosecurity of intensive pig production worldwide. The E3 ubiquitin Ligase TRIM7 has emerged as a key regulator of host Antiviral immunity, yet its role in TGEV Infection remains elusive. Here, we report that TRIM7 is abundantly expressed in porcine intestinal tissue and significantly upregulated upon TGEV challenge in IPEC-J2 cells. Functional studies demonstrated that TRIM7 restricts TGEV replication in IPEC-J2 cells through two distinct mechanisms. Firstly, molecular interaction and co-immunoprecipitation assays revealed that TRIM7 mediates ubiquitin-dependent degradation of the TGEV nucleocapsid (N) protein. Secondly, RNA-seq analysis combined with RIG-I signaling modulation experiments established that TRIM7 enhances RIG-I-mediated type I interferon (IFN) signaling to suppress viral propagation. These findings uncover a dual Antiviral role for TRIM7 in countering TGEV Infection, highlighting its potential as a therapeutic target for TGEV control.

Keywords

RIG-I signaling pathway; TRIM7; Transmissible gastroenteritis virus; type I interferon; ubiquitination.

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