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Targeting HBV cccDNA Levels: Key to Achieving Complete Cure of Chronic Hepatitis B
Wei He1,2, Zhijin Zheng1,2, Qian Zhao1,2
1Jiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123, Jiangsu, China.
Insights
Chronic hepatitis B (CHB) is hard to cure due to persistent HBV cccDNA. New strategies aim to eliminate this viral DNA for a complete cure, moving beyond current treatments.
Area of Science:
- Hepatology
- Virology
- Molecular Biology
Background:
- Chronic hepatitis B (CHB) affects many globally.
- Persistent hepatitis B virus covalently closed circular DNA (HBV cccDNA) prevents complete cure.
- Current antivirals control but do not eliminate HBV.
Purpose of the Study:
- To review novel strategies for complete CHB cure.
- To focus on targeting the HBV cccDNA template.
Main Methods:
- Inhibition of de novo HBV cccDNA synthesis.
- Degradation of existing HBV cccDNA via host factors and small molecules.
- CRISPR-Cas9 gene editing for HBV cccDNA.
- Epigenetic silencing of HBV cccDNA.
Main Results:
- Multiple therapeutic avenues are being explored to eradicate HBV cccDNA.
- These strategies offer potential for a functional cure of CHB.
- Combining approaches may be necessary for complete viral clearance.
Conclusions:
- Complete cure of CHB necessitates targeting HBV cccDNA.
- Emerging strategies show promise for eliminating the viral reservoir.
- Further research is crucial to translate these findings into clinical practice.
Abstract:
Chronic hepatitis B (CHB) caused by HBV infection has brought suffering to numerous people. Due to the stable existence of HBV cccDNA, the original template for HBV replication, chronic hepatitis B (CHB) is difficult to cure completely. Despite current antiviral strategies being able to effectively limit the progression of CHB, complete CHB cure requires directly targeting HBV cccDNA. In this review, we discuss strategies that may achieve a complete cure of CHB, including inhibition of cccDNA de novo synthesis, targeting cccDNA degradation through host factors and small molecules, CRISP-Cas9-based cccDNA editing, and silencing cccDNA epigenetically.
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