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 hepato-cellular carcinoma.Mechanistically,HBV reprograms core metabolic pathways,including glycolysis,tricarboxylic acid(TCA)cycle,oxidative phosphorylation,and lipid homeostasis,to fuel its replica-tion machinery and evade immune surveillance.This review systematically synthesizes current evi-dence on HBV-induced glucose/lipid metabolic rewiring,with particular emphasis on how viral-host crosstalk at the metabolic interface sustains viral pathogenesis.
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