SCD1 inhibits HBV replication by regulating autophagy under high lipid conditions.

IF 1.9 4区 医学 Q3 GENETICS & HEREDITY Virus Genes Pub Date : 2023-12-01 Epub Date: 2023-08-29 DOI:10.1007/s11262-023-02028-5
Xuan Du, Xiaoyi Shi, Mei Han, Xiaoyun Gao, Chuang Wang, Chunmeng Jiang, Chunwen Pu
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Abstract

Chronic hepatitis B virus (HBV) infection remains a significant public health concern worldwide. Several metabolic processes regulate HBV DNA replication, including autophagy and lipid metabolism. In this study, we clarified the effect of lipids on HBV replication and elucidated possible mechanisms. We discovered that lipid metabolic gene expression levels were negatively correlated with the HBV DNA in plasma. Our data showed that fatty acid stimulation significantly reduced HBV DNA, hepatitis B surface antigen (HBsAg), and hepatitis B e antigen (HBeAg) levels in HepG2.2.15 cells, which are human hepatoma cell cultures transfected with HBV DNA. The Stearoyl coenzyme A desaturase 1 (SCD1)-autophagy pathway has also been implicated in inhibiting HBV replication by fatty acids stimulation. SCD1 knockdown deregulates the inhibitory effect of fatty acids on HBV by enhancing autophagy. When 3 methyladenine (3MA) was added, the inhibitory effects of specific autophagy inhibitors eliminated the positive effects of SCD1 knockdown on HBV replication. Our results indicate that SCD1 participates in the regulation of inhibition of HBV replication by fatty acids stimulation through regulating autophagy.

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在高脂条件下,SCD1通过调节自噬抑制HBV复制。
慢性乙型肝炎病毒(HBV)感染仍然是世界范围内一个重大的公共卫生问题。几种代谢过程调节HBV DNA复制,包括自噬和脂质代谢。在本研究中,我们阐明了脂质对HBV复制的影响,并阐明了可能的机制。我们发现脂质代谢基因表达水平与血浆中HBV DNA呈负相关。我们的数据显示,脂肪酸刺激显著降低HepG2.2.15细胞的HBV DNA、乙型肝炎表面抗原(HBsAg)和乙型肝炎e抗原(HBeAg)水平,HepG2.2.15是转染HBV DNA的人肝癌细胞培养物。硬脂酰辅酶A去饱和酶1 (SCD1)-自噬途径也与脂肪酸刺激抑制HBV复制有关。SCD1敲低可以通过增强自噬来解除脂肪酸对HBV的抑制作用。当加入3甲基腺嘌呤(3MA)时,特异性自噬抑制剂的抑制作用消除了SCD1敲低对HBV复制的积极作用。我们的研究结果表明,SCD1通过调节自噬参与脂肪酸刺激抑制HBV复制的调控。
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来源期刊
Virus Genes
Virus Genes 医学-病毒学
CiteScore
3.30
自引率
0.00%
发文量
76
审稿时长
3 months
期刊介绍: Viruses are convenient models for the elucidation of life processes. The study of viruses is again on the cutting edge of biological sciences: systems biology, genomics, proteomics, metagenomics, using the newest most powerful tools. Huge amounts of new details on virus interactions with the cell, other pathogens and the hosts – animal (including human), insect, fungal, plant, bacterial, and archaeal - and their role in infection and disease are forthcoming in perplexing details requiring analysis and comments. Virus Genes is dedicated to the publication of studies on the structure and function of viruses and their genes, the molecular and systems interactions with the host and all applications derived thereof, providing a forum for the analysis of data and discussion of its implications, and the development of new hypotheses.
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