Yang Jingyu, Hu Xiaotong, Lv Changjie, Cheng Chuxing, Zhang Qiang, Sun Xiaomei, Du Xuezhu, Jin Meilin
State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan 430070, China.
College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China.
Transbound Emerg Dis. 2025 Jul 14;2025:2453420. doi: 10.1155/tbed/2453420. eCollection 2025.
African swine fever (ASF) is an acute infectious disease that significantly threats the global pig farming industry. At present, there is no efficient vaccine or targeted therapy for this virus, primarily because of the unclear pathogenesis of ASF virus (ASFV) infection and its interactions with host responses. Here, we established an oral infection model of ASFV in Landrace pigs and identified gene expression and metabolic changes in the pig spleen following ASFV infection using transcriptomic and metabolomic analyses. After ASFV SY-1 infection, 5556 differentially expressed genes (DEGs) were identified, wherein 2577 and 2979 were upregulated and downregulated, respectively. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed that these genes were dynamically enriched in various biological processes, including the innate immune response, inflammatory response, chemokine signaling, and signal transduction. Integrated transcriptome and metabolome analyses indicated that ASFV altered diverse pathways, including cysteine and methionine metabolism, cGMP-PKG signaling, choline metabolism in cancer, cholesterol metabolism, sphingolipid signaling, protein digestion and absorption, FoxO signaling, and central carbon metabolism in cancer. Additionally, we confirmed that metabolites, such as L-glutamate, glycerophosphocholine, and L-serine, significantly inhibit ASFV proliferation in vitro. This study improves our comprehension of the relationships between viruses and hosts, and it serves as a guide for identifying new inhibitors for ASFV.
非洲猪瘟(ASF)是一种对全球养猪业构成重大威胁的急性传染病。目前,针对这种病毒尚无有效的疫苗或靶向治疗方法,主要原因是非洲猪瘟病毒(ASFV)感染的发病机制及其与宿主反应的相互作用尚不清楚。在此,我们建立了长白猪ASFV口服感染模型,并通过转录组学和代谢组学分析确定了ASFV感染后猪脾脏中的基因表达和代谢变化。ASFV SY-1感染后,鉴定出5556个差异表达基因(DEG),其中分别有2577个和2979个上调和下调。基因本体论(GO)和京都基因与基因组百科全书(KEGG)分析表明,这些基因在各种生物过程中动态富集,包括先天免疫反应、炎症反应、趋化因子信号传导和信号转导。综合转录组和代谢组分析表明,ASFV改变了多种途径,包括半胱氨酸和甲硫氨酸代谢、cGMP-PKG信号传导、癌症中的胆碱代谢、胆固醇代谢、鞘脂信号传导、蛋白质消化和吸收、FoxO信号传导以及癌症中的中心碳代谢。此外,我们证实,L-谷氨酸、甘油磷酸胆碱和L-丝氨酸等代谢物在体外显著抑制ASFV增殖。本研究提高了我们对病毒与宿主之间关系的理解,并为鉴定ASFV的新抑制剂提供了指导。