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

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

Research output: Contribution to journalReview articlepeer-review

4 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)326-344
Number of pages19
JournalClinical and Molecular Hepatology
Volume30
Issue number3
DOIs
StatePublished - Jul 2024

Bibliographical note

Publisher Copyright:
© 2024 by Korean Association for the Study of the Liver.

Keywords

  • Epigenetic
  • Genetic
  • HCC
  • HCV
  • SVR
  • Surveillance

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