Ontology highlight
ABSTRACT:
PROVIDER: PRJNA916626 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
Project description:The natural history of chronic hepatitis B virus (HBV) infection could be divided in different phases by transaminase and HBV replication levels. However, it remains unknown how the intrahepatic transcriptomes in patients are correlated with the clinical phases. Here, we determined the intrahepatic transcriptomes of chronic hepatitis B patients and examined the role of specific groups of genes, including immune-related genes, in the control of hepatitis B virus infection.
2016-03-31 | GSE65359 | GEO
Project description:To identify gene biomarkers for different phases of chronic HBV infection, we performed RNA-seq of CD14+ monocytes from pateints in each of the phases, which was then analyzed for differntial gene expression and validated by qRT-PCR in individual samples
2024-08-28 | GSE217459 | GEO
Project description:Hepatitis B virus (HBV)-specific CD8+ T cells play a dominant role during acute-resolving HBV infection but are functionally impaired during chronic HBV infection in humans. These functional deficits have been linked with metabolic and phenotypic heterogeneity, but it has remained unclear to what extent different subsets of HBV-specific CD8+ T cells still suppress viral replication. We addressed this issue by deep profiling, functional testing and perturbation of HBV-specific CD8+ T cells during different phases of chronic HBV infection. Our data revealed a mechanism of effector CD8+ T cell attenuation that emerges alongside classical CD8+ T cell exhaustion. Attenuated HBV-specific CD8+ T cells were characterized by cytotoxic properties and a dampened effector differentiation program, determined by antigen recognition and TGFβ signaling, and were associated with viral control during chronic HBV infection. These observations identify a distinct subset of CD8+ T cells linked with immune efficacy in the context of a chronic human viral infection with immunotherapeutic potential.
2024-07-01 | GSE259231 | GEO
Project description:Hepatitis B Virus (HBV) is a small DNA virus that replicates via an episomal covalently closed circular DNA (cccDNA) that serves as the transcriptional template for viral mRNAs. The host protein, CCCTC-binding factor (CTCF), is a key regulator of cellular transcription by maintaining epigenetic boundaries, nucleosome phasing, stabilisation of long-range chromatin loops and directing alternative exon splicing. We previously reported that CTCF binds two conserved motifs within Enhancer I of the HBV genome and represses viral transcripts, however, the underlying mechanisms were not identified. We show that CTCF depletion in cells harbouring cccDNA-like HBV molecules and in de novo infected cells resulted in an increase in spliced transcripts, which was most notable in the abundant SP1 spliced transcript. In contrast, depletion of CTCF in cell lines with integrated HBV DNA had no effect on the abundance of viral transcripts and in line with this observation there was limited evidence for CTCF binding to viral integrants, suggesting that CTCF-regulation of HBV transcription is specific to episomal cccDNA. Analysis of HBV chromatin topology by Assay for Transposase Accessibility/sequencing (ATAC-Seq) revealed an accessible region spanning Enhancers I and II and the basal core promoter (BCP). Mutating the CTCF binding sites within Enhancer I resulted in a dramatic rearrangement of chromatin accessibility where the open chromatin region was no longer detected, indicating loss of the phased nucleosome up- and down- stream of the HBV enhancer/BCP. These data demonstrate that CTCF functions to regulate HBV chromatin conformation and nucleosomal positioning in episomal maintained cccDNA, which has important consequences for HBV transcription regulation.
2024-01-18 | GSE248738 | GEO
Project description:Hepatitis B Virus (HBV) is a small DNA virus that replicates via an episomal covalently closed circular DNA (cccDNA) that serves as the transcriptional template for viral mRNAs. The host protein, CCCTC-binding factor (CTCF), is a key regulator of cellular transcription by maintaining epigenetic boundaries, nucleosome phasing, stabilisation of long-range chromatin loops and directing alternative exon splicing. We previously reported that CTCF binds two conserved motifs within Enhancer I of the HBV genome and represses viral transcripts, however, the underlying mechanisms were not identified. We show that CTCF depletion in cells harbouring cccDNA-like HBV molecules and in de novo infected cells resulted in an increase in spliced transcripts, which was most notable in the abundant SP1 spliced transcript. In contrast, depletion of CTCF in cell lines with integrated HBV DNA had no effect on the abundance of viral transcripts and in line with this observation there was limited evidence for CTCF binding to viral integrants, suggesting that CTCF-regulation of HBV transcription is specific to episomal cccDNA. Analysis of HBV chromatin topology by Assay for Transposase Accessibility/sequencing (ATAC-Seq) revealed an accessible region spanning Enhancers I and II and the basal core promoter (BCP). Mutating the CTCF binding sites within Enhancer I resulted in a dramatic rearrangement of chromatin accessibility where the open chromatin region was no longer detected, indicating loss of the phased nucleosome up- and down- stream of the HBV enhancer/BCP. These data demonstrate that CTCF functions to regulate HBV chromatin conformation and nucleosomal positioning in episomal maintained cccDNA, which has important consequences for HBV transcription regulation.
2024-01-18 | GSE249278 | GEO
Project description:Histone 3 lysine 9 acetylation (H3K9ac) at transcription initiation sites is a well known marker for actively initiating and transcribing genes.The purpose of the present study was to investigate the association between H3K9ac and diverse progress of HBV infection. We employed chromatin immunoprecipitation microarray (ChIP-chip) technology to profile and compare the variations of genes H3K9ac in CD4 T cells of the CHB patients at the different clinic phases. The results showed there were lots of different genes with H3K9ac among the study groups. Comparison of genomic H3K9ac status in CD4 T cells from CHB patients at the different clinic phases
2012-08-28 | E-GEOD-40365 | biostudies-arrayexpress
Project description:Viruses employ various strategies to evade innate immunity. Despite many studies on host or viral gene expression, how the cellular proteome responds to internal or external cues, has not been fully investigated. Using a Hepatitis B Virus (HBV) replication model, we performed proteomic analyses of HBV-replicating cells in G1/S and G2/M phases, as a function of IFN-alpha, providing specific information of how HBV infection, in combination with IFN-alpha, alters the hepatocyte proteome. We identified the conserved LSm (Like-Sm1-8) proteins were differentially expressed as a function of HBV replication and IFN-alpha. Specifically, in G2/M, IFN-alpha increased protein level of LSm1, the unique subunit of cytoplasmic LSm1-7 complex involved in mRNA decay. By contrast, IFN-alpha decreased LSm8, the unique subunit of nuclear LSm2-8 complex, a chaperone of U6 spliceosomal RNA. These results suggest cytoplasmic LSm1-7 has antiviral role, whereas nuclear LSm2-8 complex is pro-viral. Employing HBV replication and infection models, siRNA-mediated knockdown of LSm1 increased the level of all viral RNAs. Conversely, knockdown of LSm8 reduced viral RNA levels, dependent on N6-adenosine methylation (m6A) of the epsilon stem-loop at the 5 end of pre-Core/pregenomic (preC/pg) RNA. Methylated RNA immunoprecipitation (MeRIP) assays demonstrated reduced viral RNA methylation upon LSm8 knockdown, dependent on the m6A modification, suggesting the LSm2-8 complex has a role in mediating this modification. Interestingly, splicing inhibitor Cp028 acting upstream of LSm2-8 complex, suppressed levels of viral RNAs without reducing the m6A modification. This observation suggests Cp028 has novel antiviral effects, likely potentiating IFN-alpha -mediated suppression of HBV biosynthesis.
2022-06-03 | MSV000089600 | MassIVE
Project description:Gene expression of CD14+ peripheral blood monocytes in different phases of chronic HBV infection
| PRJNA899046 | ENA