ReviewBiomedicines2023
Hepatitis C Virus-Lipid Interplay: Pathogenesis and Clinical Impact.
Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Risk factors for hepatocellular carcinoma: an umbrella review of systematic review and meta-analysis.Annals of medicine · 2025Pooled it
- Reduced Circulating Angiopoietin-Like Protein Levels in Crimean-Congo Hemorrhagic Fever.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026Article
- Lipid abnormalities in chronic viral hepatitis: associations and machine learning-enhanced prediction.BMC gastroenterology · 2026Article
- Hepatitis C Virus: An Overview of Its Chronic Impact on Liver Function, Metabolic Dysregulation, Inflammatory-Oxidative Pathogenesis and Epigenetic Memory.International journal of molecular sciences · 2026Review
- Association between LDL-R (exon 8 C.1171 G > A) polymorphisms and response to antiviral therapy in hepatitis C virus infection.Scientific reports · 2026Article
- Longitudinal Changes in Lipid Profile After Sustained Virological Response in Patients with Chronic Hepatitis C Treated with Direct-Acting Antivirals.Healthcare (Basel, Switzerland) · 2026Article
- Dynamic regulatory mechanism of cholesterol 25-hydroxylase-mediated antiviral response in RNA virus infections.Frontiers in cellular and infection microbiology · 2026Review
- MASLD and viral hepatitis overlap: An emerging dual burden in chronic liver disease.Hepatology forum · 2026Review
- Lipid dysregulation as a convergent pathway linking environmental exposures to stroke.Frontiers in aging neuroscience · 2026Review
- Genetic and transcriptional insights reveal hepatitis C virus as a driver of kidney cancer.Infectious agents and cancer · 2025Article
- The HCV-Dependent Inhibition of Nrf1/ARE-Mediated Gene Expression Favours Viral Morphogenesis.Viruses · 2025Article
- Article
- Changes in Hepatic Steatosis Before and After Direct-Acting Antiviral Treatment in People With HIV and Hepatitis C Coinfection.The Journal of infectious diseases · 2025Article
- Association of MASLD Phenotypes With Liver Fibrosis in Hepatitis C: The Role of Cardiometabolic Risk Factors.Journal of viral hepatitis · 2025Article
- Article
- Lipid and immune dysregulation and risk of metabolic disorders after HCV clearance in HIV/HCV-coinfected participants with cACLD: a retrospective study.Frontiers in immunology · 2025Article
- Elevated serum neprilysin levels in patients with chronic hepatitis C and metabolic dysfunction-associated steatotic liver disease: hepatic oxidative stress as an underlying mechanism.Molecular biology reports · 2024Article
- Article
- The triglyceride-synthesizing enzyme diacylglycerol acyltransferase 2 modulates the formation of the hepatitis C virus replication organelle.PLoS pathogens · 2024Article
- The Impact of Liver Steatosis on Interleukin and Growth Factors Kinetics during Chronic Hepatitis C Treatment.Journal of clinical medicine · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) infection represents the major cause of chronic liver disease, leading to a wide range of hepatic diseases, including cirrhosis and hepatocellular carcinoma. It is the leading indication for liver transplantation worldwide. In addition, there is a growing body of evidence concerning the role of HCV in extrahepatic manifestations, including immune-related disorders and metabolic abnormalities, such as insulin resistance and steatosis. HCV depends on its host cells to propagate successfully, and every aspect of the HCV life cycle is closely related to human lipid metabolism. The virus circulates as a lipid-rich particle, entering the hepatocyte via lipoprotein cell receptors. It has also been shown to upregulate lipid biosynthesis and impair lipid degradation, resulting in significant intracellular lipid accumulation (steatosis) and circulating hypocholesterolemia. Patients with chronic HCV are at increased risk for hepatic steatosis, dyslipidemia, and cardiovascular disease, including accelerated atherosclerosis. This review aims to describe different aspects of the HCV viral life cycle as it impacts host lipoproteins and lipid metabolism. It then discusses the mechanisms of HCV-related hepatic steatosis, hypocholesterolemia, and accelerated atherosclerosis.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.