ReviewViruses2021
Mechanism of Hepatitis B Virus cccDNA Formation.
Review in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
86 citing papers in PubMed, 116 citations in OpenAlex.
- Chimeric antigen receptor T (CAR-T) cell therapy in non-oncological diseases.Signal transduction and targeted therapy · 2026Review
- [The E3 ubiquitin ligase KLHL8 degrades HBx protein via the ubiquitin-proteasome pathway and inhibits HBV cccDNA transcription].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Article
- Structure-guided discovery and engineering of miniature CRISPR-Cas12m for epigenome editing.Nature structural & molecular biology · 2026Article
- Core protein mutations are key determinants of hepatitis B virus replication during the hepatitis B e antigen-negative stage.The Journal of general virology · 2026Article
- Chromatin Accessibility-Guided Targeting Identifies Structurally Constrained Regions in HBV cccDNA and Suppresses Viral Replication.International journal of molecular sciences · 2026Article
- Review
- From metabolites to chromatin: ACSS2-driven acetyl-CoA fuels H3K27ac chromatin remodeling in HBV-associated HCC: Editorial on "Acetyl-coenzyme A synthetase 2-mediated acetyl-coenzyme A accumulation promotes mitophagy and tumor growth via increased H3K27ac in hepatitis B virus-related hepatocellular carcinoma".Clinical and molecular hepatology · 2026Article
- Therapeutic Vaccines for Chronic Viral Infections: From Immune Modulation to Clinical Translation.Vaccines · 2026Review
- Stable state of hepatocyte chromatin during hepatitis B virus infection.Scientific reports · 2026Article
- Nucleotide excision repair and poly(ADP-ribose) polymerase 1 cooperate in HBV cccDNA synthesis: A potential viral therapeutic target.JHEP reports : innovation in hepatology · 2026Article
- Lead Optimization of Xanthone Derivatives as Hepatitis B Virus cccDNA Reducers: Design, Synthesis, and Bioevaluation.ACS medicinal chemistry letters · 2026Article
- hnRNPA2B1 induces HBV cccDNA degradation by recruiting APOBEC3B.Nucleic acids research · 2026Article
- ZNF638 represses the transcription of HBV closed circular DNA involving HUSH complex-mediated histone modifications of epigenetic silencing.Cell communication and signaling : CCS · 2026Article
- HBV reprograms the tumor microenvironment in hepatocellular carcinoma: mechanisms and therapeutic implications.Clinical and experimental medicine · 2026Review
- Hepatocyte-Targeted Drug Delivery Strategies for Chronic Hepatitis B: Overcoming Delivery Barriers Toward Functional Cure.Pharmaceutics · 2026Review
- Chromatin remodeler BAF maintains HBV cccDNA transcriptional competence and represents a therapeutic target.Nucleic acids research · 2026Article
- Dynamics and Sensitivity of the Lifecycle of Hepatitis B Virus.Pathogens (Basel, Switzerland) · 2026Article
- Detection and characterization of Hepatitis B virus double-stranded linear DNA-derived covalently closed circular DNA in chronic hepatitis B patients.PLoS pathogens · 2026Article
- Programmable synthesis of alkaloidal frameworks integrating Michael acceptor generates covalent probes for targeting POLE3 in HBV replication.RSC chemical biology · 2026Article
- Disrupting Viral Persistence: CRISPR/Cas9-Based Strategies for Hepatitis B and C Treatment, and Challenges.Journal of cellular and molecular medicine · 2026Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Hepatitis B virus (HBV) remains a major medical problem affecting at least 257 million chronically infected patients who are at risk of developing serious, frequently fatal liver diseases. HBV is a small, partially double-stranded DNA virus that goes through an intricate replication cycle in its native cellular environment: human hepatocytes. A critical step in the viral life-cycle is the conversion of relaxed circular DNA (rcDNA) into covalently closed circular DNA (cccDNA), the latter being the major template for HBV gene transcription. For this conversion, HBV relies on multiple host factors, as enzymes capable of catalyzing the relevant reactions are not encoded in the viral genome. Combinations of genetic and biochemical approaches have produced findings that provide a more holistic picture of the complex mechanism of HBV cccDNA formation. Here, we review some of these studies that have helped to provide a comprehensive picture of rcDNA to cccDNA conversion. Mechanistic insights into this critical step for HBV persistence hold the key for devising new therapies that will lead not only to viral suppression but to a cure.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.