Published online Jun 21, 2016. doi: 10.3748/wjg.v22.i23.5393
Peer-review started: February 2, 2016
First decision: March 7, 2016
Revised: March 21, 2016
Accepted: April 7, 2016
Article in press: April 7, 2016
Published online: June 21, 2016
AIM: To determine the genomic changes in hepatitis B virus (HBV) and evaluate their role in the development of hepatocellular carcinoma (HCC) in patients chronically infected with genotype C HBV.
METHODS: Two hundred and forty chronic hepatitis B (CHB) patients were subjected and followed for a median of 105 mo. HCC was diagnosed in accordance with AASLD guidelines. The whole X, S, basal core promoter (BCP), and precore regions of HBV were sequenced using the direct sequencing method.
RESULTS: All of the subjects were infected with genotype C HBV. Out of 240 CHB patients, 25 (10%) had C1653T and 33 (14%) had T1753V mutation in X region; 157 (65%) had A1762T/G1764A mutations in BCP region, 50 (21%) had G1896A mutation in precore region and 67 (28%) had pre-S deletions. HCC occurred in 6 patients (3%). The prevalence of T1753V mutation was significantly higher in patients who developed HCC than in those without HCC. The cumulative occurrence rates of HCC were 5% and 19% at 10 and 15 years, respectively, in patients with T1753V mutant, which were significantly higher than 1% and 1% in those with wild type HBV (P < 0.001).
CONCLUSION: The presence of T1753V mutation in HBV X-gene significantly increases the risk of HCC development in patients chronically infected with genotype C HBV.
Core tip: In the present study, we determined the genomic changes in the X, S, basal core promoter (BCP), and precore regions of hepatitis B virus (HBV), and evaluate their role in the development of hepatocellular carcinoma (HCC) in chronic hepatitis B (CHB) patients with genotype C HBV. As the results, it was suggested that T1753V mutation in X region might significantly increase the risk of HCC development in CHB patients with genotype C HBV. Also, the BCP mutations might act in synergy with T1753V or G1896A mutation, and with pre-S deletion to promote the development of HCC in these patients.