Metabolic reprogramming as a novel therapeutic target for Coxsackievirus B3

被引:0
|
作者
Kuk, Myeong Uk [1 ]
Ga, Yun Ji [1 ]
Kim, Ye Jin [1 ]
Park, Ji Yun [1 ]
Song, Eun Seon [1 ]
Lee, Haneur [1 ]
Lee, Yun Haeng [1 ]
Ko, Gahyun [1 ]
Kim, Jae Kwang [1 ]
Yeh, Jung-Yong [1 ]
Kwon, Hyung Wook [1 ,2 ]
Byun, Youngjoo [3 ]
Park, Joon Tae [1 ,2 ]
机构
[1] Incheon Natl Univ, Coll Life Sci & Bioengn, Div Life Sci, Incheon 22012, South Korea
[2] Incheon Natl Univ, Convergence Res Ctr Insect Vectors, Incheon 22012, South Korea
[3] Korea Univ, Coll Pharm, Sejong 30019, South Korea
关键词
Coxsackievirus B3; metabolic alteration; glycolysis inhibitors; antiviral effect; CELLULAR METABOLOME; GLUCOSE-LEVELS; REPLICATION; 2-DEOXY-D-GLUCOSE; CELLS;
D O I
10.1080/19768354.2022.2141318
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:275 / 282
页数:8
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