Shan Yiyi, Xiao Qi, He Kongwang, Wu Shenglong, Bao Wenbin, Wu Zhengchang
Key Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design of Jiangsu Province, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Institute of Veterinary Medicine, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, China.
Vet Sci. 2024 Mar 20;11(3):135. doi: 10.3390/vetsci11030135.
Porcine circovirus type 2 (PCV2) is the main pathogen causing post-weaning multisystemic wasting syndrome (PMWS), which mainly targets the body's immune system and poses a serious threat to the global pig industry. 5-Azacytidine is a potent inhibitor of DNA methylation, which can participate in many important physiological and pathological processes, including virus-related processes, by inhibiting gene expression. However, the impact of 5-Aza on PCV2 replication in cells is not yet clear. We explored the impact of 5-Aza on PCV2 infection utilizing PK15 cells as a cellular model. Our objective was to gain insights that could potentially offer novel therapeutic strategies for PCV2. Our results showed that 5-Aza significantly enhanced the infectivity of PCV2 in PK15 cells. Transcriptome analysis revealed that PCV2 infection activated various immune-related signaling pathways. 5-Aza may activate the MAPK signaling pathway to exacerbate PCV2 infection and upregulate the expression of inflammatory and apoptotic factors.
猪圆环病毒2型(PCV2)是引起断奶后多系统消耗综合征(PMWS)的主要病原体,该综合征主要针对机体免疫系统,对全球养猪业构成严重威胁。5-氮杂胞苷是一种有效的DNA甲基化抑制剂,它可以通过抑制基因表达参与许多重要的生理和病理过程,包括与病毒相关的过程。然而,5-氮杂胞苷对PCV2在细胞中复制的影响尚不清楚。我们利用PK15细胞作为细胞模型,探索了5-氮杂胞苷对PCV2感染的影响。我们的目标是获得可能为PCV2提供新治疗策略的见解。我们的结果表明,5-氮杂胞苷显著增强了PCV2在PK15细胞中的感染性。转录组分析显示,PCV2感染激活了各种免疫相关信号通路。5-氮杂胞苷可能激活丝裂原活化蛋白激酶(MAPK)信号通路,加剧PCV2感染并上调炎症和凋亡因子的表达。