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Detection of Low Copy Number Integrated Viral DNA Formed by In Vitro Hepatitis B Infection
Published on: November 7, 2018
Abnormal immunity and gene mutation in patients with severe hepatitis-B
1Department of Infectious Diseases, the Second Hospital, China Medical University, Shenyang 110004, Liaoning Province, China.
World Journal of Gastroenterology
|September 13, 2003
Summary
Hepatitis B virus (HBV) precore mutations are common in severe cases, leading to immune dysfunction and increased mortality. These mutations promote T-lymphocyte imbalance and elevated cytokine levels, contributing to severe liver damage.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Hepatitis B virus (HBV) infection is a global health concern.
- The precore 1896 site mutation in HBV is associated with disease progression.
Purpose of the Study:
- To investigate the role of HBV precore 1896 site mutations in severe hepatitis B.
- To evaluate associated immune system abnormalities and gene mutations.
Main Methods:
- Restriction fragment length polymorphism (RFLP) analysis to detect HBV precore 1896 mutations.
- Enzyme-linked immunosorbent assay (ELISA) to measure cytokine levels (TNF-alpha, IFN-gamma, IL-6, IL-8).
- Alkaline phosphatase anti-alkaline phosphatase (APAAP) technique to detect T lymphocyte subgroups.
Main Results:
- A high infective rate (52.5%) of HBV mutant strain was observed in severe hepatitis B patients.
- Mutant strains were associated with lower CD8+ T lymphocyte percentages and higher CD4+/CD8+ ratios.
- Elevated levels of TNF-alpha, IFN-gamma, IL-6, and IL-8 were found in severe hepatitis B patients, particularly in the mutant group.
- Mortality was significantly higher (100%) in patients infected with the HBV mutant strain compared to the wild-type (0.9%).
Conclusions:
- HBV precore 1896 mutations are prevalent in severe hepatitis B and contribute to immune dysregulation.
- The mutant strain induces significant immune disorders, including lymphocyte activation and cytokine release.
- HBV DNA mutation appears to be an adaptive response to altered host immunity, exacerbating liver damage.
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