Related Experiment Video

Updated: Aug 15, 2025

Use of Viral Entry Assays and Molecular Docking Analysis for the Identification of Antiviral Candidates against Coxsackievirus A16
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Use of Viral Entry Assays and Molecular Docking Analysis for the Identification of Antiviral Candidates against Coxsackievirus A16

Published on: July 15, 2019

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Metabolic reprogramming as a novel therapeutic target for Coxsackievirus B3

Myeong Uk Kuk1, Yun Ji Ga1, Ye Jin Kim1

  • 1Division of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon, Korea.

Animal Cells and Systems
|January 6, 2023
PubMed

Insights

Coxsackievirus B3 infection alters host cell metabolism by increasing glycolysis. Inhibiting this metabolic pathway with glycolysis inhibitors effectively reduces viral load, offering a potential new treatment strategy for Coxsackievirus B3.

Area of Science:

  • Virology
  • Metabolic pathways
  • Host-pathogen interactions

Background:

  • Coxsackievirus B3 (CVB3) is an enterovirus causing severe human diseases like myocarditis and pancreatitis.
  • Current therapeutic options for CVB3 infections are limited.
  • Understanding CVB3's interaction with host cell metabolism is crucial for developing treatments.

Purpose of the Study:

  • To investigate the metabolic alterations induced by CVB3 infection in host cells.
  • To explore the potential of targeting host cell metabolism as an antiviral strategy against CVB3.

Main Methods:

  • Measuring extracellular acidification rate (ECAR) to assess glycolysis levels.
  • Utilizing gas chromatography-mass spectrometry (GC-MS) for metabolite analysis.
  • Evaluating the efficacy of glycolysis inhibitors (2-Deoxy-D-glucose, sodium oxide) in reducing CVB3 titers.

Main Results:

  • CVB3 infection significantly increases host cell glycolysis, indicated by elevated ECAR.
  • Metabolomic analysis confirmed CVB3-induced metabolic reprogramming.
  • Treatment with glycolysis inhibitors markedly reduced CVB3 viral titers post-infection.

Conclusions:

  • CVB3 manipulates host cell metabolism, specifically enhancing glycolysis, to facilitate its replication.
  • Inhibiting glycolysis presents a promising therapeutic strategy against CVB3 infections.
  • Targeting host metabolic pathways offers a novel approach for controlling enterovirus replication.

Keywords:
Coxsackievirus B3antiviral effectglycolysis inhibitorsmetabolic alteration

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