Abstract

Despite breakthroughs in antiviral therapies, chronic viral hepatitis B and C are still the major causes of liver fibrosis and hepatocellular carcinoma (HCC). Importantly, even in patients with controlled infection or viral cure, the cancer risk cannot be fully eliminated, highlighting a persisting oncogenic pressure imposed by epigenetic imprinting and advanced liver disease. Reliable and minimally invasive biomarkers for early fibrosis and for residual HCC risk in HCV-cured patients are urgently needed. Chronic infection with HBV and/or HCV dysregulates oncogenic and profibrogenic signaling within the host, also displayed in the secretion of soluble factors to the blood. The study of virus-dysregulated signaling pathways may, therefore, contribute to the identification of reliable minimally invasive biomarkers for the detection of patients at early-stage liver disease potentially complementing existing noninvasive methods in clinics. With a focus on virus-induced signaling events, this review provides an overview of candidate blood biomarkers for liver disease and HCC risk associated with chronic viral hepatitis and epigenetic viral footprints.

Highlights

  • In Europe, it is estimated that 10–15% of hepatocellular carcinoma (HCC) are caused by hepatitis B virus (HBV) infection, while 70% are caused by hepatitis C virus (HCV) infection, HCV being the major risk factor for HCC development [10]

  • Both viruses contribute to liver fibrosis and HCC risk by multiple factors involving a dysregulation of host signal transduction through viral proteins, miRNAs, virus-induced growth factor and cytokine expression or antiviral responses that cumulate in a pro-fibrotic and pro-oncogenic environment in the liver [11,12,13,14,15,16,17]

  • With a focus on virus-induced signaling events, this review provides an overview of the candidate blood biomarkers of fibrotic liver disease and HCC risk associated with chronic viral hepatitis

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Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. An estimated 180 million people live with hepatitis B virus (HBV) and 75 million with hepatitis C virus (HCV), and for most, testing and treatment remain beyond reach [9] Both viruses share similar as well as distinct mechanisms contributing to liver disease and cancer. In Europe, it is estimated that 10–15% of HCCs are caused by HBV infection, while 70% are caused by HCV infection, HCV being the major risk factor for HCC development [10] Both viruses contribute to liver fibrosis and HCC risk by multiple factors involving a dysregulation of host signal transduction through viral proteins, miRNAs, virus-induced growth factor and cytokine expression or antiviral responses that cumulate in a pro-fibrotic and pro-oncogenic environment in the liver [11,12,13,14,15,16,17]. With a focus on virus-induced signaling events, this review provides an overview of the candidate blood biomarkers of fibrotic liver disease and HCC risk associated with chronic viral hepatitis

Viral Hepatitis B and C
Antiviral Therapies
Fibrosis and HCC Screening in the Clinics—State of the Art
Signaling Pathways Associated with Candidate Serum Biomarkers
Virus-Induced Epigenetic Changes as Biomarkers
Findings
Discussion and Perspectives

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