摘要
Hepatitis B virus(HBV)establishes chronic infection through strategic manipulation of host metabolic networks,driving a spectrum of hepatic pathologies ranging from hepatitis to cirrhosis and hepatocellular carcinoma.Mechanistically,HBV reprograms core metabolic pathways,including glycolysis,tricarboxylic acid(TCA)cycle,oxidative phosphorylation,and lipid homeostasis,to fuel its replication machinery and evade immune surveillance.This review systematically synthesizes current evidence on HBV-induced glucose/lipid metabolic rewiring,with particular emphasis on how viral-host crosstalk at the metabolic interface sustains viral pathogenesis.
基金
supported by the National Natural Science Foundation of China(82202497)
the National Key R&D Program of China(2023YFC2306800)
the Fundamental Research Funds for the Central Universities(226-2024-00129).
