Qiao Wen-Ting, Yao Xin, Lu Wei-Hong, Zhang Yu-Qian, Malhi Kanwar Kumar, Li Hui-Xin, Li Jin-Long
College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China.
State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150001, PR China.
Int J Biol Macromol. 2024 Jun;270(Pt 2):132408. doi: 10.1016/j.ijbiomac.2024.132408. Epub 2024 May 14.
Porcine Epidemic Diarrhea Virus (PEDV) is a highly contagious virus that causes Porcine Epidemic Diarrhea (PED). This enteric disease results in high mortality rates in piglets, leading to significant financial losses in the pig industry. However, vaccines cannot provide sufficient protection against epidemic strains. Spike (S) protein exposed on the surface of virion mediates PEDV entry into cells. Our findings imply that matrine (MT), a naturally occurring alkaloid, inhibits PEDV infection targeting S protein of virions and biological process of cells. The GLY434 residue in the autodocking site of the S protein and MT conserved based on sequence comparison. This study provides a comprehensive analysis of viral attachment, entry, and virucidal effects to investigate how that MT inhibits virus replication. MT inhibits PEDV attachment and entry by targeting S protein. MT was added to cells before, during, or after infection, it exhibits anti-PEDV activities and viricidal effects. Network pharmacology focuses on addressing causal mechanisms rather than just treating symptoms. We identified the key genes and screened the cell apoptosis involved in the inhibition of MT on PEDV infection in network pharmacology. MT significantly promotes cell apoptosis in PEDV-infected cells to inhibit PEDV infection by activating the MAPK signaling pathway. Collectively, we provide the biological foundations for the development of single components of traditional Chinese medicine to inhibit PEDV infection and spread.
猪流行性腹泻病毒(PEDV)是一种高度传染性病毒,可引起猪流行性腹泻(PED)。这种肠道疾病在仔猪中导致高死亡率,给养猪业造成重大经济损失。然而,疫苗无法为流行毒株提供足够的保护。病毒粒子表面暴露的刺突(S)蛋白介导PEDV进入细胞。我们的研究结果表明,苦参碱(MT)这种天然生物碱可通过靶向病毒粒子的S蛋白和细胞的生物学过程来抑制PEDV感染。基于序列比较,S蛋白自对接位点中的GLY434残基与MT保守。本研究对病毒附着、进入和杀病毒作用进行了全面分析,以研究MT如何抑制病毒复制。MT通过靶向S蛋白抑制PEDV的附着和进入。在感染前、感染期间或感染后将MT添加到细胞中,它都表现出抗PEDV活性和杀病毒作用。网络药理学侧重于解决因果机制而非仅仅治疗症状。我们在网络药理学中确定了关键基因并筛选了参与MT抑制PEDV感染的细胞凋亡。MT通过激活MAPK信号通路显著促进PEDV感染细胞中的细胞凋亡,从而抑制PEDV感染。总的来说,我们为开发抑制PEDV感染和传播的单味中药成分提供了生物学基础。