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Updated: Jan 16, 2026
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Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
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HBV and host metabolic crosstalk: Reprogramming pathways for viral replication and pathogenesis.
YanYing Yan1, Zhiqiang Wei1, Min Zheng1
1State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310000, China.
Virologica Sinica
|September 29, 2025
Summary
Hepatitis B virus (HBV) infection reprograms host metabolism, altering glucose and lipid pathways to support viral replication and disease progression. Understanding this metabolic rewiring is key to developing new therapies for chronic HBV.
Area of Science:
- Hepatology
- Virology
- Metabolic pathways
Background:
- Chronic Hepatitis B virus (HBV) infection leads to significant liver damage, including cirrhosis and hepatocellular carcinoma.
- HBV infection involves complex interactions with host cellular machinery.
Purpose of the Study:
- To systematically review the current evidence on how HBV alters host glucose and lipid metabolism.
- To elucidate the mechanisms by which viral-host metabolic crosstalk contributes to HBV pathogenesis.
Main Methods:
- Systematic literature review of studies investigating HBV and host metabolic pathways.
- Analysis of viral-induced reprogramming of glycolysis, TCA cycle, oxidative phosphorylation, and lipid homeostasis.
Main Results:
- HBV strategically manipulates host metabolic networks to fuel viral replication.
- Viral reprogramming affects key pathways including glucose metabolism and lipid homeostasis.
- Metabolic alterations are crucial for immune evasion and sustained viral pathogenesis.
Conclusions:
- HBV infection induces profound metabolic changes in hepatocytes.
- Targeting these metabolic alterations presents a potential therapeutic strategy for chronic HBV infection.
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