Hepatitis B virus
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR121861.fastq.gz | Fastqsanger.gz | |||
| DRR121862.fastq.gz | Fastqsanger.gz | |||
| DRR121863.fastq.gz | Fastqsanger.gz | |||
| DRR121864.fastq.gz | Fastqsanger.gz | |||
| DRR121865.fastq.gz | Fastqsanger.gz |
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Project description:Hepatitis B virus (HBV) infection could cause hepatitis, liver cirrhosis and hepatocellular carcinoma. HBV-mediated pathogenesis is only partially understood, but X protein (HBx) reportedly possesses oncogenic potential. Exosomes are small membrane vesicles with diverse functions released by various cells including hepatocytes, and HBV harnesses cellular exosome biogenesis and export machineries for virion morphogenesis and secretion. Therefore, HBV infection might cause changes in exosome contents with functional implications for both virus and host. In this project, exosome protein content changes induced by HBV and HBx were quantitatively analyzed by SILAC/LC-MS/MS. Exosomes prepared from SILAC-labeled hepatoma cell line Huh-7 transfected with HBx, wildtype or HBx-null HBV replicon plasmids were analyzed by LC-MS/MS.
2014-10-09 | PXD001339 | Pride
Project description:<p>BACKGROUND: The pathological and physiological characteristics between HBsAg-positive HBV infection and occult hepatitis B infection (OBI) are currently unclear. This study aimed to explore the immune microenvironment in the peripheral circulation of OBI patients through integration of proteomic and metabolomic sequencing, and to identify molecular biomarkers for clinical diagnosis of HBsAg-positive HBV and OBI.</p><p>METHODS: This research involved collection of plasma from 20 patients with OBI (negative for HBsAg but positive for HBV DNA, with HBV DNA levels < 200 IU/mL), 20 patients with HBsAg-positive HBV infection and 10 healthy individuals. Mass spectrometry-based detection was used to analyze the proteome, while nuclear magnetic resonance spectroscopy was employed to study the metabolomic phenotypes. Differential molecule analysis, pathway enrichment and functional annotation, as well as weighted correlation network analysis (WGCNA), were conducted to uncover the characteristics of HBV-related liver disease. Prognostic biomarkers were identified using machine learning algorithms, and their validity was confirmed in a larger cohort using enzyme linked immunosorbent assay (ELISA).</p><p>RESULTS: HBsAg-positive HBV individuals showed higher age and ALT levels (p=0.010) when compared to OBI patients. The influence of HBV infection on metabolic functions and inflammation was evident through the analysis of distinct metabolic pathways in HBsAg-positive HBV and OBI groups. Tissue tracing demonstrated a connection between Kupffer cells and HBsAg-positive HBV infection, as well as between hepatocytes and OBI. Immune profiling revealed the correlation between CD4 Tem cells, memory B cells and OBI, enabling a rapid response to infection reactivation through cytokine secretion and antibody production.</p>
2024-11-05 | MTBLS11406 | MetaboLights
Project description:Hepatitis B virus (HBV) infection could cause hepatitis, liver cirrhosis and hepatocellular carcinoma. HBV-mediated pathogenesis is only partially understood, but X protein (HBx) reportedly possesses oncogenic potential. Exosomes are small membrane vesicles with diverse functions released by various cells including hepatocytes, and HBV harnesses cellular exosome biogenesis and export machineries for virion morphogenesis and secretion. Therefore, HBV infection might cause changes in exosome contents with functional implications for both virus and host. In this project, exosome protein content changes induced by HBV and HBx were quantitatively analyzed by SILAC/LC-MS/MS. Exosomes prepared from SILAC-labeled hepatoma cell line Huh-7 transfected with HBx, wildtype or HBx-null HBV replicon plasmids were analyzed by LC-MS/MS.
