ArticleClinical and molecular hepatology2025
Distinct inflammatory imprint in non-cirrhotic and cirrhotic patients before and after direct-acting antiviral therapy.
Article in Clinical and molecular hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Hepatitis C elimination: is it time to redefine the goals?Nature reviews. Gastroenterology & hepatology · 2026Article
- Clinical implications of residual changes following HCV clearance: Editorial on "Distinct inflammatory imprint in non-cirrhotic and cirrhotic patients before and after direct-acting antiviral therapy".Clinical and molecular hepatology · 2026Article
- IFNL4-rs12979860 CC genotype predisposes to accelerated terminal exhaustion and senescence in HIV/HCV-chronic infection.Journal of translational medicine · 2025Article
- HBV Dominance Is Associated With a Distinct Inflammatory Milieu in HBV/HCV Coinfection.Journal of viral hepatitis · 2025Article
- Gut microbiota-immunity cascade in hepatocellular carcinoma: mechanisms and therapeutic opportunities.Oncology reviews · 2025Review
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15 authors.
Funding
Abstract
BACKGROUND/
aimsHepatitis C virus (HCV) infection remains a global health challenge, leading to chronic liver disease, cirrhosis, and hepatocellular carcinoma (HCC). Despite the high efficacy of direct-acting antiviral therapy in achieving sustained virologic response (SVR), concerns persist regarding long-term immune alterations and residual risks, particularly in cirrhotic patients.
methodsThis study investigates 75 soluble immune mediator (SIM) profiles in 102 chronic HCV patients, stratified by cirrhosis status, at therapy initiation, end of treatment, and long-term follow-up (median 96 weeks). Findings were compared with 51 matched healthy controls and validated in an independent cohort of 47 cirrhotic patients, 17 of whom developed HCC.
resultsWe observed significant SIM alterations at baseline, with cirrhotic patients displaying a more profoundly dysregulated inflammatory milieu. Despite an overall decline in inflammatory markers following SVR, persistent alterations were evident, particularly in cirrhotic patients. Notably, those with liver stiffness exceeding 14 kPa exhibited sustained inflammatory dysregulation, correlating with liver elastography values. Key SIM such as interleukin (IL)-6, IL-8, urokinase plasminogen activator, and hepatocellular growth factor remained elevated and were associated with HCC development. Network analysis highlighted their roles in liver fibrosis, regeneration, and carcinogenesis.
conclusionThese findings underscore the importance of early antiviral intervention to prevent cirrhosis-related sequelae. Future studies should explore the mechanistic pathways linking chronic inflammation, fibrosis, and oncogenesis to identify predictive biomarkers and novel therapeutic targets. Addressing persistent immune alterations post-HCV clearance may improve long-term outcomes, particularly in patients with advanced liver disease.
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