M-HBsAg
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB36242 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:CLONING OF RECOMBINANT PLASMIDS pPIC3.5-S AND pPIC9-S ENCODING THE S REGION OF THE HUMAN HEPATITIS B VIRUS (HBV)
| PRJEB36259 | ENA
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: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
Project description:Hepatitis B virus (HBV) is an enveloped, coated, non-cytopathic and hepatotropic partially double-stranded DNA virus in the family Hepadnaviridae genus Orthohepadnavirus. Despite significant progress in the availability of safe vaccines and antiviral therapies against HBV, it still affects approximately 257 million people worldwide and is responsible for about 887,000 deaths per year around the world [4]. HBV infection, which are associated with acute and chronic liver failure responses to viruses attacked the liver, can result in inactive carrier state, chronic hepatitis, or fulminant hepatitis and put them at high risk to develop advanced liver fibrosis and cirrhosis, and even hepatocellular cancer. Many viral factors, which could affect the disparity of clinical outcomes or disease prognosis during chronic HBV infection, have been reported in previous studies; among them, the viral genotype, as well as HBV mutations ascribing the virus to a certain phenotype, was reported to be the most important factor influencing viral pathogenesis, including the change of host immune recognition, the enhanced virulence with increased HBV replication and the facilitation of cell attachment or penetration.
2022-02-17 | PXD025968 | Pride
Project description:Here, we examined the host response relative of SACC-PHHs infected with either hepatitis B virus (HBV) alone or both HBV/hepatitis delta virus (HDV) co-infection compared to non-infected controls.
2019-06-18 | GSE112118 | GEO
Project description:We applied small RNA Solexa sequencing technology to identify microRNA expression in human liver samples from surgically removed liver tissues including three normal liver tissues (distal normal liver tissue of liver hemangioma), an hepatitis B virus (HBV)-infected liver, a severe chronic hepatitis B liver, two HBV-related hepatocellular carcinoma (HCC), an hepatitis C virus (HCV)-related HCC, and an HCC without HBV or HCV infection. All samples were collected with the informed consent of the patients and the experiments were approved by the ethics committee of Second Military Medical University, Shanghai, China. We investigated the miRNome in human normal liver and suggested some deregulated abundantly expressed microRNAs in HCC. center_name: National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, China. Examination of miRNome in human liver samples from surgically removed liver tissues including three normal liver tissues (distal normal liver tissue of liver hemangioma), an hepatitis B virus (HBV)-infected liver tissue, a severe chronic hepatitis B liver tissue, an HBV-related hepatocellular carcinoma (HCC) tissue and adjacent liver tissues of different regions,an HBV-related HCC tissue and adjacent liver tissue, an hepatitis C virus (HCV)-related HCC tissue and adjacent liver tissue, and an HCC without HBV or HCV infection and adjacent liver tissue. All 15 human liver tissue samples.
2010-04-10 | E-GEOD-21279 | biostudies-arrayexpress
Project description:Background and Aims: Whether hepatitis B virus (HBV) could play a direct role in hepatocarcinogenesis remains uncertain. The 3' end nonsense mutations of HBV PreS/S gene have been found to encode transcriptional transactivation activity, suggesting these mutations may contribute to HBV-associated oncogenesis. Recently, we have identified a potent oncogenic HBV surface (S) gene nonsense mutant sW182*. Results: Gene expression microarray study revealed that sW182* mutant was significantly enriched by gene sets associated with cell cycle regulation, DNA repair, or genome instability. The transforming growth factor-induced (TGFBI) gene was downregulated in the sW182* mutant clones, and irresponsive to TGF- treatment. The level of Cyclin D1, a negatively regulated TGFBI target, was highly elevated in sW182* mutant cells. Exogenous expression of TGFBI alleviated the oncogenic activity of sW182* in mouse xenograft study. In human HBV-related HCC cancerous tissue, expression of TGFBI was downregulated in 25 of the 55 (45%) patients. Conclusions: Dysregulation of transforming growth factor-induced (TGFBI) gene is involved in the oncogenic activity of the sW182* mutant of hepatitis B virus S gene. This has never been described before. NIH3T3 cells were stably transfected with plasmids encoding the wild type PreS/S gene or the nonsense mutant (sW182*) of HBV PreS/S gene. Totoal RNAs were extracted from those stable clones for gene expression microarray analysis using Illumina MouseRef-8 V2 BeadChip.
2014-07-30 | E-GEOD-50180 | biostudies-arrayexpress
Project description: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 proteomic sequencing, and to identify molecular biomarkers for clinical diagnosis of HBsAg-positive HBV and OBI. 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.
2024-08-04 | PXD054566 |
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:In patient serum, HBsAg particles can outnumber HBV particles by 1000:1 or higher. To explore the interactions between HBsAg and hepatocytes, concentrating on the possible effects of persistently secreting HBsAg on the functions of host cells, we have used the S gene of a full-length HBV isolate derived from an HBsAg chronic carrier (code No. C8, GenBank accession No. AF461363), cloned into pCMV vector to transfect HepG2 cells. G418 resistant clones secreting HBsAg were selected to establish permanent cell lines, and control clones transfected only with the vector were passaged as well to serve as controls. Cells were separately collected on the fourth and the eighth day after seeding, and gene expression profiles of both cell clones were studied and compared by microarray. Totally, 340 genes were suppressed and 673 genes were induced by the expression of HBsAg on the fourth day, whereas 219 genes were down-regulated and 683 genes were up-regulated on the eighth day. Arbitrarily, changes of genes detected on both 4th and 8th day cultures were selected for further study. Many cellular functions such as immune response, xenobiotic metabolism, ubiquitin pathway, transcription regulation were affected by HBsAg expression, indicating a close association between HBsAg and host cells. Experiment Overall Design: HBsAg particles are composed of viral envelope proteins and outnumber HBV virions by 1000:1 or even higher. This unique characteristic of HBV remains to be one of the challenges in basic and clinical aspects of viral hepatitis B. Experiment Overall Design: In this study, we want to explore the interactions between HBsAg and hepatocytes, concentrating on the effects of persistently secreting HBsAg on host cell functions.
2008-06-13 | E-GEOD-4549 | biostudies-arrayexpress