ArticleHepatology international2016
Elevated hepatic lipid and interferon stimulated gene expression in HCV GT3 patients relative to non-alcoholic steatohepatitis.
Article in Hepatology international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 35 citations in OpenAlex.
- The Dual Role of IP-10/CXCL10 in Liver Injury: From Pathogenic Mediator to Clinical Biomarker and Therapeutic Target.Drug design, development and therapy · 2026Review
- Sex differences in murine MASH induced by a fructose-palmitate-cholesterol-enriched diet.JHEP reports : innovation in hepatology · 2025Article
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- Common molecular basis for MASH and hepatitis C revealed via systems biology approach.Frontiers in oncology · 2024Article
- Shared biomarkers and immune cell infiltration signatures in ulcerative colitis and nonalcoholic steatohepatitis.Scientific reports · 2023Article
- The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms.Biomolecules · 2023Review
- Differences of core genes in liver fibrosis and hepatocellular carcinoma: Evidence from integrated bioinformatics and immunohistochemical analysis.World journal of gastrointestinal oncology · 2022Article
- Identification of key biomarkers and immune infiltration in systemic lupus erythematosus by integrated bioinformatics analysis.Journal of translational medicine · 2021Article
- Article
- Signature molecules expressed differentially in a liver disease stage-specific manner by HIV-1 and HCV co-infection.PloS one · 2018Article
- HCV-induced regulatory alterations of IL-1β, IL-6, TNF-α, and IFN-ϒ operative, leading liver en-route to non-alcoholic steatohepatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Review
- Review
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimsHCV GT-3 has a more pronounced effect on hepatic steatosis and host lipids than other HCV genotypes and is proving less responsive to all oral interferon-free treatment with direct acting antiviral agents. As both HCV GT3 infection and NASH can result in steatosis and cirrhosis, we asked whether hepatic transcriptional profiles reflective of the host response to inflammation differed based on the etiology of injury.
methodsHepatic gene expression was determined for 48 pre-selected genes known to be associated with hepatic interferon signaling and lipid metabolic pathways in treatment-naïve HCV GT-3 (n = 9) and NASH (n = 14) patients.
resultsGenes with significantly higher expression in HCV included chemokines CXCL10, CXCL11 interferon IFNA2, interferon receptors IFNAR1, IL10RB negative regulators of interferon signaling SOCS3, USP18, JAK/STAT and IRF family members STAT1, STAT2, and IRF, and TGFB family members TGFB1, TGFBR1, and TGFBR2 and other ISGs like OAS2, IF127, IF144 and ISG15. HCV infection was also associated with higher expression of genes associated with lipid metabolism APOE, APOL3, SREBF1 and HMBS. Furthermore, our results suggest that, in HCV GT3-infected patients, IL28B (CC) genotype is associated with lower baseline ISG expression such as IRF9, ISG15, MX1, STAT1, CXCL10, CXCL11, and IFI27 compared to CT/TT genotype.
conclusionsHCV GT-3 and NASH both induce hepatic steatosis and inflammation, while HCV GT-3 infection is uniquely associated with elevated transcription of hepatic ISGs and genes associated with lipid metabolism. These changes likely reflect the unique host response to HCV replication distinct from the inflammatory response induced by NASH.
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