柯萨奇病毒B3(CVB3)是属于肠道病毒属的单链RNA病毒。CVB3是与心肌炎等严重疾病相关的人类病原体,扩张型心肌病,和胰腺炎。然而,目前尚无治疗CVB3感染的干预措施.在这项研究中,我们发现CVB3通过增加糖酵解水平诱导宿主细胞的代谢改变,如胞外酸化速率(ECAR)的增加所示。CVB3介导的代谢改变通过使用气相色谱-质谱(GC-MS)的代谢物变化分析来确认。根据调查结果,已经提出了一种抑制糖酵解的策略来治疗CVB3感染。的确,糖酵解抑制剂(2-脱氧-D-葡萄糖,氧化钠)显着降低CVB3感染后的CVB3滴度,表明糖酵解抑制剂可以用作有效的抗病毒剂。一起来看,我们的研究结果揭示了一种通过调节宿主细胞代谢来控制CVB3感染的新机制。
Coxsackievirus B3 (CVB3) is a single-stranded RNA virus that belongs to the Enterovirus genus. CVB3 is a human pathogen associated with serious conditions such as myocarditis, dilated cardiomyopathy, and pancreatitis. However, there are no therapeutic interventions to treat CVB3 infections. In this study, we found that CVB3 induced metabolic alteration in host cells through increasing glycolysis level, as indicated by an increase in the extracellular acidification rate (ECAR). CVB3-mediated metabolic alteration was confirmed by metabolite change analysis using gas chromatography-mass spectrometry (GC-MS). Based on findings, a strategy to inhibit glycolysis has been proposed to treat CVB3 infection. Indeed, glycolysis inhibitors (2-Deoxy-D-glucose, sodium oxide) significantly reduced CVB3 titers after CVB3 infection, indicating that glycolysis inhibitors can be used as effective antiviral agents. Taken together, our results reveal a novel mechanism by which CVB3 infection is controlled by regulation of host cell metabolism.