ReviewACS infectious diseases2019
Virological Basis for the Cure of Chronic Hepatitis B.
Review in ACS infectious diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 57 citations in OpenAlex.
- 4-Diketopyrrole-2-carboxamide derivatives affecting HBV capsid assembly: structure-activity relationship around the GLP-26 scaffold.Organic & biomolecular chemistry · 2026Article
- A visible assay for evaluating the inhibitory activity of drug and antibody against HBV infection.Microbiology spectrum · 2026Article
- MAFLD is linked to lower HBV DNA levels in chronic hepatitis B: clinical and transcriptomic insights.Frontiers in medicine · 2026Article
- Triterpenoids CDDO and CDDO-EA Inhibit the Replication of Hepatitis B Virus by Modulating Nucleocapsid Assembly.International journal of molecular sciences · 2025Article
- Antiviral and immune modulatory activities of STING agonists in a mouse model of persistent hepatitis B virus infection.PLoS pathogens · 2025Article
- Utility of Serum HBV RNA Measurement During Nucleoside/Nucleotide Analog Therapy in Chronic Hepatitis B Patients.International journal of molecular sciences · 2025Article
- HBV capsid assembly modulators differentially modulate the assembly of wild-type and drug-resistant core protein chimeric nucleocapsids and empty capsids.PLoS pathogens · 2025Article
- Article
- Unveiling the Molecular Architecture of HBV Spherical Subviral Particles: Structure, Symmetry, and Lipid Dynamics.Viruses · 2024Review
- Article
- Novel Approaches to Inhibition of HBsAg Expression from cccDNA and Chromosomal Integrants: A Review.Journal of clinical and translational hepatology · 2023Review
- Identification of novel tetrahydroquinoxaline derived phenyl ureas as modulators of the hepatitis B virus nucleocapsid assembly.European journal of medicinal chemistry · 2023Article
- Liver Cell Type-Specific Targeting by Nanoformulations for Therapeutic Applications.International journal of molecular sciences · 2023Review
- Heat Shock Protein Family A Member 1 Promotes Intracellular Amplification of Hepatitis B Virus Covalently Closed Circular DNA.Journal of virology · 2023Article
- Dual role of neddylation in transcription of hepatitis B virus RNAs from cccDNA and production of viral surface antigen.JHEP reports : innovation in hepatology · 2022Article
- Identification of STAU1 as a regulator of HBV replication by TurboID-based proximity labeling.iScience · 2022Article
- PRKDC promotes hepatitis B virus transcription through enhancing the binding of RNA Pol II to cccDNA.Cell death & disease · 2022Article
- 4-Oxooctahydroquinoline-1(2H)-carboxamides as hepatitis B virus (HBV) capsid core protein assembly modulators.Bioorganic & medicinal chemistry letters · 2022Article
- Novel Therapies of Hepatitis B and D.Microorganisms · 2021Review
- Hepatitis B virus nucleocapsid uncoating: biological consequences and regulation by cellular nucleases.Emerging microbes & infections · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Hepatitis B virus (HBV) has infected one-third of world population, and 240 million people are chronic carriers, to whom a curative therapy is still not available. Similar to other viruses, persistent HBV infection relies on the virus to exploit host cell functions to support its replication and efficiently evade host innate and adaptive antiviral immunity. Understanding HBV replication and concomitant host cell interactions is thus instrumental for development of therapeutics to disrupt the virus-host interactions critical for its persistence and cure chronic hepatitis B. Although the currently available cell culture systems of HBV infection are refractory to genome-wide high throughput screening of key host cellular factors essential for and/or regulating HBV replication, classic one-gene (or pathway)-at-a-time studies in the last several decades have already revealed many aspects of HBV-host interactions. An overview of the landscape of HBV-hepatocyte interaction indicates that, in addition to more tightly suppressing viral replication by directly targeting viral proteins, disruption of key viral-host cell interactions to eliminate or inactivate the covalently closed circular (ccc) DNA, the most stable HBV replication intermediate that exists as an episomal minichromosome in the nucleus of infected hepatocyte, is essential to achieve a functional cure of chronic hepatitis B. Moreover, therapeutic targeting of integrated HBV DNA and their transcripts may also be required to induce hepatitis B virus surface antigen (HBsAg) seroclearance and prevent liver carcinogenesis.
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.