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The Role of HBx Mutations in Chronic Hepatitis B with Acute Exacerbation
Xiaobei Chen1, Jinzhi Shi1, Ping Zhou2
1Department of Infectious Diseases, East Campus, Renmin Hospital of Wuhan University, Wuhan 430223, China.
Insights
Specific Hepatitis B virus X protein (HBx) mutations are linked to chronic hepatitis B acute exacerbation (CHB-AE) and liver failure. These HBx mutations may indicate disease severity and serve as therapeutic targets.
Area of Science:
- Hepatology
- Virology
- Molecular Biology
Background:
- Hepatitis B virus (HBV) infection causes significant global health issues, including chronic complications like cirrhosis and hepatocellular carcinoma (HCC).
- Acute exacerbation of chronic hepatitis B (CHB-AE) is a common early clinical sign.
- The Hepatitis B virus X protein (HBx) is crucial for viral replication and HCC development.
Purpose of the Study:
- To investigate the association between Hepatitis B virus X protein (HBx) mutations and the progression of chronic hepatitis B acute exacerbation (CHB-AE).
- To explore the role of HBx mutations in relation to viral load, patient demographics, and response to antiviral therapy in CHB-AE and HBV-related liver failure.
Main Methods:
- Retrospective analysis of 33 hospitalized CHB-AE patients and 31 HBV-related liver failure patients in mainland China (January 2017 - June 2018).
- Genotyping of Hepatitis B virus X protein (HBx) mutations.
- Statistical analysis to correlate HBx mutations with clinical parameters, HBV DNA levels, and patient age.
Main Results:
- Single mutation 36 of HBx was more prevalent in CHB-AE patients, while Joint Mutation 1 was more frequent in HBV-related liver failure patients.
- HBx mutations (Single mutation 36, Joint Mutations 2 & 3) correlated with high HBV DNA levels, whereas Joint mutation 1 was associated with low HBV DNA.
- Specific mutations (Single mutation 36, Joint Mutation 2) were more common in younger patients (<35 years), and Joint mutation 1 in older patients (≥35 years).
- Antiviral therapy significantly reduced Joint mutation 1 prevalence from 82.98% to 29.41%.
Conclusions:
- Specific HBx mutations are significantly associated with viral replication levels, disease progression (CHB-AE vs. liver failure), and patient demographics.
- These HBx mutations may function as valuable molecular markers for assessing disease severity.
- Identified HBx mutations could represent potential therapeutic targets for managing CHB-AE and HBV-related liver failure.
Abstract:
Hepatitis B virus (HBV) infection remains a significant global health burden, primarily due to its chronic complications, including acute exacerbation, cirrhosis, hepatocellular carcinoma (HCC), and related sequelae. Acute exacerbation of chronic hepatitis B (CHB-AE) is common and often represents the earliest clinical manifestation. The Hepatitis B virus X protein (HBx) (17-kDa) is not only essential for viral replication but also plays a role in the development of HCC. To investigate the role of HBx mutation in CHB-AE progression, we enrolled 33 hospitalized CHB-AE patients and 31 patients with HBV-related liver failure (controls) from mainland China between January 2017 and June 2018. Single mutation 36 of HBx was significantly more prevalent in CHB-AE patients (p < 0.05), whereas Joint Mutation 1 was more frequent in HBV-related liver failure patients (p < 0.05). HBx mutations, including Single mutation 36 and Joint Mutations 2 and 3, were significantly associated with high HBV DNA levels (p < 0.05), while Joint mutation 1 predominated in the low HBV DNA group (p < 0.01). Age-stratified analysis showed that Single mutation 36 and Joint Mutation 2 were more common in younger patients (<35 years old) (p < 0.05), whereas Joint mutation 1 was more frequent in older age (≥35 years old) (p < 0.05). Moreover, antiviral therapy markedly reduced the prevalence of Joint mutation 1 from 82.98% in treatment-naïve patients to 29.41% in treatment-experienced patients (p < 0.0001). These findings suggest that specific HBx mutations are associated with viral replication levels, disease progression, and patient demographics. Such mutations may serve as molecular markers for disease severity and potential therapeutic targets in both CHB-AE and HBV-related liver failure.
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