ArticleGut2007
The genotype 3-specific hepatitis C virus core protein residue phenylalanine 164 increases steatosis in an in vitro cellular model.
Article in Gut, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 106 citations in OpenAlex.
- Chronic viral hepatitis with concurrent metabolic dysfunction-associated steatotic liver disease: dual etiology challenges.Clinical and molecular hepatology · 2026Review
- Metabolic Dysfunction-Associated Steatotic Liver Disease in Chronic Hepatitis C Virus Infection: From Basics to Clinical and Nutritional Management.Clinics and practice · 2024Review
- The effect of different direct antivirals on hepatic steatosis in nondiabetic and naïve hepatitis C-infected Egyptian patients.The Egyptian journal of internal medicine · 2023Article
- Lipid Droplet-Associated Proteins Perilipin 1 and 2: Molecular Markers of Steatosis and Microvesicular Steatotic Foci in Chronic Hepatitis C.International journal of molecular sciences · 2022Article
- The Impact of Steatosis on Chronic Hepatitis C Progression and Response to Antiviral Treatments.Biomedicines · 2021Review
- Article
- Lipid Droplets in Health and Disease.Lipids in health and disease · 2017Review
- Increased hepatic expression of miRNA-122 in patients infected with HCV genotype 3.Medical microbiology and immunology · 2016Article
- Genotype-specific differences in structural features of hepatitis C virus (HCV) p7 membrane protein.Biochimica et biophysica acta · 2015Article
- Insulin resistance and its consequences in chronic hepatitis C.Clinical and experimental hepatology · 2015Review
- Adiponectin serum level in chronic hepatitis C infection and therapeutic profile.World journal of hepatology · 2015Review
- The Replacement of 10 Non-Conserved Residues in the Core Protein of JFH-1 Hepatitis C Virus Improves Its Assembly and Secretion.PloS one · 2015Article
- Elevated miR-33a and miR-224 in steatotic chronic hepatitis C liver biopsies.World journal of gastroenterology · 2014Article
- Insulin resistance and liver steatosis in chronic hepatitis C infection genotype 3.World journal of gastroenterology · 2014Review
- Origin of hepatitis C virus genotype 3 in Africa as estimated through an evolutionary analysis of the full-length genomes of nine subtypes, including the newly sequenced 3d and 3e.The Journal of general virology · 2014Article
- Production and pathogenicity of hepatitis C virus core gene products.World journal of gastroenterology · 2014Review
- Pathogenesis and significance of hepatitis C virus steatosis: an update on survival strategy of a successful pathogen.World journal of gastroenterology · 2014Review
- Autophagy in hepatitis C virus-host interactions: potential roles and therapeutic targets for liver-associated diseases.World journal of gastroenterology · 2014Review
- Hepcidin and the iron enigma in HCV infection.Virulence · 2014Review
- Full-length sequences of 11 hepatitis C virus genotype 2 isolates representing five subtypes and six unclassified lineages with unique geographical distributions and genetic variation patterns.The Journal of general virology · 2012Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsThe prevalence and severity of liver steatosis are higher in patients infected with genotype 3 hepatitis C virus (HCV) than in patients infected with other genotypes. HCV core protein is known to affect lipid metabolism, inducing lipid droplet accumulation both in vitro and in vivo. An in vitro cellular model was used to investigate whether an HCV core protein with residues specific to genotype 3 increased this phenomenon.
methodsSequence comparisons for HCV core protein domain II, which is known to interact with lipid droplets, identified the phenylalanine (F) residue at position 164 as the only residue specific to genotype 3. The area covered by lipid droplets in sections of cells producing a wild-type genotype 1a HCV core protein was compared with that in cells producing a Y164F mutant protein.
resultsCumulative lipid droplet area was significantly greater in sections of cells producing the Y164F mutant HCV core protein than in cells producing the wild-type protein (p<0.001). The frequency of cell sections containing more than 3 mum(2) of lipid droplets, in particular, was higher for the mutant than for the wild-type protein.
conclusionThe data provide a molecular explanation for HCV genotype 3-specific lipid accumulation. This difference between genotypes may be due to phenylalanine having a higher affinity for lipids than tyrosine (Y). These observations provide useful information for further studies of the mechanisms involved in HCV-induced steatosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.