Metabolic reprogramming as a novel therapeutic target for Coxsackievirus B3.
Myeong Uk KukYun Ji GaYe Jin KimJi Yun ParkEun Seon SongHaneur LeeYun Haeng LeeGahyun KoJae Kwang KimJung-Yong YehHyung-Wook KwonYoungjoo ByunJoon Tae ParkPublished in: Animal cells and systems (2022)
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.
Keyphrases
- gas chromatography mass spectrometry
- endothelial cells
- single cell
- stem cells
- physical activity
- high glucose
- blood pressure
- oxidative stress
- metabolic syndrome
- adipose tissue
- cell death
- high resolution
- dna methylation
- cell cycle arrest
- weight loss
- skeletal muscle
- insulin resistance
- binding protein
- solid phase extraction