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Peer-reviewedCC BY 4.0Virulence

NLRP3 inflammasome in major swine viral infections: Host defense and viral antagonism

  • Ya-Di Guo1,2,3
  • Hang-Tian Mei1,2,3
  • Yang Wang1,2,3
  • Yu-Xin Xiang1,2,3
  • Ying-Nan Li1,2,3
  • Guo-Yu Yang1,2,3
  • Jiang Wang1,2,3,4
  • Lei Zeng1,2,3
  • Bei-Bei Chu1,2,3,4,5,6
  • Sheng-Li Ming1,2,3
6 affiliations
  1. 1College of Veterinary Medicine, Henan Agricultural University, Zhengzhou, Henan Province, China
  2. 2Key Laboratory of Animal Biochemistry and Nutrition, Ministry of Agriculture and Rural Affairs, Zhengzhou, Henan Province, China
  3. 3Key Laboratory of Veterinary Biotechnology of Henan Province, Henan Agricultural University, Zhengzhou, Henan Province, China
  4. 4Ministry of Education Key Laboratory for Animal Pathogens and Biosafety, Henan Agricultural University, Zhengzhou, Henan Province, China
  5. 5Longhu Advanced Immunization Laboratory, Henan Agricultural University, Zhengzhou, Henan Province, China
  6. 6International Joint Research Center of National Animal Immunology, Henan Agricultural University, Zhengzhou, Henan Province, China
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Abstract

The NLRP3 inflammasome is a cytosolic signaling platform that drives caspase-1-dependent maturation of IL-1β and IL-18 and gasdermin D (GSDMD)-mediated pyroptosis. During infection with major porcine viruses – including African swine fever virus, porcine reproductive and respiratory syndrome virus, pseudorabies virus, porcine epidemic diarrhea virus, transmissible gastroenteritis virus, and porcine circovirus type 2, NLRP3 exerts opposing effects: moderate activation restricts viral propagation, whereas sustained stimulation drives tissue injury. We review how structurally unrelated viral proteins converge on limited upstream events – endolysosomal damage, ion flux, mitochondrial injury, ER stress, and the ubiquitin–autophagy network. Because genetically distinct porcine pathogens exploit this same regulatory axis, it represents a shared point of vulnerability. We assess therapeutic options targeting NLRP3 assembly, GSDMD pore formation, and host proteostasis, and highlight questions requiring validation in porcine cells and pigs.

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Cite

BibTeXRIS
BibTeX
@article{guo2026nlrp3,
  title = {{NLRP3 inflammasome in major swine viral infections: Host defense and viral antagonism}},
  author = {Ya-Di Guo and Hang-Tian Mei and Yang Wang and Yu-Xin Xiang and Ying-Nan Li and Guo-Yu Yang and Jiang Wang and Lei Zeng and Bei-Bei Chu and Sheng-Li Ming},
  journal = {Virulence},
  year = {2026},
  month = oct,
  doi = {10.1080/21505594.2026.2753323},
  url = {https://doi.org/10.1080/21505594.2026.2753323},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - NLRP3 inflammasome in major swine viral infections: Host defense and viral antagonism
AU  - Ya-Di Guo
AU  - Hang-Tian Mei
AU  - Yang Wang
AU  - Yu-Xin Xiang
AU  - Ying-Nan Li
AU  - Guo-Yu Yang
AU  - Jiang Wang
AU  - Lei Zeng
AU  - Bei-Bei Chu
AU  - Sheng-Li Ming
PY  - 2026
DA  - 2026/10/29
JO  - Virulence
DO  - 10.1080/21505594.2026.2753323
UR  - https://doi.org/10.1080/21505594.2026.2753323
AB  - The NLRP3 inflammasome is a cytosolic signaling platform that drives caspase-1-dependent maturation of IL-1β and IL-18 and gasdermin D (GSDMD)-mediated pyroptosis. During infection with major porcine viruses – including African swine fever virus, porcine reproductive and respiratory syndrome virus, pseudorabies virus, porcine epidemic diarrhea virus, transmissible gastroenteritis virus, and porcine circovirus type 2, NLRP3 exerts opposing effects: moderate activation restricts viral propagation, whereas sustained stimulation drives tissue injury. We review how structurally unrelated viral proteins converge on limited upstream events – endolysosomal damage, ion flux, mitochondrial injury, ER stress, and the ubiquitin–autophagy network. Because genetically distinct porcine pathogens exploit this same regulatory axis, it represents a shared point of vulnerability. We assess therapeutic options targeting NLRP3 assembly, GSDMD pore formation, and host proteostasis, and highlight questions requiring validation in porcine cells and pigs.
SN  - 2150-5594
SN  - 2150-5608
ER  -