Li Shuo, Mo Jiacong, Fang Yinxiang, Chen Xijiao, Chen Ming, Wang Shishi, Li Huizi, Ning Zhangyong
College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
Int J Biol Macromol. 2024 Nov;281(Pt 1):136197. doi: 10.1016/j.ijbiomac.2024.136197. Epub 2024 Oct 2.
Senecavirus A (SVA) induced porcine idiopathic vesicular disease (PIVD) has been spread worldwide due to persistent infection, causing economic losses in swine industry. Host factors play an important role in replication of SVA, while, the interaction of migration inhibitory factor (MIF) and the virus has not been verified. Here, MIF facilitates the replication of SVA by enhancing the glycolysis via hypoxia-inducible factor alpha (HIF-1α) was reported. SVA infection up-regulates the expression of MIF in 3D4/21 cells, and infection experiment of cells with overexpression and interference expression of MIF showed that MIF facilitates the replication of SVA. MIF promoted the glycolysis in SVA infection to facilitate its replication by enhancing the accumulation of lactate and decreasing the production of adenosine triphosphate (ATP) and inhibiting the expression of retinoic acid-inducible gene I (RIG-I), mitochondrial antiviral-signaling protein (MAVS), interferon regulatory factor 3 (IRF3), interferon-beta (IFN-β), IFN-α, interferon-stimulating gene 15 (ISG15), and ISG56. Meanwhile, specific inhibitor verified MIF facilitates the replication of SVA by enhancing glycolysis. Further results showed MIF induces the increased expression of HIF-1α, which enhances MIF-induced glycolysis. These results provide new data on host factors in replication of SVA, as well as better understanding the role of MIF in virus infection.
A组赛内卡病毒（SVA）引发的猪特发性水疱病（PIVD）因持续感染已在全球范围内传播，给养猪业造成经济损失。宿主因子在SVA复制中起重要作用，然而，迁移抑制因子（MIF）与该病毒的相互作用尚未得到证实。在此，有报道称MIF通过缺氧诱导因子α（HIF-1α）增强糖酵解来促进SVA的复制。SVA感染上调3D4/21细胞中MIF的表达，对MIF进行过表达和干扰表达的细胞感染实验表明MIF促进SVA的复制。MIF通过增强乳酸积累、减少三磷酸腺苷（ATP）生成以及抑制视黄酸诱导基因I（RIG-I）、线粒体抗病毒信号蛋白（MAVS）、干扰素调节因子3（IRF3）、干扰素-β（IFN-β）、IFN-α、干扰素刺激基因15（ISG15）和ISG56的表达，促进SVA感染中的糖酵解以利于其复制。同时，特异性抑制剂证实MIF通过增强糖酵解促进SVA的复制。进一步结果表明MIF诱导HIF-1α表达增加，从而增强MIF诱导的糖酵解。这些结果为SVA复制中的宿主因子提供了新数据，也有助于更好地理解MIF在病毒感染中的作用。
