1. Academic Validation
  2. Resveratrol inhibits porcine deltacoronavirus infection by activating SIRT1 to promote interferon production in vitro

Resveratrol inhibits porcine deltacoronavirus infection by activating SIRT1 to promote interferon production in vitro

  • Microb Pathog. 2026 Jan:210:108159. doi: 10.1016/j.micpath.2025.108159.
Songqi Wang 1 Zhicheng Liu 2 Jingjing Nie 2 Yunzhi Qu 2 Chunhong Zhang 2 Jianfeng Zhang 2 Jin Chen 3 Liting Hou 3 Yu Lu 3 Haiyan Shen 4 Renwei Su 5
Affiliations

Affiliations

  • 1 College of Veterinary Medicine, South China Agricultural University, Guangzhou, China; Key Laboratory of Livestock Disease Prevention and Treatment of Guangdong Province, Institute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
  • 2 Key Laboratory of Livestock Disease Prevention and Treatment of Guangdong Province, Institute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
  • 3 Institute of Veterinary Immunology &Engineering, Jiangsu Academy of Agricultural Sciences, Nanjing, Jiangsu, 210014, China; GuoTai (Taizhou) Center of Technology Innovation for Veterinary Biologicals, Taizhou, 225300, China.
  • 4 Key Laboratory of Livestock Disease Prevention and Treatment of Guangdong Province, Institute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangzhou, China. Electronic address: [email protected].
  • 5 College of Veterinary Medicine, South China Agricultural University, Guangzhou, China. Electronic address: [email protected].
Abstract

Porcine deltacoronavirus (PDCoV) is a major pathogen that causes clinical diarrhea in piglets, resulting in substantial economic losses to the pig farming industry. Because of its host diversity, PDCoV can infect multiple species such as cattle, chickens, turkeys, mice, and even humans, posing a considerable threat to public health security. Currently, effective commercial drugs for PDCoV Infection remain unavailable. In this study, we noted that resveratrol (Res) treatment effectively inhibited PDCoV replication in the porcine small intestinal epithelial cell line, IPEC-J2. Mechanistically, Res treatment increased SIRT1 expression, and the SIRT1 Inhibitor EX-527 could block Res's Antiviral activity. SIRT1 overexpression inhibited PDCoV replication, whereas mutant SIRT1 lacking deacetylase activity did not affect PDCoV replication. These results indicated that the deacetylation activity of SIRT1 is critical for the anti-PDCoV effects of Res. We also found that Res treatment significantly elevated IFN-β mRNA levels and activated IRF3 phosphorylation via SIRT1. In conclusion, Res can activate SIRT1, upregulating the interferon signaling pathway and promoting IFN-β production, thereby inhibiting PDCoV replication. As such, Res may be a promising therapeutic agent for PDCoV control, facilitating the development of novel anti-PDCoV drugs.

Keywords

Antiviral activity; IFN-β; Porcine deltacoronavirus; SIRT1.

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