Liver Carcinogenesis Suppression in Chronic Hepatitis B in the Nucleoside Analogues Era

In Vivo. 2024 Jan-Feb;38(1):40-47. doi: 10.21873/invivo.13408.

Abstract

There is a strong association between the distribution of Hepatitis B virus (HBV) carriers and the incidence of hepatocellular carcinoma (HCC). About 60% of HCC in Japan is caused by viral hepatitis. Ten to 15 percent of hepatitis virus-related HCCs derive from HBV. Recently, antiviral therapy against HBV has developed, and interferon therapy and nucleos(t)ide analogues (NAs) are currently the standard of care. NAs exhibit antiviral activity by inhibiting DNA polymerase and suppressing HBV replication. NAs are highly effective in suppressing HBV-DNA and improving alanine aminotransferase. The long-term treatment goal for chronic hepatitis B is HB surface antigen (HBsAg) loss. However, the number of patients who achieve HBsAg loss by NA (i.e., functional cure) is low and there have been cases of HCC incidence during (or after) NA therapy. In this article, we review the efficacy of NA therapy in suppressing HBV-derived carcinogenesis.

Keywords: Hepatitis B virus; carcinogenesis; cccDNA; hepatitis B surface antigen; nucleos(t)ide analogue; review.

Publication types

  • Review

MeSH terms

  • Antiviral Agents / therapeutic use
  • Carcinoma, Hepatocellular* / drug therapy
  • Carcinoma, Hepatocellular* / epidemiology
  • Carcinoma, Hepatocellular* / etiology
  • DNA, Viral / genetics
  • Hepatitis B Surface Antigens
  • Hepatitis B virus
  • Hepatitis B, Chronic* / complications
  • Hepatitis B, Chronic* / drug therapy
  • Humans
  • Liver Neoplasms* / drug therapy
  • Liver Neoplasms* / epidemiology
  • Liver Neoplasms* / etiology
  • Nucleosides / therapeutic use

Substances

  • Nucleosides
  • Hepatitis B Surface Antigens
  • Antiviral Agents
  • DNA, Viral