2017-03-29 | MSV000080794 | MassIVE
Project description:Hepatitis B virus (HBV) infection is a major health problem worldwide. Recent evidence suggests that various viruses can manipulate the infection process by secretion of specific viral and cellular components into exosomes, small nanometer-sized (30-150 nm) vesicles secreted from various cells. However, the impact of HBV replication on hepatocytes produced exosomes has not been fully delineated. In this work, an HBV-inducible cell line HepAD38 was used to directly compare changes in the protein content of exosomes secreted from HepAD38 cells with or without HBV replication. Exosomes were isolated from conditioned medium of HepAD38 cell cultures and the purity of exosomes were confirmed by transmission electron microscopy (TEM) and Western immunoblotting assays. Ion-intensity based label-free LC−MS/MS quantitation technologies were applied to analyze protein content of HBV-exosomes and HBV-free-exosomes. A total of 1412 exosomal proteins were identified, in which the abundance of 35 proteins were significantly altered. Strikingly, 5 subunit proteins from the 26S proteasome complex, including PSMC1, PSMC2, PSMD1, PSMD7 and PSMD14 were consistently enhanced in HBV-exosomes. Bioinformatic analysis of differential exosomal proteins revealed the significant enrichment of components involved in proteasomal catabolic process. Proteasome activity assays further suggested that HBV-exosomes had enhanced proteolytic activity compared to HBV-free-exosomes. Furthermore, Human peripheral monocytes incubated with HBV-exosomes induced a significant lower level of IL-6 secretion compared to HBV-free-exosomes. Irreversible inhibition of proteasomal activity within exosome restored the IL-6 induction in monocytes. These results suggest that transmission of proteasome subunit proteins by HBV-exosomes might modulate the innate sensing of pro-inflammatory molecules in the recipient monocytes. These results revealed the composition and potential function of exosomes produced during HBV replication, thus provide a new perspective on the role of exosomes in HBV-host interaction.
2017-03-01 | PXD004724 | Pride
Project description:Hepatitis B virus (HBV) infection is a major health problem worldwide. Recent evidence suggests that various viruses can manipulate the infection process by secretion of specific viral and cellular components into exosomes, small nanometer-sized (30-150 nm) vesicles secreted from various cells. However, the impact of HBV replication on hepatocytes produced exosomes has not been fully delineated. In this work, an HBV-inducible cell line HepAD38 was used to directly compare changes in the protein content of exosomes secreted from HepAD38 cells with or without HBV replication. Exosomes were isolated from conditioned medium of HepAD38 cell cultures and the purity of exosomes were confirmed by transmission electron microscopy (TEM) and Western immunoblotting assays. Ion-intensity based label-free LC?MS/MS quantitation technologies were applied to analyze protein content of HBV-exosomes and HBV-free-exosomes. A total of 1412 exosomal proteins were identified, in which the abundance of 35 proteins were significantly altered. Strikingly, 5 subunit proteins from the 26S proteasome complex, including PSMC1, PSMC2, PSMD1, PSMD7 and PSMD14 were consistently enhanced in HBV-exosomes. Bioinformatic analysis of differential exosomal proteins revealed the significant enrichment of components involved in proteasomal catabolic process. Proteasome activity assays further suggested that HBV-exosomes had enhanced proteolytic activity compared to HBV-free-exosomes. Furthermore, Human peripheral monocytes incubated with HBV-exosomes induced a significant lower level of IL-6 secretion compared to HBV-free-exosomes. Irreversible inhibition of proteasomal activity within exosome restored the IL-6 induction in monocytes. These results suggest that transmission of proteasome subunit proteins by HBV-exosomes might modulate the innate sensing of pro-inflammatory molecules in the recipient monocytes. These results revealed the composition and potential function of exosomes produced during HBV replication, thus provide a new perspective on the role of exosomes in HBV-host interaction.
2017-03-29 | MSV000080718 | MassIVE
Project description:Human SNU cell lines derived from hepatocellular carcinomas associated with chronic hepatitis B virus (HBV) infection were examined. The analysis of intracellular RNA and DNA markers of HBV replication and examination of HBV RNA reads coverage of selected regions on HBV-related RNAs and polyadenylation positions within HBV sequence using RNA-sequencing suggested absence of HBV replication in SNU-423, SNU-368 SNU-398, SNU-182, SNU-449, SNU-475, SNU-354, SNU-739 and SNU-387 cells, while SNU-761 and SNU-886 still could maintain residual HBV replication. The undetectable intracellular HBV core antigen (HBcAg) and absence of significant levels of secreted core-associated and virion-associated HBV DNA confirmed the absence or profound suppression of HBV replication in parental SNU cell lines. Various 5'-human-HBV-3' and 5'-HBV-human-3' RNAs transcribed from integrated HBV DNA were found in most of SNU cell lines. The 5'-HBV-human-3' junctions suggested that several SNU cell lines could generate 5'-HBV-human-3' RNAs encoding HBV envelope proteins. The known and novel spliced HBV RNAs were detected in SNU-886, SNU-739, SNU-387, SNU-761, and SNU-354 cells. At least some of them were generated independently of HBV replication. All SNU cell lines could not support efficient HBV replication after transfection with the vector initiating efficient HBV replication in Huh7 cells. This was reflected by three distinct accumulation patterns of HBV replication markers, undetectable intracellular HBcAg, and by the lack of considerable levels of secreted core-bound and virion-associated HBV DNA. Overall, SNU cell lines represent valuable model systems for detailed analysis of integrant-transcribed HBV RNAs, spliced HBV RNAs, and mechanisms of suppression of HBV genome replication.
