fig1

Figure 1. The mechanisms of HBV-induced hepatocarcinogenesis: the current understanding. The interplay between HBV infection, age, and genetic predisposition leads to chronic inflammation. Inflammatory mediators such as IL-6, STAT3, TNF-α, and NF-κB are activated in this process. These factors not only upregulate the expression of APOBEC but also downregulate the expression of the UNG, resulting in an APOBEC-UNG imbalance. This imbalance fosters both HBV mutation and somatic cell mutation. While most of the mutated HBV are eliminated by the immune system, a minority survives and integrates into the genome of these residual somatic cells. This integration triggers the activation of the EMT and oncogenic pathways, potentially leading to the development of HCC. Created with Biorender (https://www.biorender.com/) and Bioart (https://bioart.niaid.nih.gov/). HBV: Hepatitis B virus; HCC: hepatocellular carcinoma; IL-6: interleukin-6; STAT3: signal transducer and activator of transcription 3; TNF-α: tumor necrosis factor α; NF-κB: nuclear factor‐kappa B; APOBEC: apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like; UNG: uracil-N-glycosylase; EMT: epithelial-mesenchymal transition.