ArticleJournal of virology2018
Asymmetric Modification of Hepatitis B Virus (HBV) Genomes by an Endogenous Cytidine Deaminase inside HBV Cores Informs a Model of Reverse Transcription.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 34 citations in OpenAlex.
- Negative cooperativity drives activity of capsid-directed antivirals against hepatitis B virus.Science advances · 2026Article
- Mechanisms of APOBEC3 Packaging into HIV-1.Viruses · 2026Review
- DNA synthesis inside the hepatitis B virus creates a high-energy spool.bioRxiv : the preprint server for biology · 2026Article
- Hepatitis B Virus Nucleocapsid Assembly.Journal of molecular biology · 2025Review
- Mechanisms of Hepatitis B Virus cccDNA and Minichromosome Formation and HBV Gene Transcription.Viruses · 2024Review
- Transient and tunable CRISPRa regulation of APOBEC/AID genes for targeting hepatitis B virus.Molecular therapy. Nucleic acids · 2023Article
- Host-mediated RNA editing in viruses.Biology direct · 2023Review
- Gene Editing Technologies to Target HBV cccDNA.Viruses · 2022Review
- Core Protein-Directed Antivirals and Importin β Can Synergistically Disrupt Hepatitis B Virus Capsids.Journal of virology · 2022Article
- Viral Phrenology.Viruses · 2021Article
- Potential capacity of interferon-α to eliminate covalently closed circular DNA (cccDNA) in hepatocytes infected with hepatitis B virus.Gut pathogens · 2021Review
- Article
- CancerFrontiers in immunology · 2021Article
- The Role of APOBECs in Viral Replication.Microorganisms · 2020Review
- The evolution and clinical impact of hepatitis B virus genome diversity.Nature reviews. Gastroenterology & hepatology · 2020Review
- Clearing of Foreign Episomal DNA from Human Cells by CRISPRa-Mediated Activation of Cytidine Deaminases.International journal of molecular sciences · 2020Article
- Footprint of the host restriction factors APOBEC3 on the genome of human viruses.PLoS pathogens · 2020Article
- Replenishment of Hepatitis B Virus cccDNA Pool Is Restricted by Baseline Expression of Host Restriction Factors In Vitro.Microorganisms · 2019Article
- Mapping the Interactions of HBV cccDNA with Host Factors.International journal of molecular sciences · 2019Review
- Effects of Moloney Leukemia Virus 10 Protein on Hepatitis B Virus Infection and Viral Replication.Viruses · 2019Article
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
Cytidine deaminases inhibit replication of a broad range of DNA viruses by deaminating cytidines on single-stranded DNA (ssDNA) to generate uracil. While several lines of evidence have revealed hepatitis B virus (HBV) genome editing by deamination, it is still unclear which nucleic acid intermediate of HBV is modified. Hepatitis B virus has a relaxed circular double-stranded DNA (rcDNA) genome that is reverse transcribed within virus cores from a RNA template. The HBV genome also persists as covalently closed circular DNA (cccDNA) in the nucleus of an infected cell. In the present study, we found that in HBV-producing HepAD38 and HepG2.2.15 cell lines, endogenous cytidine deaminases edited 10 to 25% of HBV rcDNA genomes, asymmetrically with almost all mutations on the 5' half of the minus strand. This region corresponds to the last half of the minus strand to be protected by plus-strand synthesis. Within this half of the genome, the number of mutations peaks in the middle. Overexpressed APOBEC3A and APOBEC3G could be packaged in HBV capsids but did not change the amount or distribution of mutations. We found no deamination on pregenomic RNA (pgRNA), indicating that an intact genome is encapsidated and deaminated during or after reverse transcription. The deamination pattern suggests a model of rcDNA synthesis in which pgRNA and then newly synthesized minus-sense single-stranded DNA are protected from deaminase by interaction with the virus capsid; during plus-strand synthesis, when enough dsDNA has been synthesized to displace the remaining minus strand from the capsid surface, the single-stranded DNA becomes deaminase sensitive.
Indexed as
Identifiers
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.