Hepatitis B virus infection and alcohol consumption

Abstract

Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer, and the second most common cause of cancer deaths worldwide. The top three causes of HCC are hepatitis B virus (HBV), hepatitis C virus (HCV), and alcoholic liver disease. Owing to recent advances in direct-acting antiviral agents, HCV can now be eradicated in almost all patients. HBV infection and alcoholic liver disease are expected, therefore, to become the leading causes of HCC in the future. However, the association between alcohol consumption and chronic hepatitis B in the progression of liver disease is less well understood than with chronic hepatitis C. The mechanisms underlying the complex interaction between HBV and alcohol are not fully understood, and enhanced viral replication, increased oxidative stress and a weakened immune response could each play an important role in the development of HCC. It remains controversial whether HBV and alcohol synergistically increase the incidence of HCC. Herein, we review the currently available literature regarding the interaction of HBV infection and alcohol consumption on disease progression.

Keywords: Entecavir; Genetic factors; Hepatocellular carcinoma; Interferon.

Figure 1

The mechanisms of activation of hepatic stellate cells during chronic liver injury, resulting in synthesis of excess extracellular matrix. Once chronic liver injury has occurred, damaged hepatocytes, activated sinusoidal cells, platelets, and recruited inflammatory cells release various profibrogenic cytokines, which activate hepatic stellate cells, resulting in synthesis of excess extracellular matrix, such as type I and type III collagens. ECM: Extracellular matrix; IL: Interleukin; PDGF: Platelet-derived growth factor; TGF-β: Transforming growth factor-β; TNF-α: Tumor necrosis factor-α.