ArticleJournal of molecular biology2007
The sequence of the RNA primer and the DNA template influence the initiation of plus-strand DNA synthesis in hepatitis B virus.
Article in Journal of molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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
30 citing papers in PubMed, 42 citations in OpenAlex.
- Structural organization of HBV pgRNA genome driven by phase separation in capsid confinement.Nature communications · 2026Article
- The Role of Integrated HBV DNA in the Quest for a Cure in HIV/HBV co-infection.Current HIV/AIDS reports · 2025Review
- Genome integration of human DNA oncoviruses.Journal of virology · 2025Review
- [Exploring the reasons for liver cancer occurrence still after long-term nucleos(t)ide analogue therapy in patients with chronic hepatitis B].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024Review
- Identification of Host Proteins Involved in Hepatitis B Virus Genome Packaging.Journal of proteome research · 2024Article
- The impact of integrated hepatitis B virus DNA on oncogenesis and antiviral therapy.Biomarker research · 2024Review
- Article
- Pregenomic RNA Launch Hepatitis B Virus Replication System Facilitates the Mechanistic Study of Antiviral Agents and Drug-Resistant Variants on Covalently Closed Circular DNA Synthesis.Journal of virology · 2022Article
- Hepatitis B Virus DNA Integration: In Vitro Models for Investigating Viral Pathogenesis and Persistence.Viruses · 2021Review
- DNA Engineering and Hepatitis B Virus Replication.Frontiers in microbiology · 2021Article
- Characterization of the Termini of Cytoplasmic Hepatitis B Virus Deproteinated Relaxed Circular DNA.Journal of virology · 2020Article
- Preclinical Profile and Characterization of the Hepatitis B Virus Core Protein Inhibitor ABI-H0731.Antimicrobial agents and chemotherapy · 2020Article
- Recent Advances in Understanding, Diagnosing, and Treating Hepatitis B Virus Infection.Microorganisms · 2020Review
- Hepatitis B Virus Virions Produced Under Nucleos(t)ide Analogue Treatment Are Mainly Not Infectious Because of Irreversible DNA Chain Termination.Hepatology (Baltimore, Md.) · 2020Article
- Mouse models for hepatitis B virus research.Laboratory animal research · 2018Review
- Hepatitis B virus: virology, molecular biology, life cycle and intrahepatic spread.Hepatology international · 2017Review
- Review
- Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle.Journal of visualized experiments : JoVE · 2017Article
- In Vitro Enzymatic and Cell Culture-Based Assays for Measuring Activity of HBV RNaseH Inhibitors.Methods in molecular biology (Clifton, N.J.) · 2017Article
- Core protein: A pleiotropic keystone in the HBV lifecycle.Antiviral research · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
For hepadnaviruses, the RNA primer for plus-strand DNA synthesis is generated by the final RNase H cleavage of the pregenomic RNA at an 11 nt sequence called DR1 during the synthesis of minus-strand DNA. This RNA primer initiates synthesis at one of two distinct sites on the minus-strand DNA template, resulting in two different end products; duplex linear DNA or relaxed circular DNA. Duplex linear DNA is made when initiation of synthesis occurs at DR1. Relaxed circular DNA, the major product, is made when the RNA primer translocates to the sequence complementary to DR1, called DR2 before initiation of DNA synthesis. We studied the mechanism that determines the site of the final RNase H cleavage in hepatitis B virus (HBV). We showed that the sites of the final RNase H cleavage are always a fixed number of nucleotides from the 5' end of the pregenomic RNA. This finding is similar to what was found previously for duck hepatitis B virus (DHBV), and suggests that all hepadnaviruses use a similar mechanism. Also, we studied the role of complementarity between the RNA primer and the acceptor site at DR2 in HBV. By increasing the complementarity, we were able to increase the level of priming at DR2 over that seen in the wild-type virus. This finding suggests that the level of initiation of plus-strand DNA synthesis at DR2 is sub-maximal for wild-type HBV. Finally, we studied the role of the sequence at the 5' end of the RNA primer that is outside of the DR sequence. We found that substitutions or insertions in this region affected the level of priming at DR1 and DR2.
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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.