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

## TL;DR

TRIM7 helps fight TGEV in pigs by breaking down a viral protein and boosting the immune response, offering a new way to control the virus.

## Contribution

This study reveals TRIM7's dual role in suppressing TGEV through N protein degradation and RIG-I activation.

## Key findings

- TRIM7 mediates ubiquitin-dependent degradation of the TGEV nucleocapsid (N) protein.
- TRIM7 enhances RIG-I-mediated type I interferon signaling to suppress TGEV replication.
- TRIM7 is upregulated in porcine intestinal tissue upon TGEV challenge.

## 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.

The online version contains supplementary material available at 10.1186/s13567-025-01610-z.