Citation: YanYing Yan, Zhiqiang Wei, Min Zheng, Mengji Lu, Xueyu Wang. HBV and host metabolic crosstalk: Reprogramming pathways for viral replication and pathogenesis .VIROLOGICA SINICA, 2025, 40(5) : 685-693.  http://dx.doi.org/10.1016/j.virs.2025.09.008

HBV and host metabolic crosstalk: Reprogramming pathways for viral replication and pathogenesis

  • 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.

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    HBV and host metabolic crosstalk: Reprogramming pathways for viral replication and pathogenesis

      Corresponding author: Mengji Lu, mengji.lu@uni-due.de
      Corresponding author: Xueyu Wang, xueyuwang@zju.edu.cn
    • a. State 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;
    • b. Institute of Virology, University Hospital Essen, University of Duisburg-Essen, Essen 45122, Germany

    Abstract: 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.

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