ArticleNature communications2025
Episomal and integrated hepatitis B transcriptome mapping uncovers heterogeneity with the potential for drug-resistance.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Peripheral Biomarkers in Chronic Hepatitis D Infection: A Review.Journal of viral hepatitis · 2026Review
- [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 key role for the exoribonuclease XRN1 in regulating the hepatitis B viral transcriptome.iScience · 2026Article
- A preS2 aa1-26-specific humoural response marks functional cure in chronic HBV infection.EBioMedicine · 2026Article
- HBx-Associated Reactivation of the IGF2 Locus in Chronic HBV Infection and HBV-Related Hepatocarcinogenesis: Evidence Boundaries and Biomarker Implications.Biomedicines · 2026Review
- HBV HBx protein masks epigenetic reader Spindlin1 via an inter-molecular zinc finger to subvert transcriptional control.Nature communications · 2026Article
- Article
- Veterinary Herpesviruses: Experimental Tools for Transcriptomics and Neuroscience.Veterinary sciences · 2026Review
- Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Hepatitis B virus (HBV) is a small DNA virus that establishes chronic infection and drives progressive liver disease and cancer; presenting a global health problem with more than 250 million infections. HBV replicates via an episomal covalently-closed-circular DNA (cccDNA) and integrated viral DNA fragments are linked to carcinogenesis. Current treatments only suppress HBV replication and there is a global initiative to develop genome targeting therapies, including siRNAs, antisense oligonucleotides and epigenetic modifiers specific for HBV cccDNA. However, our knowledge of the cccDNA and integrant transcriptomes is confounded by overlapping viral RNAs. Using targeted long-read sequencing we mapped the HBV transcriptome in liver biopsies from eleven treatment naïve patients. Probe enrichment yielded robust sequencing libraries and identified cccDNA-derived genomic and sub-genomic transcripts, and a repertoire of previously uncharacterised spliced, truncated and chimeric viral RNAs. Assigning viral transcripts to their respective DNA templates revealed differential promoter activity in cccDNA and integrants, with implications for the efficacy of epigenetic modifiers. Integrant-derived transcripts showed vast diversity in the viral-host junctions, posing a challenge for current nucleotide-targeting therapies. cccDNA was a source of genetic polymorphism, with distinct viral lineages present in the surface antigen encoding region, providing an insight into hepadnavirus evolution during chronic infection.
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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.