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Related Experiment Video

Updated: Oct 19, 2025

Lipidomics and Transcriptomics in Neurological Diseases

Lipidomics and Transcriptomics in Neurological Diseases

Published on: March 18, 2022

Integrated Metabolomics and Transcriptomics Analyses Reveal Metabolic Landscape in Neuronal Cells during JEV

Mengyuan Li¹, Jiali Yang², Chuantao Ye¹

¹Department of Infectious Diseases, Tangdu Hospital, Air Force Medical University, Xi'an, 710038, China.

Virologica Sinica

|September 24, 2021

Summary

Japanese encephalitis virus (JEV) infection alters neuron metabolism, boosting glycolysis and lipid breakdown to fuel viral replication. Targeting these metabolic pathways offers new strategies against JEV encephalitis.

Keywords:

Japanese encephalitis virus (JEV)Metabolic reprogramming Metabolomics Transcriptomics

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Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line

Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line

Published on: August 9, 2014

Area of Science:

Neuroscience
Virology
Metabolomics

Background:

Japanese encephalitis virus (JEV) causes significant viral encephalitis in Asia.
Understanding JEV's interaction with host cell metabolism is crucial for elucidating pathogenesis and identifying antiviral targets.

Purpose of the Study:

To investigate the metabolic reprogramming of neurons during the early stages of JEV infection.
To identify key metabolic pathways supporting JEV replication and encephalitis progression.

Main Methods:

Integrated analysis of metabolomics and transcriptomics data from JEV-infected neurons.
Pharmacological inhibition of key metabolic pathways (glycolysis, pentose phosphate pathway).

Main Results:

JEV infection increased glycolysis and pentose phosphate pathway (PPP) flux while impairing oxidative phosphorylation (OXPHOS).
Lipid metabolism showed catabolic patterns facilitating precursor biosynthesis for viral replication.
Inhibiting glycolysis and PPP reduced JEV propagation.
Upregulation of pro-inflammatory lipid metabolites was observed, potentially contributing to encephalitis.

Conclusions:

JEV infection induces specific metabolic reprogramming in neurons, characterized by altered glucose and lipid metabolism.
Metabolic pathways, particularly glycolysis and PPP, are essential for JEV replication.
Targeting host cell metabolism presents a promising antiviral strategy against JEV.