Unmet needs in the post-direct-acting antivirals era: The risk and molecular mechanisms of hepatocellular carcinoma after hepatitis C virus eradication

• Published in: Clinical and molecular hepatology Vol. 30; no. 3; pp. 326 - 344
• Main Authors: Huang, Chung-Feng, Awad, Manar Hijaze, Gal-Tanamy, Meital, Yu, Ming-Lung
• Format: Journal Article
• Language: English
• Published: Korea (South) The Korean Association for the Study of the Liver 01.07.2024; Korean Association for the Study of the Liver; 대한간학회
• Subjects: Antiviral Agents - therapeutic use; Carcinoma, Hepatocellular - etiology; epigenetic; genetic; hcc; hcv; Hepacivirus - genetics; Hepatitis C, Chronic - complications; Hepatitis C, Chronic - drug therapy; Humans; Liver Neoplasms - etiology; Liver Neoplasms - pathology; Review; Risk Factors; surveillance; Sustained Virologic Response; svr; 내과학; Genetic; HCC; HCV; Epigenetic; Surveillance; SVR
• ISSN: 2287-2728; 2287-285X; 2287-285X
• DOI: 10.3350/cmh.2024.0155

Hepatitis C virus (HCV) infection is one of the major etiologies of hepatocellular carcinoma (HCC) with approximately 30% of HCC being due to HCV infection worldwide. HCV eradication by antivirals greatly reduces the risk of HCC; nevertheless, HCC remains to occur in chronic hepatitis C (CHC) patients who have achieved a sustained virological response (SVR). The proportion of post-SVR HCC among newly diagnosed HCC patients is increasing in the direct-acting antiviral (DAA) era and might be due to preexisting inflammatory and fibrotic liver backgrounds, immune dysregulation between host and virus interactions, as well as host epigenetic scars, genetic predispositions and alternations. By means of applying surrogate markers and adopting risk stratification, HCC surveillance should be consistently performed in high-risk populations. In this review, we discuss the possible molecular mechanism, risk factors, and HCC surveillance strategy for HCC development after HCV eradication in CHC patients.