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Updated: May 27, 2026

Detection of Low Copy Number Integrated Viral DNA Formed by In Vitro Hepatitis B Infection
Published on: November 7, 2018
[Mutations in precore/basal core promoter regions and viral polymerase in patients with chronic hepatitis B]
Ainhoa Gutiérrez1, Isabel Viciana, Francisca Rius
1Servicio de Microbiología, Hospital Virgen de la Victoria, Málaga, España.
Insights
Hepatitis B virus (HBV) mutations in the C and P genes are common in chronic hepatitis B patients, often leading to antiviral treatment failure. Early detection of these mutations is crucial for effective patient management.
Area of Science:
- Hepatology
- Virology
- Genetics
Context:
- Chronic hepatitis B (CHB) is a significant global health concern.
- Hepatitis B virus (HBV) infection can lead to serious liver disease.
- Antiviral treatment failure in CHB is a growing clinical challenge.
Purpose:
- To investigate the prevalence of HBV C and P gene mutations in CHB patients.
- To determine the association between specific mutations and antiviral treatment outcomes.
- To identify common HBV genotypes in the studied population.
Summary:
- Genotyping of HBV C and P genes was performed on 75% of CHB patients over five years.
- Mutations in precore/basal core promoter regions were found in 75% of patients.
- Antiviral resistance mutations were present in 37% of patients, with genotypes A and D being most frequent.
Impact:
- Findings highlight the high prevalence of HBV mutations contributing to treatment failure.
- Early detection of resistance mutations is recommended to optimize CHB management.
- Understanding genotype distribution aids in predicting treatment response and disease progression.
Background:
Variations of C gene give rise to precore and basal core mutations, which influence HBeAg expression The antiviral treatment failure is due to the presence of variations in the gene P, which cause mutations in the viral polymerase.
Methods:
We performed genotyping of HBV P gene by sequencing, and gene C in patients with chronic hepatitis B over a period of five years.
Results:
A total of 75% of the patients had some mutation in precore or in basal core promoter regions, and 37% demonstrated resistance mutations to antiviral treatment. The most frequent genotypes were A and D.
Conclusions:
The presence of mutations in core/precore regions in patients with chronic hepatitis has led to tighter control of these patients. Detecting for resistance should be done as quickly as possible before there is an increase in viral load.
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