An overview of hepatitis B virus in gastric carcinogenesis: from clinical association to molecular mechanisms

Previous studies have established that Hepatitis B virus (HBV) infection contributes to the development of cirrhosis and hepatocellular carcinoma (HCC). In recent years, growing attention has been directed towards the association between HBV and extrahepatic malignant tumors, particularly gastric cancer (GC), with increasing evidence suggesting that HBV infection may elevate the risk of GC. Several meta-analyses have examined the link between HBV and GC. However, the underlying pathogenic mechanisms remain poorly understood. This study conducts a systematic review of existing research to investigate the association between HBV infection and GC risk. Additionally, it offers a comprehensive analysis of the epidemiological data, virological characteristics, and molecular mechanisms. The available evidence suggests that HBV may contribute to GC development and progression through mechanisms such as HBV DNA integration, regulation of HBx protein, chronic inflammation, and immune dysregulation. However, limitations in the current literature—such as reliance on single-source samples, insufficient control of confounding factors, and limited mechanistic studies—should be acknowledged. Large-scale, multicenter, prospective studies with clearly defined mechanisms are needed to further clarify the causal relationship between HBV and GC and to identify potential biomarkers. In conclusion, addressing HBV-related GC is a critical clinical and public health priority.