Zhang Jiaxuan, Ling Ning, Lei Yu, Peng Mingli, Hu Peng, Chen Min
Key Laboratory of Molecular Biology for Infectious Diseases, Ministry of Education, Department of Infectious Diseases, Institute for Viral Hepatitis, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Front Microbiol. 2021 Mar 11;12:636897. doi: 10.3389/fmicb.2021.636897. eCollection 2021.
Hepatitis B virus (HBV) is considered a "metabolic virus" and affects many hepatic metabolic pathways. However, how HBV affects lipid metabolism in hepatocytes remains uncertain yet. Accumulating clinical studies suggested that compared to non-HBV-infected controls, chronic HBV infection was associated with lower levels of serum total cholesterol and triglycerides and a lower prevalence of hepatic steatosis. In patients with chronic HBV infection, high ALT level, high body mass index, male gender, or old age was found to be positively correlated with hepatic steatosis. Furthermore, mechanisms of how HBV infection affected hepatic lipid metabolism had also been explored in a number of studies based on cell lines and mouse models. These results demonstrated that HBV replication or expression induced extensive and diverse changes in hepatic lipid metabolism, by not only activating expression of some critical lipogenesis and cholesterolgenesis-related proteins but also upregulating fatty acid oxidation and bile acid synthesis. Moreover, increasing studies found some potential targets to inhibit HBV replication or expression by decreasing or enhancing certain lipid metabolism-related proteins or metabolites. Therefore, in this article, we comprehensively reviewed these publications and revealed the connections between clinical observations and experimental findings to better understand the interaction between hepatic lipid metabolism and HBV infection. However, the available data are far from conclusive, and there is still a long way to go before clarifying the complex interaction between HBV infection and hepatic lipid metabolism.
乙型肝炎病毒(HBV)被认为是一种“代谢病毒”,会影响许多肝脏代谢途径。然而,HBV如何影响肝细胞中的脂质代谢仍不确定。越来越多的临床研究表明,与未感染HBV的对照组相比,慢性HBV感染与血清总胆固醇和甘油三酯水平较低以及肝脂肪变性患病率较低有关。在慢性HBV感染患者中,高ALT水平、高体重指数、男性或老年被发现与肝脂肪变性呈正相关。此外,基于细胞系和小鼠模型的多项研究也探讨了HBV感染影响肝脏脂质代谢的机制。这些结果表明,HBV复制或表达会引起肝脏脂质代谢广泛而多样的变化,不仅会激活一些关键的脂肪生成和胆固醇生成相关蛋白的表达,还会上调脂肪酸氧化和胆汁酸合成。此外,越来越多的研究发现了一些潜在靶点,可通过降低或增强某些脂质代谢相关蛋白或代谢物来抑制HBV复制或表达。因此,在本文中,我们全面回顾了这些出版物,揭示了临床观察结果与实验结果之间的联系,以便更好地理解肝脏脂质代谢与HBV感染之间的相互作用。然而,现有数据远非结论性的,在阐明HBV感染与肝脏脂质代谢之间的复杂相互作用之前,仍有很长的路要走。