3^rd Edition of Infectious Diseases World Conference 2026

Abstract

Hepatitis B virus (HBV) integration into the human genome causes hepatocellular carcinoma (HCC). The present study used inverse nested PCR; the full sequence of HBV DNA fragments of the chrX: 111009033 integration site was detected (987 bp), containing two fragments of double-stranded linear DNA with the same orientation (1,744-1,094 and 1,565-1,228 nt). By reverse transcription‑quantitative PCR, HBV‑cell fusion transcript was observed in HepG2.2.15 cells. The mean copy number of this site in cells with H₂O₂ treatment (8.73x10⁻²±1.65x10⁻² copies/cell) was significantly higher than that in the cells without H₂O₂ treatment (3.02x10⁻²±2.33x10⁻² copies/cell; P<0.0001). The mean levels of P21‑activated kinase 3 (PAK3) were 15.67±5.65 copies/cell in HepG2.2.15 cells with H₂O₂ treatment, significantly higher than in the cells without H₂O₂ treatment (11.34±4.58 copies/cell, P=0.0076) and in HepG2 cells (5.92±1.54 copies/cell, P<0.0001). A significant difference in PAK3 levels was also found between HepG2.2.15 cells without H₂O₂ treatment and HepG2 cells (11.34±4.58 vs. 5.92±1.54 copies/cell, P<0.0001). The average copy numbers of the integration site chrX: 111009033 were positively correlated with the average levels of PAK3 (P=0.0013). The overall trend of PAK3 expression was significantly increased in HepG2. 2.15 cells with H₂O₂ treatment compared with that in HepG2. 2.15 cells without H₂O₂ treatment (37.63±8.16 and 31.38±7.94, P=0.008) and HepG2 cells (21.67±7.88, P<0.0001). In summary, the chrX: 11009033 integration site may originate from primary human hepatocytes, the occurrence and clonal expansion of which may upregulate PAK3 expression, which may contribute to hepatocarcinogenesis.