ArticleThe Journal of clinical investigation2025
Transcription of hepatitis B surface antigen shifts from cccDNA to integrated HBV DNA during treatment.
Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed.
- Single-Cell Hepatitis B Sequencing Reveals Distinct Viral Infection Events Consistent With Superinfection.The Journal of infectious diseases · 2026Article
- Differential Hepatitis B Surface Antigen Glycan Isomer Kinetics Between Tenofovir Alafenamide and Entecavir: Hepatocellular Carcinoma Risk Stratification in Hepatitis B e Antigen-Positive Patients.Journal of viral hepatitis · 2026Article
- [Clinical significance and occurrence mechanism of hepatitis B virus DNA integration].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- A preS2 aa1-26-specific humoural response marks functional cure in chronic HBV infection.EBioMedicine · 2026Article
- Hepatitis B virus RNA and hepatitis B surface antigen kinetics predict treatment outcomes in children with chronic hepatitis B.Frontiers in cellular and infection microbiology · 2026Article
- Research Progress on Mechanisms of Immune Tolerance Induced by Hepatitis B Surface Antigen in Chronic HBV Infection.Journal of immunology research · 2026Review
- Review
- Beyond viral suppression: combining PEG-interferon with novel immunotherapies for functional cure of chronic hepatitis B.Frontiers in cellular and infection microbiology · 2026Review
- Exploratory analysis of lamivudine legacy and clonal selection of HBs truncation mutants in HBV-related hepatocellular carcinoma.Infectious agents and cancer · 2025Article
- The Role of Integrated HBV DNA in the Quest for a Cure in HIV/HBV co-infection.Current HIV/AIDS reports · 2025Review
- The Role of Liver Biopsy and Fine Needle Aspiration in Novel HBV Therapeutics in HIV and HBV Coinfection.Current HIV/AIDS reports · 2025Review
- Recurrence risk factors for chronic hepatitis B virus-infected patients who achieve functional cure with pegylated interferon-α-2b-based therapy: a multicenter pilot study.Virology journal · 2025Observational
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
The cornerstone of functional cure for chronic hepatitis B (CHB) is hepatitis B surface antigen (HBsAg) loss from blood. HBsAg is encoded by covalently closed circular DNA (cccDNA) and HBV DNA integrated into the host genome (iDNA). Nucleos(t)ide analogs (NUCs), the mainstay of CHB treatment, rarely lead to HBsAg loss, which we hypothesized was due to continued iDNA transcription despite decreased cccDNA transcription. To test this, we applied a multiplex droplet digital PCR that identifies the dominant source of HBsAg mRNAs to 3,436 single cells from paired liver biopsies obtained from 10 people with CHB and HIV receiving NUCs. With increased NUC duration, cells producing HBsAg mRNAs shifted their transcription from chiefly cccDNA to chiefly iDNA. This shift was due to both a reduction in the number of cccDNA-containing cells and diminished cccDNA-derived transcription per cell; furthermore, it correlated with reduced detection of proteins deriving from cccDNA but not iDNA. Despite this shift in the primary source of HBsAg, rare cells remained with detectable cccDNA-derived transcription, suggesting a source for maintaining the replication cycle. Functional cure must address both iDNA and residual cccDNA transcription. Further research is required to understand the significance of HBsAg when chiefly derived from iDNA.
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.