Functional study on the mutations of HBV X gene
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ABSTRACT:
PROVIDER: PRJNA742360 | ENA |
REPOSITORIES: ENA
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Project description:The in vitro HBV infection assay system was established in primary human hepatocytes (PXB cells) infected with HBV derived from the plasmid containing 1.3-mer HBV genome. Comprehensive and functional studies were performed by small interfering RNA knockdown and vector transfection experiments of the related genes and analyzed using microarray to reveal the host factors related to HBV regulation. Knockdown of STAT1 increased viral products in HBV-transfected HepG2 cells, but unexpectedly decreased in HBV-infected PXB cells. In RNA microarray analysis, STAT1 knockdown induced changes in intracellular molecules related to metabolism and protein synthesis in PXB cells, but not in HepG2 cells.
2025-01-16 | GSE253496 | GEO
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:This SuperSeries is composed of the SubSeries listed below.
2022-03-02 | GSE179127 | GEO
Project description:Study of HBV and HDV transcriptomic modulation
| PRJNA798970 | ENA
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.
2014-07-30 | GSE50180 | GEO
Project description:Background: Hepatitis B (HBV) and human immunodeficiency virus (HIV) co-infection is a common occurrence globally, with significant morbidity and mortality. Both viruses lead to dysregulated immune responses including changes in natural killer (NK) cells, a key component of antiviral defense and a promising target for HBV cure strategies. In this study we used high-throughput single cell analysis to explore the immune cell landscape in people with HBV mono-infection and HIV/HBV co-infection, on antiviral therapy, with emphasis on identifying the distinctive characteristics of NK cell subsets. Results: Our data show striking differences in the transcriptional programs of NK cells. HIV/HBV co-infection was characterized by an overrepresentation of adaptive, KLRC2 expressing NK cells, including a higher abundance of a chemokine enriched (CCL3/CCL4) adaptive cluster. The NK cell remodeling in HIV/HBV co-infection was reflected in enriched activation pathways shared with T cells, including CD3 phosphorylation and ZAP-70 translocation that can mediate stronger ADCC responses and a bias towards chemokine/cytokine signaling. By contrast HBV mono-infection imposed a stronger cytotoxic profile on NK cells and a more prominent signature of exhaustion with higher circulating levels of HBsAg. Mirroring the transcriptomic analysis, phenotypic alterations in the NK cell pool in co-infection were consistent with increased ‘adaptiveness’ and better capacity for ADCC compared to HBV mono-infection. Overall an adaptive NK cell signature correlated inversely with circulating levels of HBsAg and HBV-RNA in our cohort. Conlcusions: This study provides new insights into the differential transcriptional signature and functional profile of NK cells in HBV and HIV/HBV co-infection, highlighting new pathways that can be manipulated to tailor NK cell-focused approaches to advance cure strategies in the different population groups.
2024-08-01 | GSE241183 | GEO
Project description:HBV gene expression in HBV-infected primary human hepatocytes.
2022-07-15 | GSE208115 | GEO
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:A genome-wide functional study of 3’UTR mutations in advanced prostate cancer
| PRJNA824026 | ENA