Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hepatitis B virus

ABSTRACT: Kinetics of Hepatitis B surface antigen (HBsAg) quasispecies during REP2139-Ca therapy in HBeAg+ chronic HBV infection

PROVIDER: PRJNA478149 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7535310_1.fastq.gz	Fastqsanger.gz
	SRR7535310_2.fastq.gz	Fastqsanger.gz
	SRR7535320_1.fastq.gz	Fastqsanger.gz
	SRR7535320_2.fastq.gz	Fastqsanger.gz
	SRR7535330_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 71

Similar Datasets

Smart-seq for HBs-specific CD8+ T cells sorted from C57BL/6 mice and C57BL/6-Tg (HBV Alb-1) Bri44 HBV transgenic mice liver

Project description:Previous studies have paid more attention to hepatitis B e antigen (HBeAg) intrauterine exposure, however the effect of solely hepatitis B surface antigen (HBsAg) exposure on the immune response of offspring against hepatitis B virus (HBV) is still unclear. In this study, we investigated whether HBsAg intrauterine exposure affected the offspring's immune response against HBV and the relevant mechanism, which is important for the prevention of HBV mother-to-infant transmission.

2021-12-01 | GSE162718 | GEO

Characterization of Hepatitis B Virus Transcripts in Chronically HBV-infected Chimpanzees and Patients Treated with ARC-520 siRNA Demonstrates Transcriptional Silencing of cccDNA

Project description:Full-length hepatitis B virus (HBV) transcripts of chimpanzees and patients treated with multidose (MD) HBV siRNA ARC-520 and entecavir (ETV) were characterized by single-molecule real-time (SMRT) sequencing, identifying multiple types of transcripts with the potential to encode HBx, HBsAg, HBeAg, core, and polymerase, as well as transcripts likely to be derived from dimers of dslDNA, and these differed between HBeAg-positive (HBeAg+) and HBeAg-negative (HBeAg−) individuals. HBV transcripts from the last follow-up ~30 months post-ARC-520 treatment were categorized from one HBeAg+ (one of two previously highly viremic patients that became HBeAg− upon treatment and had greatly reduced cccDNA products) and four HBeAg− patients. The previously HBeAg+ patient received a biopsy that revealed that he had 3.4 copies/cell cccDNA (two to three orders of magnitude more cccDNA than HBeAg− chimpanzees) but expressed primarily truncated X and HBsAg from iDNA, like two patients that were HBeAg− at the start of the study and had one copy/cell cccDNA. No HBV transcripts were detected in two other HBeAg− patients that had ~0.3 copies/cell cccDNA, one of which had seroconverted for HBsAg. The paucity of cccDNA-derived transcripts in the presence of high cccDNA demonstrates the transcriptional silencing of HBV following MD siRNA treatment with ETV.

2024-12-17 | GSE279971 | GEO

Spatial transcriptomics reveals a low extent of transcriptionally active hepatitis B virus integration in patients with HBsAg loss

Project description:Hepatitis B virus (HBV) can integrate into the chromosomes of infected hepatocytes, contributing to the production of hepatitis B surface antigen (HBsAg) and to hepatocarcinogenesis. We performed spatial transcriptomics to investigate the intrahepatic cell heterogeneity and the spatial distribution of transcriptionally active HBV integration events in different phases of chronic HBV infection. Our analysis revealed that transcriptionally active HBV integration occurred in chronically HBV-infected patients in different phases, including those patients with HBsAg loss, and antiviral treatment was associated with a decreased number and extent of viral integrations.

2023-09-30 | GSE243367 | GEO

The immune landscape and mechanism of hepatitis B virus surface antigen clearance [CITEseq]

Project description:Hepatitis B virus (HBV) surface antigen (HBsAg) clearance constitutes the hallmark of resolution of acute infection and is a therapeutic goal for functional cure of chronic hepatitis B. Here, we reveal the immunological landscape and mechanism of HBsAg clearance in mice. After acquiring nonopsonized HBsAg, B cells prime CD4+ T cell responses by CCR5- and EBI2-guided interaction with CD4+ T cells at follicular and interfollicular regions, respectively. Monocyte-derived macrophages transport complement-opsonized HBsAg to follicular dendritic cells (FDCs) to maintain germinal center reaction. Batf3+ XCR1+ conventional type 1 DCs (cDC1s) acquire and present HBsAg by MHC-I cross-dressing to drive CD8+ T cell responses in liver. We map the antigen-presenting cell (APC)-T cell crosstalk landscape and identify key costimulatory signals. The immune responses in patients with acute HBV infection are revealed by a single-cell transcriptome atlas. These findings revolutionize our understanding of anti-HBV immune responses and would lead to immunotherapeutic strategies for HBsAg clearance.

