ArticleMolecular therapy : the journal of the American Society of Gene Therapy2010
Zinc-finger nucleases as a novel therapeutic strategy for targeting hepatitis B virus DNAs.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
What it found
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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.
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Who cites it
91 citing papers in PubMed, 183 citations in OpenAlex.
- Reconstructing the complex architecture of the genome with molecular scissors: applying genome editing technology in precision medicine.Frontiers in genome editing · 2026Review
- Disrupting Viral Persistence: CRISPR/Cas9-Based Strategies for Hepatitis B and C Treatment, and Challenges.Journal of cellular and molecular medicine · 2026Review
- Genomic medicine in hepatology: mechanisms and liver treatment strategies.Molecular medicine (Cambridge, Mass.) · 2025Review
- Potential Applications of RNase P Ribozyme Against Hepatitis B Virus.Molecules (Basel, Switzerland) · 2025Review
- Article
- Prospects of viral vector-mediated delivery of sequences encoding anti-HBV designer endonucleases.Gene therapy · 2025Review
- The impact of integrated hepatitis B virus DNA on oncogenesis and antiviral therapy.Biomarker research · 2024Review
- The potential of HBV cure: an overview of CRISPR-mediated HBV gene disruption.Frontiers in genome editing · 2024Review
- AAV Immunotoxicity: Implications in Anti-HBV Gene Therapy.Microorganisms · 2023Review
- Review
- New Treatment Options in Chronic Hepatitis B: How Close Are We to Cure?Infectious diseases & clinical microbiology · 2023Review
- Hepatitis B Virus Epsilon (ε) RNA Element: Dynamic Regulator of Viral Replication and Attractive Therapeutic Target.Viruses · 2023Review
- HBV Infection and Host Interactions: The Role in Viral Persistence and Oncogenesis.International journal of molecular sciences · 2023Review
- Gene Editing Technologies to Target HBV cccDNA.Viruses · 2022Review
- Role of hepatitis B virus in development of hepatocellular carcinoma: Focus on covalently closed circular DNA.World journal of hepatology · 2022Review
- Gene editing and its applications in biomedicine.Science China. Life sciences · 2022Review
- Review
- Viral hepatitis: Innovations and expectations.World journal of gastroenterology · 2022Review
- Chronic hepatitis B: New potential therapeutic drugs target.World journal of virology · 2022Review
- Toward a complete cure for chronic hepatitis B: Novel therapeutic targets for hepatitis B virus.Clinical and molecular hepatology · 2022Review
31 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
5 authors at 2 institutions in 1 country.
Funding
Abstract
Hepatitis B virus (HBV) chronically infects 350-400 million people worldwide and causes >1 million deaths yearly. Current therapies prevent new viral genome formation, but do not target pre-existing viral genomic DNA, thus curing only approximately 1/2 of patients. We targeted HBV DNA for cleavage using zinc-finger nucleases (ZFNs), which cleave as dimers. Co-transfection of our ZFN pair with a target plasmid containing the HBV genome resulted in specific cleavage. After 3 days in culture, 26% of the target remained linear, whereas approximately10% was cleaved and misjoined tail-to-tail. Notably, ZFN treatment decreased levels of the hepatitis C virus pregenomic RNA by 29%. A portion of cleaved plasmids are repaired in cells, often with deletions and insertions. To track misrepair, we introduced an XbaI restriction site in the spacer between the ZFN sites. Targeted cleavage and misrepair destroys the XbaI site. After 3 days in culture, approximately 6% of plasmids were XbaI-resistant. Thirteen of 16 clones sequenced contained frameshift mutations that would lead to truncations of the viral core protein. These results demonstrate, for the first time, the possibility of targeting episomal viral DNA genomes using ZFNs.
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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.