Punicalagin Inhibits African Swine Fever Virus Replication by Targeting Early Viral Stages and Modulating Inflammatory Pathways
文献类型: 外文期刊
第一作者: Geng, Renhao
作者: Geng, Renhao;Yin, Dan;Lv, Hui;Zhou, Xiaoyu;Bao, Chunhui;Shao, Hongxia;Qian, Kun;Qin, Aijian;Geng, Renhao;Yin, Dan;Lv, Hui;Zhou, Xiaoyu;Bao, Chunhui;Shao, Hongxia;Qian, Kun;Qin, Aijian;Liu, Yingnan;Chen, Hongjun;Gong, Lang
作者机构:
关键词: African swine fever virus; library screen; punicalagin; replication stages; NF-kappa B/STAT3/NLRP3
期刊名称:VETERINARY SCIENCES ( 影响因子:2.3; 五年影响因子:2.4 )
ISSN:
年卷期: 2024 年 11 卷 9 期
页码:
收录情况: SCI
摘要: Simple Summary The spread of the African swine fever virus (ASFV) poses a great threat to the global pig industry and new measures for prevention and control are urgently needed. With no effective vaccines, drug development against ASFV is crucial. This study screened 536 antiviral compounds and identified that punicalagin, from pomegranate peel, significantly inhibited ASFV replication in various cell lines in vitro. Punicalagin acted on early viral replication stages, including attachment and internalization, and directly inactivated the virus. Finally, it was found that punicalagin could modulate the NF-kappa B/STAT3/NLRP3 signaling pathway, reducing ASFV-induced inflammation. These results provide an experimental basis for the use of punicalagin in developing anti-ASFV candidate drugs.Abstract African swine fever (ASF), caused by the African swine fever virus (ASFV), has resulted in significant losses in the global pig industry. Considering the absence of effective vaccines, developing drugs against ASFV may be a crucial strategy for its prevention and control in the future. In this study, punicalagin, a polyphenolic substance extracted from pomegranate peel, was found to significantly inhibit ASFV replication in MA-104, PK-15, WSL, and 3D4/21 cells by screening an antiviral compound library containing 536 compounds. Time-of-addition studies demonstrated that punicalagin acted on early viral replication stages, impinging on viral attachment and internalization. Meanwhile, punicalagin could directly inactivate the virus according to virucidal assay. RT-qPCR and Western blot results indicated that punicalagin modulated the NF-kappa B/STAT3/NLRP3 inflammasome signaling pathway and reduced the levels of inflammatory mediators induced by ASFV. In conclusion, this study reveals the anti-ASFV activity of punicalagin and the mechanism of action, which may have great potential for developing effective drugs against ASFV.
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