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Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle
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Glycometabolism regulates hepatitis C virus release.
Tao Yu1,2, Qiankun Yang1,2, Fangling Tian1,2,3
1Unit of Viral Hepatitis, Institut Pasteur of Shanghai, CAS Key Laboratory of Molecular Virology and Immunology, Chinese Academy of Sciences, Shanghai, China.
Plos Pathogens
|July 23, 2021
Summary
Hepatitis C virus (HCV) release is blocked by altering cell metabolism from glycolysis to oxidative phosphorylation. This metabolic shift traps infectious HCV particles inside cells, suggesting new therapeutic targets.
Area of Science:
- Hepatology
- Virology
- Cell Metabolism
Background:
- Hepatoma-derived cell lines are used for Hepatitis C virus (HCV) propagation.
- Cells utilize aerobic glycolysis in glucose but switch to oxidative phosphorylation in galactose.
Purpose of the Study:
- To investigate how modulating glycolysis in hepatocytes affects HCV infection.
- To understand the mechanisms regulating HCV release and transmission.
Main Methods:
- Culturing hepatoma cells in glucose versus galactose media.
- Assessing HCV entry, replication, assembly, and release.
- Investigating the role of multivesicular bodies (MVBs), MAPK-p38 phosphorylation, and cell-to-cell transmission.
Main Results:
- HCV release, but not entry, replication, or assembly, was blocked in galactose medium, causing virion accumulation in MVBs.
- Blocking MVB-lysosome fusion or adding pro-inflammatory cytokines restored HCV release in galactose.
- MAPK-p38 phosphorylation mediated this glycometabolic regulation of HCV release.
- HCV cell-to-cell transmission remained unaffected by glycometabolism.
Conclusions:
- Glycometabolism significantly regulates the efficiency and route of HCV release from hepatocytes.
- HCV may exploit host cell metabolic states to promote cell-to-cell spread, potentially evading immune responses.
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