2025-09-15 | GSE298154 | GEO
Project description:The low frequency of HBV-specific CD8+ T cells in the peripheral blood of CHB patients has limited studies of the mechanisms underlying HBV-induced T cell exhaustion. Similar to the expansion defect displayed in HBV-specific CD8+ T cells, TCR-induced proliferation of global CD8+ T cells is impaired in a fraction of chronic HBV (CHB) patients. Thus, examining the molecular regulation of global CD8+ T cell function in CHB patients may provide insight into the exhaustion of HBV-specific CD8+ T cells. We used microarrays to detail the global programme of gene expression of CD8 T cells from CHB patients who have not received anti-viral treatment. Fifteen milliliters of blood was drawn from eachof three CHB patients and three healthy donors. PBMCs were enriched using Ficoll, and CD8+ T cells were purified using positive selection beads to a purity of >95% (Miltenyi Biotec, Auburn, CA). Total RNA was extracted using a mirVana isolation kit (Life Technologies, Carlsbad, CA).
2016-07-01 | E-GEOD-51489 | biostudies-arrayexpress
Project description:HBV Episomal Variants after CRISPR-Cas9 Editing
| PRJEB51625 | ENA
Project description:Viral infection leads to heterogeneous cellular outcomes ranging from resistance to virion amplification and cell death. In this study, we apply single-cell techniques to analyze diverse fate trajectories during Epstein-Barr virus (EBV) lytic reactivation in three B cell models. We expand upon the previous finding that c-Myc regulates lytic reactivation and determine that MYC downregulation during the lytic phase is correlated with a loss of germinal center (GC) B cell expression signatures. Consistent with prior work, lytic induction yields both abortive and complete reactivation. Abortive lytic cells, which express high STAT3 and initiate but do not complete the lytic cycle, also upregulate NF-kB and IRF3 pathway target genes. Cells that proceeded through the full lytic cycle exhibited unexpected and striking expression of genes associated with cellular reprogramming, developmental progenitor phenotypes, and cytokine upregulation. Distinct subpopulations of lytic cells further displayed variable profiles for transcripts known to escape virus-mediated host shutoff. These data reveal previously unknown and promiscuous outcomes of lytic reactivation with broad implications for viral replication and EBV-associated oncogenesis.
2024-10-31 | GSE272763 | GEO
Project description:Hepatitis B virus (HBV) infection is a globally significant threaten to global health, with the potential to progress to hepatitis and hepatocellular carcinoma (HCC). Despite the availability of a vaccine, a population with non-responders, emphasizing the need for continued research into HBV-mediated immune responses. Interleukin-33 (IL-33) has emerged as a pivotal player in chronic inflammation and cancer, yet its role in specific viral contexts remains elusive. Here, we demonstrate the immune mechanisms underlying HBV infection and its contribution to HCC development. HBV with liver carcinogens induced IL-33 expression. Utilizing IL-33 and ST2 knockout mice, we demonstrate impaired HBV- mediated tumor progression, highlighting the critical involvement of IL-33 axis. Furthermore, we identify ST2 positive regulatory T cells (Treg) is a major effector cells with IL-33 in HBV-infected mice. ST2-deficient Tregs triggers immune cell infiltration, accompanied by reduced expression of immunosuppressive cytokines such as IL-10. Blocking this axis with STATIN, IL-33 inhibitor, shows promise therapeutic drug in chronic hepatitis and HCC in human subjects. In conclusion, our study reveals that IL-33/Treg axis as a critical mediator in hepatitis and its cancer development.
2025-05-14 | GSE269528 | GEO