2024-07-01 | GSE207541 | GEO

The immune landscape and mechanism of hepatitis B virus surface antigen clearance [RNA-Seq]

2024-07-01 | GSE207539 | GEO

Association of HBsAg levels with differential gene expression in NK, CD8 T, and memory B cells in treated patients with chronic HBV

Project description:Hepatitis B surface antigen (HBsAg) secretion may impact the immune response in chronic hepatitis B virus (HBV) infection. Therapeutic approaches to suppress HBsAg production are being investigated. Our study aims to examine the immunomodulatory effects of high and low levels of circulating HBsAg by analyzing single-cell RNA sequencing data (scRNAseq) from blood and liver fine-needle aspirates (FNA). This will help to better understand anti-HBV immunity.

2024-01-01 | GSE247322 | GEO

Clinical cure of chronic hepatitis B is dependent on activation and perpetuation of a robust CD4+ T cell response

Project description:Hepatitis B virus (HBV) is a major global pathogen that often leads to immune-mediated progressive liver injury and liver cancer. While seroclearance of the surface antigen (HBsAg) defines clinical cure and reduces disease-associated risks, HBsAg clearance is rarely observed and remains therapeutically elusive. Here we overcome some of the challenges to studying immune mechanisms of HBsAg clearance in chronic hepatitis B (CHB) using our mouse model of age-dependent HBsAg clearance and persistence, and samples from our BeNEG-DO trial that provided longitudinal PBMCs from patients who either cleared HBsAg or retained stable HBsAg levels after stopping nucleos(t)ide analog therapy. We show that young mice fail to clear HBsAg and have an impaired ability to efficiently initiate and sustain an HBV-specific CD4+ T cell response. We also demonstrate a role for CD4+ T cells in hepatic leukocyte organization, HBV-specific CD8+ T cell cytotoxicity, and ultimately HBsAg clearance. Upstream of the CD4+ T cell response, we reveal that hepatic dendritic cells, particularly cDC2s, direct effective CD4+ T cell activation and differentiation. Studies in CHB patients identified immune features of HBsAg clearance that overlap with the mouse model, including Th1 and cytotoxic CD4+ T cell activation and CD8+ T cell cytotoxic effector function. These findings identify an important role for potent CD4+ T cell activation in the clinical cure of CHB, and illuminate potential immunotherapeutic targets for enhancing CD4+ T cell responses to achieve greater HBsAg clearance rates.

2026-04-29 | GSE291286 | GEO

Development of an Optimized Epigenetic Silencer to Transcriptionally Inactivate Viral DNA in Chronic Hepatitis B [HybridCaptureMethylseq]

Project description:Approved chronic hepatitis B (CHB) therapies rarely result in functional cure, as they fail to permanently silence all transcriptionally active hepatitis B virus (HBV) DNA. CRMA-1001 employs an optimized epigenetic silencer that represses viral transcription through targeted deposition of DNA methylation on episomal and integrated HBV DNAs. In HBV mouse models, a single dose of CRMA-1001 produced >3 log10 reductions in viral biomarkers, which correlated with de novo methylation of HBV DNA. Three doses resulted in up to 90% of animals with undetectable hepatitis B surface antigen (HBsAg) and HBV DNA by 6 months post-treatment. In non-human primates, CRMA-1001 induced transient liver transaminase elevations only at the highest dose tested. Expression and DNA methylation profiling revealed no detectable unintended targets in the human genome. These findings support the initiation of clinical development of CRMA-1001 as a finite treatment course with the potential for functional cure in individuals living with CHB.

2026-06-28 | GSE318226 | GEO

Development of an Optimized Epigenetic Silencer to Transcriptionally Inactivate Viral DNA in Chronic Hepatitis B [RNAseq]

2026-06-28 | GSE318225 | GEO

Development of an Optimized Epigenetic Silencer to Transcriptionally Inactivate Viral DNA in Chronic Hepatitis B [NHPAmpliconBisulfiteseq]

2026-06-28 | GSE319072 | GEO