Hepatitis B virus integration and hepatocarcinogenesis.

Area of Science:

• Hepatology
• Virology
• Oncology

Background:

• Hepatitis B virus (HBV) is a primary cause of hepatocellular carcinoma (HCC), particularly in Southeast Asia.
• Persistent HBV infection affects approximately 350 million people globally.
• HBV contributes to HCC through direct and indirect oncogenic pathways.

Purpose of the Study:

• To review the mechanisms by which HBV promotes hepatocellular carcinoma (HCC) development.
• To summarize the specific roles of the HBV X (HBx) protein and preS/S envelope protein in tumorigenesis.
• To discuss current concerns and future research perspectives in HBV-related liver cancer.

Main Methods:

• Literature review of HBV's role in HCC pathogenesis.
• Analysis of HBV DNA integration, ecDNA formation, and viral protein-mediated oncogenesis.
• Synthesis of information on HBx and preS/S protein functions in cancer development.

Main Results:

• HBV DNA integration can cause insertional mutagenesis and genomic instability.
• Extrachromosomal circular DNA (ecDNA) facilitates viral and host oncogene expression.
• HBx and preS/S proteins modulate host gene expression, promoting tumorigenesis.

Conclusions:

• HBV infection is a significant driver of HCC through complex molecular mechanisms.
• Understanding the roles of HBx and preS/S proteins is crucial for targeted therapies.
• Further research is needed to address concerns and explore new perspectives in managing HBV-related liver cancer.