Journal
METABOLITES
Volume 10, Issue 8, Pages -Publisher
MDPI
DOI: 10.3390/metabo10080302
Keywords
Enterovirus; metabolic profiling; hNPCs; glucose homeostasis
Categories
Funding
- Respiratory Viral Research Foundation Limited
- Hui Hoy and Chow Sin Lan Charity Fund Limited
- Chan Yin Chuen Memorial Charitable Foundation
- Hong Kong Hainan Commercial Association South China Microbiology Research Fund
- Health and Medical Research Fund of the Food and Health Bureau [19180502, HKM-15-M04]
- Research Grants Council, Hong Kong Special Administrative Region Government [17126919]
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EnterovirusA71 (EV-A71) is a common cause of hand, foot, and mouth disease. Severe EV-A71 infections may be associated with life-threatening neurological complications. However, the pathogenic mechanisms underlying these severe clinical and pathological features remain incompletely understood. Metabolites are known to play critical roles in multiple stages of the replication cycles of viruses. The metabolic reprogramming induced by viral infections is essential for optimal virus replication and may be potential antiviral targets. In this study, we applied targeted metabolomics profiling to investigate the metabolic changes of induced pluripotent human stem cell (iPSC)-derived neural progenitor cells (NPCs) upon EV-A71 infection. A targeted quantitation of polar metabolites identified 14 candidates with altered expression profiles. A pathway enrichment analysis pinpointed glucose metabolic pathways as being highly perturbed upon EV-A71 infection. Gene silencing of one of the key enzymes of glycolysis, 6-phosphofructo-2-kinase (PFKFB3), significantly suppressed EV-A71 replication in vitro. Collectively, we demonstrated the feasibility to manipulate EV-A71-triggered host metabolic reprogramming as a potential anti-EV-A71 strategy.
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