Tracking down the epigenetic footprint of hcv-induced hepatocarcinogenesis

Tom Domovitz, Meital Gal-Tanamy

Research output: Contribution to journalReview articlepeer-review

17 Scopus citations

Abstract

Hepatitis C virus (HCV) is a major cause of death and morbidity globally and is a leading cause of hepatocellular carcinoma (HCC). Incidence of HCV infections, as well as HCV-related liver diseases, are increasing. Although now, with new direct acting antivirals (DAAs) therapy available, HCV is a curable cancer-associated infectious agent, HCC prevalence is expected to continue to rise because HCC risk still persists after HCV cure. Understanding the factors that lead from HCV infection to HCC pre-and post-cure may open-up opportunities to novel strategies for HCC prevention. Herein, we provide an overview of the reported evidence for the induction of alterations in the transcriptome of host cells via epigenetic dysregulation by HCV infection and describe recent reports linking the residual risk for HCC post-cure with a persistent HCV-induced epigenetic signature. Specifically, we discuss the contribution of the epigenetic changes identified following HCV infection to HCC risk pre-and post-cure, the molecular pathways that are epigenetically altered, the downstream effects on expression of cancer-related genes, the identification of targets to prevent or revert this cancer-inducing epigenetic signature, and the potential contribution of these studies to early prognosis and prevention of HCC as an approach for reducing HCC-related mortality.

Original languageEnglish
Article number551
Pages (from-to)1-16
Number of pages16
JournalJournal of Clinical Medicine
Volume10
Issue number3
DOIs
StatePublished - 2 Feb 2021

Bibliographical note

Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.

Keywords

  • Direct acting antivirals (DAAs)
  • Epigenetic signature
  • Hepatitis C virus (HCV)
  • Hepatocellular carcinoma (HCC)

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