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Published on: February 1, 2017
Different hepatitis B virus core gene mutations in children with chronic infection and hepatocellular carcinoma
1Department of Paediatrics, Hospital and College of Medicine, National Taiwan University, Taipei, Taiwan.
Insights
Hepatitis B virus (HBV) core gene mutations accumulate in children with chronic infection and hepatocellular carcinoma (HCC). HCC patients exhibit distinct mutation patterns, suggesting a role in pediatric liver cancer development.
Area of Science:
- Hepatology
- Virology
- Pediatric Oncology
Background:
- The role of hepatitis B virus (HBV) precore/core antigen mutations in persistent infection and liver disease remains debated.
- Understanding HBV mutations is crucial for managing chronic infections and preventing liver cancer.
Purpose of the Study:
- To analyze HBV core gene sequence changes in children with chronic HBV infection.
- To investigate the association between these mutations and the development of hepatocellular carcinoma (HCC) in pediatric patients.
Main Methods:
- Studied 31 children with chronic HBV infection and documented hepatitis B e antigen seroconversion.
- Analyzed HBV core gene sequences from serum samples of chronic HBV patients and 12 children with HBV-related HCC.
- Compared mutation profiles before and after seroconversion in chronic cases.
Main Results:
- Mutations frequently occurred at core gene codons 21, 147, 65, and precore stop codon 28 in chronic HBV patients.
- Hepatocellular carcinoma patients showed distinct mutations at core codons 74, 87, and 159.
- Significantly more mutations were observed in the core gene of HCC patients compared to chronic HBV-infected children (p=0.013).
Conclusions:
- HBV core region mutation accumulation differs between pediatric HCC patients and those with chronic HBV infection.
- These distinct mutation patterns may offer insights into the pathogenesis of pediatric hepatocellular carcinoma.
Background:
The significance of mutations of hepatitis B virus (HBV) precore/core antigen in causing persistent infection and subsequent liver diseases is debatable.
Aim:
To investigate HBV core gene sequence changes in children with chronic HBV infection and their implications in hepatocellular carcinoma (HCC).
Methods:
Thirty one chronic HBV infected children with documented hepatitis B e antigen seroconversion selected from 415 long term carrier children and 12 HBV related HCC children were studied. Four serial serum samples before and after hepatitis B e antigen seroconversion from each of the 31 children, and one serum sample taken from the 12 HCC children were subjected to HBV core gene sequence analysis.
Results:
Mutations accumulated as chronic infection persisted and most frequently occurred at core gene codon 21 (29%), codon 147 (29%), codon 65 (16%), and precore stop codon 28 (74%) in the 31 chronic HBV infected children. Core gene mutation sites in HCC children were identified at core codons 74, 87, and 159. HCC children had more mutations in the core gene than those with chronic HBV infection (p=0.013).
Conclusion:
Accumulation of mutations of HBV core region in HCC children differ from those in chronic HBV infected children. This may be a clue to the pathogenesis of paediatric HCC.
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