ArticlePloS one2014
HCV 3a core protein increases lipid droplet cholesteryl ester content via a mechanism dependent on sphingolipid biosynthesis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Hepatitis C virus NS3/4A protease cleaves SPG20, a key regulator of lipid droplet turnover, to promote lipid droplet formation.Journal of virology · 2025Article
- Ceramide homeostasis in hepatic lipid droplets.Biochemical Society transactions · 2025Review
- Infection with the hepatitis C virus causes viral genotype-specific differences in cholesterol metabolism and hepatic steatosis.Scientific reports · 2022Article
- What role for cellular metabolism in the control of hepatitis viruses?Frontiers in immunology · 2022Review
- Insights Into the Biogenesis and Emerging Functions of Lipid Droplets From Unbiased Molecular Profiling Approaches.Frontiers in cell and developmental biology · 2022Review
- Viral Hepatitis and Hepatocellular Carcinoma: State of the Art.Pathogens (Basel, Switzerland) · 2021Review
- Sterol O-acyltransferase 2 chaperoned by apolipoprotein J facilitates hepatic lipid accumulation following viral and nutrient stresses.Communications biology · 2021Article
- Profiling of MicroRNA Targets Using Activity-Based Protein Profiling: Linking Enzyme Activity to MicroRNA-185 Function.Cell chemical biology · 2021Article
- Seipin negatively regulates sphingolipid production at the ER-LD contact site.The Journal of cell biology · 2019Article
- Runx1 Role in Epithelial and Cancer Cell Proliferation Implicates Lipid Metabolism and Scd1 and Soat1 Activity.Stem cells (Dayton, Ohio) · 2018Article
- Comparative Transcriptomic Response of Primary and Immortalized Macrophages to Murine Norovirus Infection.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Hepatitis C Virus-Genotype 3: Update on Current and Emergent Therapeutic Interventions.Current infectious disease reports · 2017Review
- Hepatitis C virus and cardiovascular: A review.Journal of advanced research · 2017Review
- Entangled in a membranous web: ER and lipid droplet reorganization during hepatitis C virus infection.Current opinion in cell biology · 2016Review
- Hepatitis C virus infection: Are there still specific problems with genotype 3?World journal of gastroenterology · 2015Review
- The SwissLipids knowledgebase for lipid biology.Bioinformatics (Oxford, England) · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) infected patients often develop steatosis and the HCV core protein alone can induce this phenomenon. To gain new insights into the pathways leading to steatosis, we performed lipidomic profiling of HCV core protein expressing-Huh-7 cells and also assessed the lipid profile of purified lipid droplets isolated from HCV 3a core expressing cells. Cholesteryl esters, ceramides and glycosylceramides, but not triglycerides, increased specifically in cells expressing the steatogenic HCV 3a core protein. Accordingly, inhibitors of cholesteryl ester biosynthesis such as statins and acyl-CoA cholesterol acyl transferase inhibitors prevented the increase of cholesteryl ester production and the formation of large lipid droplets in HCV core 3a-expressing cells. Furthermore, inhibition of de novo sphingolipid biosynthesis by myriocin - but not of glycosphingolipid biosynthesis by miglustat - affected both lipid droplet size and cholesteryl ester level. The lipid profile of purified lipid droplets, isolated from HCV 3a core-expressing cells, confirmed the particular increase of cholesteryl ester. Thus, both sphingolipid and cholesteryl ester biosynthesis are affected by the steatogenic core protein of HCV genotype 3a. These results may explain the peculiar lipid profile of HCV-infected patients with steatosis.
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