Evidence map›Paper›PMID 41803964›Full record

ArticleVeterinary research2026

TGEV activates RIG-I/IFN-β/STAT1 axis to promote NLRC5-mediated SLA-I upregulation.

Wenqian Wang, Mengyao Ma, Haojie Bai, Yinhe Sun, Borui Liu, Ao Gao, Qihao Pan, Dongfang Zheng, Muzi Li, Weili Jiang and 4 more

Abstract read
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In one paragraph

Article in Veterinary research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Wenqian Wang *College of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Mengyao Ma *College of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Haojie BaiCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Yinhe SunCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Borui LiuCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Ao GaoCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Qihao PanCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Dongfang ZhengCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Muzi LiCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Weili JiangCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Shijie MaCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Zhanyong WeiCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Honglei ZhangCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China. zhanghonglei@henau.edu.cn.
Lanlan ZhengCollege of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China. lanlan@henau.edu.cn.

Funding

Basic Research Program of Henan Higher Education Institutions Key Scientific Research Project 26ZX011Innovative Research Team (in Science and Technology) in University of Henan Province 24IRTSTHN034Interdisciplinary Innovation Research Group Project of Natural Science Foundation of Henan Province of China 232300421001National Natural Science Foundation of China 32473045
6 · The paper itself

Abstract

Porcine transmissible gastroenteritis virus (TGEV) is a major pathogen causing acute diarrhea and high mortality in neonatal piglets, yet the interplay between TGEV infection and host immune responses, particularly swine leukocyte antigen class I (SLA-I) mediated antigen presentation and type I interferon (IFN) signaling, remains poorly defined. This study aimed to clarify how TGEV modulates SLA-I expression through NOD-like receptor family CARD domain containing 5 (NLRC5) and the underlying signaling pathways. Since TGEV infection was shown to induce SLA-I upregulation in porcine intestinal tissues, we used swine testicular (ST) cells to investigate the expression dynamics of retinoic acid inducible gene I (RIG-I)/IFN-β/signal transducer and activator of transcription 1 (STAT1) axis. TGEV infection significantly upregulated SLA-I and NLRC5 in ST cells, with high expression coinciding with active viral replication, while NLRC5 inhibited TGEV proliferation. Furthermore, TGEV upregulated SLA-I and NLRC5 expression via RIG-I activation, which triggered downstream IFN-β secretion and subsequent STAT1 phosphorylation, thereby facilitating the induction of SLA-I and NLRC5. Moreover, the TGEV open reading frame 7 (ORF7) protein was identified as a critical viral effector contributing to SLA-I and NLRC5 upregulation. Collectively, TGEV infection activates the RIG-I/IFN-β/STAT1 axis to promote NLRC5 mediated SLA-I upregulation, which inhibits TGEV proliferation, elucidating a novel immune regulatory mechanism that balances viral replication and host antiviral defense and providing insights for targeted management strategies against porcine enteric coronaviruses.

Indexed as

Gastroenteritis, Transmissible, of SwineHistocompatibility Antigens Class IIntracellular Signaling Peptides and ProteinsTransmissible gastroenteritis virusAnimalsInterferon-betaMaleSignal TransductionSTAT1 Transcription FactorSwineUp-RegulationHistocompatibility Antigens Class IInterferon-betaIntracellular Signaling Peptides and ProteinsSTAT1 Transcription FactorNLRC5Porcine transmissible gastroenteritis virusSLA-Iviral proliferation

Identifiers

PMID41803964
PMCPMC13085429

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.