ArticleLipids in health and disease2017
Hepatitis B virus inhibits the in vivo and in vitro synthesis and secretion of apolipoprotein C3.
Article in Lipids in health and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Genetic insights into the interaction between chronic hepatitis B virus infection and metabolic syndrome.Virulence · 2025Article
- APOC3 as a potential prognostic factor for hepatitis B virus-related acute-on-chronic liver failure.Medicine · 2025Article
- Small hepatitis B virus surface antigen (SHBs) induces dyslipidemia by suppressing apolipoprotein-AII expression through ER stress-mediated modulation of HNF4α and C/EBPγ.Journal of virology · 2024Article
- What role for cellular metabolism in the control of hepatitis viruses?Frontiers in immunology · 2022Review
- Review
- Multifaceted Interaction Between Hepatitis B Virus Infection and Lipid Metabolism in Hepatocytes: A Potential Target of Antiviral Therapy for Chronic Hepatitis B.Frontiers in microbiology · 2021Review
- Serum apolipoprotein C3 levels are negatively associated with hepatitis B virus DNA in HBeAg-negative chronic hepatitis B patients.Lipids in health and disease · 2019Article
- Insulin resistance exhibits varied metabolic abnormalities in nonalcoholic fatty liver disease, chronic hepatitis B and the combination of the two: a cross-sectional study.Diabetology & metabolic syndrome · 2019Article
- The evaluation of serum lipid profile in chronic Hepatitis B patients at a Tertiary Care Centre in Western India: A cross-sectional study.Annals of African medicineObservational
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundHepatitis B virus (HBV) infection in the body can damage liver cells and cause disorders in blood lipid metabolism. Apolipoprotein C3 (ApoC3) plays an important role in the regulation of lipid metabolism, but no study on the HBV regulation of ApoC3 has been reported. This purpose of this study was to investigate the effect of HBV on ApoC3 expression and its regulatory mechanism.
methodsThe expression levels of ApoC3 mRNA and protein in the human hepatoma cell lines HepG2 and HepG2.2.15 were determined using real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot. The HepG2 cells were co-transfected with the ApoC3 gene promoter and either HBV-infected clone pHBV1.3 or its individual genes. The changes in luciferase activity were assayed. The expression levels of ApoC3 mRNA and protein were determined using RT-qPCR and Western blot. The content of ApoC3 in the supernatant of the cultured cells was determined using an enzyme-linked immunosorbent assay (ELISA). The sera were collected from 149 patients with HBV infection and 102 healthy subjects at physical examination as the normal controls. The serological levels of ApoC3 in the HBV group and the normal control group were determined using ELISA. The contents of serum triglyceride (TG) and very-low-density lipoprotein (VLDL) in the HBV patients and the normal control were determined using an automatic biochemical analyser.
resultsThe expression levels of ApoC3 mRNA and protein were lower in the HepG2.2.15 cells than in the HepG2 cells. pHBV1.3 and its X gene could inhibit the activity of the ApoC3 promoter and its mRNA and protein expression. The serum levels of ApoC3, VLDL and TG were 65.39 ± 7.48 μg/ml, 1.24 ± 0.49 mmol/L, and 0.46 ± 0.10 mmol/L in the HBV patients and 41.02 ± 6.88 μg/ml, 0.76 ± 0.21 mmol/L, 0.29 ± 0.05 mmol/L in the normal controls, respectively, statistical analysis revealed significantly lower serum levels of ApoC3, VLDL and TG in HBV patients than in the normal controls (P < 0.05).
conclusionHBV can inhibit the in vivo and in vitro synthesis and secretion of ApoC3.
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