Hepatitis B virus-induced cirrhosis: Mechanisms, global variations, and treatment advances

Abstract

We focus on hepatitis B virus (HBV)-induced cirrhosis, global differences, and the evolution of antiviral treatment strategies. Chronic HBV (CHB) infection affects more than 250 million people globally, leading to cirrhosis and hepatocellular carcinoma. The aim of this article was to synthesize the current understanding of the pathophysiological mechanisms and clinical consequences of HBV-induced cirrhosis, and explore differences in disease progression between geographic regions. Disease progression varies across regions due to differences in HBV subtypes, transmission routes, and immune responses. The challenge of late diagnosis and treatment, particularly in resource-limited areas, highlights the urgency and importance of CHB service expansion. Modern nucleos(t)ide analogues, such as tenofovir and entecavir, have emerged as the main therapeutic regimens to improve clinical outcomes in patients by suppressing viral replication and attenuating liver fibrosis. However, drug resistance challenges highlight the need for ongoing research and personalized treatment strategies. This article highlights the mechanisms and impact of cirrhosis progression in the context of CHB infection, aiming to reduce the incidence of cirrhosis and its serious consequences, thereby improving the long-term health of CHB patients worldwide, especially in Africa.

Keywords: Chronic hepatitis B virus; Hepatitis B virus-induced cirrhosis; Nucleos(t)ide analogues.

Figure 1

Hepatitis B virus is transmitted through blood or body fluids, which leads to infection of hepatocytes in the liver. The virus particle is composed of an outer envelope containing surface proteins (HBs) and an inner nucleocapsid containing core proteins (HBc) and relaxed circular DNA (rcDNA). Upon entry into hepatocytes via the sodium taurocholate cotransporting polypeptide receptor, the viral rcDNA is transported to the nucleus where it is converted into covalently closed circular DNA (cccDNA). This cccDNA serves as a template for viral transcription and replication, leading to the production of new viral particles. Some of the infected hepatocytes experience necrosis or apoptosis as a result of viral replication, while others excrete viral particles by bile. Chronic hepatitis B infection can cause persistent liver damage, eventually leading to liver cirrhosis and significant loss of liver function. NTCP: Sodium taurocholate cotransporting polypeptide receptor; rcDNA: Relaxed circular DNA; CHB: Chronic hepatitis B; HBV: Hepatitis B virus.