Unmet needs in the post-DAA era: the risk and molecular mechanisms of hepatocellular carcinoma after HCV eradication

Huang, Chung-Feng; Awad, Manar Hijaze; Gal-Tanamy, Meital; Yu, Ming-Lung

doi:.0..

Review

Unmet needs in the post-DAA era: the risk and molecular mechanisms of hepatocellular carcinoma after HCV eradication

Chung-Feng Huang^1,2,3, Manar Hijaze Awad⁴, Meital Gal-Tanamy⁴, Ming-Lung Yu^1,2,5

¹Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital; College of Medicine and Center for Liquid Biopsy and Cohort Research, Kaohsiung Medical University, Kaohsiung, Taiwan
²Faculty of Internal Medicine and Hepatitis Research Center, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
³Ph.D. Program in Translational Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, and Academia Sinica, Taiwan
⁴Molecular Virology Lab, The Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel
⁵School of Medicine and Doctoral Program of Clinical and Experimental Medicine, College of Medicine and Center of Excellence for Metabolic Associated Fatty Liver Disease, National Sun Yat-sen University, Kaohsiung, Taiwan

Correspondence :

Meital Gal-Tanamy ,
Email: Meital.Tanamy@biu.ac.il
Ming-Lung Yu ,
Email: fish6069@gmail.com

Received: March 1, 2024 Revised: April 26, 2024 Accepted: April 26, 2024
*Chung-Feng Huang and Manar Hijaze Awad contributed equally to this work.

ABSTRACT

Hepatitis C virus (HCV) is one of the major etiologies of hepatocellular carcinoma 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 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 DAA era and might be due to preexisting inflammatory and fibrotic liver background, immune dysregulation between host and virus interaction, as well as host epigenetic scar, 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 surveillance strategy for HCC development after HCV eradication.

KeyWords: HCV; HCC; SVR; genetic; epigenetic; surveillance