ArticleJournal of virology2008
Zinc finger proteins designed to specifically target duck hepatitis B virus covalently closed circular DNA inhibit viral transcription in tissue culture.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 92 citations in OpenAlex.
- ZNF148 inhibits HBV replication by downregulating RXRα transcription.Virology journal · 2024Article
- Novel Approaches to Inhibition of HBsAg Expression from cccDNA and Chromosomal Integrants: A Review.Journal of clinical and translational hepatology · 2023Review
- Review
- Drug Discovery Study Aimed at a Functional Cure for HBV.Viruses · 2022Review
- Role of hepatitis B virus in development of hepatocellular carcinoma: Focus on covalently closed circular DNA.World journal of hepatology · 2022Review
- Hepatitis B Core-Related Antigen and New Therapies for Hepatitis B.Microorganisms · 2021Review
- Improved Specificity and Safety of Anti-Hepatitis B Virus TALENs Using Obligate HeterodimericViruses · 2021Article
- Review
- Hepatitis B: Current Status of Therapy and Future Therapies.Gastroenterology clinics of North America · 2020Review
- Genome editing for the treatment of tumorigenic viral infections and virus-related carcinomas.Frontiers of medicine · 2018Review
- Towards HBV curative therapies.Liver international : official journal of the International Association for the Study of the Liver · 2018Review
- New Viral and Immunological Targets for Hepatitis B Treatment and Cure: A Review.Infectious diseases and therapy · 2017Review
- The state of gene therapy research in Africa, its significance and implications for the future.Gene therapy · 2017Review
- New directions in hepatitis B therapy research.Clinical and experimental hepatology · 2017Review
- New Direct-Acting Antiviral Agents and Immunomodulators for Hepatitis B Virus Infection.Gastroenterology & hepatology · 2017Article
- MicroRNA-20b suppresses the expression of ZFP-148 in viral myocarditis.Molecular and cellular biochemistry · 2017Article
- The gRNA-miRNA-gRNA Ternary Cassette Combining CRISPR/Cas9 with RNAi Approach Strongly Inhibits Hepatitis B Virus Replication.Theranostics · 2017Article
- Treatment of hepatitis B virus: an update.Future microbiology · 2016Review
- New horizon for radical cure of chronic hepatitis B virus infection.World journal of hepatology · 2016Article
- Eradication Strategies for Chronic Hepatitis B Infection.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duck hepatitis B virus (DHBV) is a model virus for human hepatitis B virus (HBV), which infects approximately 360 million individuals worldwide. Nucleoside analogs can decrease virus production by inhibiting the viral polymerase; however, complete clearance by these drugs is not common because of the persistence of the HBV episome. HBV DNA is present in the nucleus as a covalently closed circular (cccDNA) form, where it drives viral transcription and progeny virus production. cccDNA is not the direct target of antiviral nucleoside analogs and is the source of HBV reemergence when antiviral therapy is stopped. To target cccDNA, six different zinc finger proteins (ZFP) were designed to bind DNA sequences in the DHBV enhancer region. After the binding kinetics were assessed by using electrophoretic mobility shift assays and surface plasmon resonance, two candidates with dissociation constants of 12.3 and 40.2 nM were focused on for further study. The ZFPs were cloned into a eukaryotic expression vector and cotransfected into longhorn male hepatoma cells with the plasmid pDHBV1.3, which replicates the DHBV life cycle. In the presence of each ZFP, viral RNA was significantly reduced, and protein levels were dramatically decreased. As a result, intracellular viral particle production was also significantly decreased. In summary, designed ZFPs are able to bind to the DHBV enhancer and interfere with viral transcription, resulting in decreased production of viral products and progeny virus genomes.
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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.