ReviewJournal of medical virology2026
Hepatitis C Virus and Type 2 Diabetes: Mechanisms, Clinical Impact, and Post-DAA Management.
Review in Journal of medical virology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Hepatitis C virus inhibits the E2F2/PI3K/AKT signaling pathway through miR-378b and leads to glycolipid metabolism disorders in the liver.Molecular biology reports · 2026Article
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.
Funding
Abstract
Hepatitis C virus (HCV) infection remains a major global health burden despite advances in direct-acting antiviral (DAA) therapies. Beyond hepatic complications such as cirrhosis and hepatocellular carcinoma (HCC), HCV has been strongly linked to metabolic disorders, particularly type 2 diabetes mellitus (T2DM). Epidemiological evidence demonstrates a higher prevalence of diabetes among HCV-infected individuals, with variations across geographic regions and populations. Mechanistically, HCV induces insulin resistance (IR) through multiple pathways, including direct interference of viral proteins with insulin signaling, oxidative stress, cytokine imbalance, impaired lipid metabolism, and pancreatic β-cell dysfunction. T2DM further worsens HCV outcomes by accelerating fibrosis, increasing the risk of HCC, and elevating all-cause mortality. Importantly, clearance of HCV with DAAs improves IR, reduces diabetes incidence, and lowers cardiovascular risks. Integrated prevention and management strategies targeting both viral eradication and glycemic control are essential to optimize outcomes. This review aims to bridge mechanistic insights with clinical evidence, facilitating strategies that improve outcomes in HCV-associated metabolic disease.
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.