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Early mutation of precore (A1896) region prior to core promoter region mutation leads to decrease of HBV replication
Insights
Hepatitis B virus (HBV) precore (preC) mutations are linked to lower HBV DNA levels and potential remission in carriers. This suggests preC mutations may control HBV replication, impacting disease progression.
Area of Science:
- Hepatology
- Virology
- Molecular Biology
Background:
- Hepatitis B virus (HBV) mutations, specifically precore (preC) and core promoter (CP) mutations, are implicated in the clinical course of chronic HBV infection.
- Understanding the relationship between these mutations and viral load is crucial for predicting disease outcomes.
Purpose of the Study:
- To investigate the association between preC and CP mutations and serum HBV DNA levels in HBe-antibody-positive HBV carriers.
- To determine if specific mutation patterns correlate with different clinical stages of HBV infection, including asymptomatic carriers (ASC), chronic hepatitis with normal ALT (CH-ASC), chronic hepatitis (CH), and hepatocellular carcinoma (HCC).
Main Methods:
- Genotyping of preC and CP mutations in HBV DNA from 158 patients across four clinical groups (ASC, CH-ASC, CH, HCC).
- Quantification of serum HBV DNA levels.
- Statistical analysis to compare mutation frequencies and HBV DNA levels across clinical groups.
Main Results:
- Nearly all patients (99.2%) exhibited mutations in either CP or preC.
- The presence of only the preC mutation (A1896) was significantly higher in asymptomatic carriers (52.2%) compared to CH (16.1%) and HCC (8.0%) groups (P < 0.01).
- Patients with only the preC mutation consistently showed lower HBV DNA levels across all clinical stages.
Conclusions:
- The precore (preC) mutation, particularly A1896, appears to be associated with lower HBV replication and may contribute to the remission of hepatitis.
- The sequence of mutations, with preC mutation potentially preceding CP mutation, might play a role in controlling HBV replication and influencing disease progression.
Abstract:
To evaluate the relationship between mutations and clinical courses, we investigated precore (preC) and core promoter (CP) mutations and serum HBV DNA levels in HBe-antibody-positive HBV carriers. Fifty-six asymptomatic carriers (ASC), 29 patients with chronic hepatitis who showed normal ALT levels for more than two years (CH-ASC), 31 patients with chronic hepatitis (CH), and 32 patients with hepatocellular carcinoma (HCC) were studied. Almost all patients (99.2%) had mutations in either CP or preC. Mutation only in preC (A1896) was present in 52.2% with ASC, 25.0% with CH-ASC, 16.1% with CH, and 8.0% with HCC, and was significantly higher in ASC (P < 0.01). The patients with only preC mutation showed low HBV DNA levels in each clinical stage. The mutation of preC (A1896) prior to the mutation of CP might control the replication of HBV, which leads to the remission of hepatitis.