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Changes of mRNA expression levels in HBV-infected human primary hepatocytes and those cells treated with bionanocapsules containing microRNA-93.

ABSTRACT: Human primary hepatocytes isolated from chimeric mice were infected with HBV for 7 days. The comprehensive changes of mRNA levels were determined by mRNA array. Also, microRNA93 was delivered into those cells using bionanocapsules to determine the effects of rescue expression of miR93 in HBV replicating cells, because we found that miR93 expression level was downregulated in HBV-infected hepatocytes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE55928 | GEO | 2014/03/15

SECONDARY ACCESSION(S): PRJNA241334

REPOSITORIES: GEO

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Changes of mRNA expression levels in HBV-infected human primary hepatocytes and those cells treated with bionanocapsules containing microRNA-93.

Project description:Human primary hepatocytes isolated from chimeric mice were infected with HBV for 7 days. The comprehensive changes of mRNA levels were determined by mRNA array. Also, microRNA93 was delivered into those cells using bionanocapsules to determine the effects of rescue expression of miR93 in HBV replicating cells, because we found that miR93 expression level was downregulated in HBV-infected hepatocytes. mRNA expression levels were compared in among control cells, HBV-infected cells, miR93 delivered cells, and HBV-infected cells with miR93 delivered, by 25K mRNA arrays.

2014-03-15 | E-GEOD-55928 | biostudies-arrayexpress

Changes of microRNA expression levels in HBV-infected human primary hepatocytes

Project description:Human primary hepatocytes isolated from chimeric mice were infected with HBV for 7 days. The comprehensive changes of miRNA levels were determined by miRNA array. MicroRNA expression levels were compared in between control and HBV-replicating primary hepatocytes by 2K microRNA microarrays

2014-03-15 | E-GEOD-55929 | biostudies-arrayexpress

Effect of two compounds on HBV gene expression in HBV-infected primary human hepatocytes.

Project description:HBV gene expression in HBV-infected primary human hepatocytes.

2022-07-15 | GSE208115 | GEO

Selective depletion of HBV-infected hepatocytes by class A capsid assembly modulators require high levels of intrahepatic HBV core protein

Project description:Several classes of capsid assembly modulators (CAMs) are currently being developed for chronic hepatitis B (CHB) cure. Both class A (CAM-A) and class E (CAM-E) CAMs disrupt nucleocapsid assembly and reduce extracellular hepatitis B virus (HBV) DNA. However, only CAM-As have been shown to reduce the number of HBV-infected cells in the animal models. However, there has been limited efficacy to date of CAM-A molecules achieving this secondary mechanism of HBV-infected cell clearance in CHB clinical trials. To investigate this disconnect, we performed comparative experiments with tool compounds from each class to further explore these unique features and antiviral activity of CAM-A across HBV-infected primary human hepatocytes (PHH), as well as in two different HBV mouse models (immunodeficient mice repopulated with human hepatocytes and AAV-HBV). Mechanistic studies in HBV-infected PHH revealed that CAM-A, but not CAM-E, induced dose-dependent aggregation of HBV core protein (HBc) in the nucleus. Experiments with siRNA, resulted in identification of the ubiquitin-binding protein p62 as a factor negatively regulating the size of these aggregates. Furthermore, we found that only the CAM-A is able to induce HBc-positive cell death in vivo with the loss of HBV-infected cells positively correlated to the levels of intrahepatic HBc. Profiling of intrahepatic HBc levels across CHB patient liver biopsies demonstrated a significantly lower level of HBc per hepatocyte than either of the HBV mouse models. Taken together, these data demonstrate that CAMs of class A have a unique secondary mechanism that has potential to specifically affect viability of HBV-infected hepatocytes. At the same time, the clearance of infected hepatocytes may depend on the level of HBc expression thereby limiting the therapeutic potential for this class of molecules.

2024-05-21 | GSE260966 | GEO

HBcore-specific CXCR6+CD8 T cells during persistent HBV replication in mice lose their effector function and have high CREM activity

Project description:We investigated molecular profiles of CD8 T cells in persistent experimental Hepatitis B virus (HBV) infection. To this end, we established a preclinical in vivo model where HBV-replicating hepatocytes were cleared by virus-specific immunity after infection with 107 IU Ad-HBV, whereas persistent HBV replication developed after infection with 108 IU Ad-HBV, revealed by high serum HBeAg levels, high numbers of HBV genome copies and of HBcorepos hepatocytes in liver tissue. To overcome variable surface expression of the T cell receptor during chronic infection and unequivocally identify HBV-specific CD8 T cells, we adoptively transferred naïve CD45.1+HBcore-specific CD8 T cells from Cor93 transgenic mice (HBcoreCD8 T cells) the day before Ad-HBV infection. After clearance of HBV-replicating hepatocytes (d44 p.i.), liver CD45.1+HBcoreCD8 T cells expressed either CXCR6 or CX3CR1, and in the spleen only CX3CR1+ CD8 T cells were detected. Next, we evaluated the transcriptional profile of FACSorted HBcoreCD8 T cells after resolved compared to persistent infection employing SmartSeq2. The resulting dataset is reported here.

2024-05-08 | GSE214151 | GEO

Gene expression response to HBV infection in PHH

Project description:Hepatitis B virus (HBV) is known for its ability to interact with the host cell DNA methylation machinery. In HBV-infected hepatocytes, this interaction leads to chronic liver diseases, including hepatocellular carcinoma (HCC). We studied the extent of genomic changes induced by natural HBV infection in human primary hepatocytes. Transcriptome and methylome profiles were obtained at different time points post-infection to identify HBV-specific alterations. Although gene expression and DNA methylation do not directly correlate, they both seem to reflect the effect of cell culture and viral infection at different levels.These changes in the hepatocyte cellular program shed light on the initial events leading to HBV-associated liver diseases.

2016-01-01 | GSE72068 | GEO

HBV Infection and DNA Stimulation Induce a Unique Innate Immune Response in Hepatocytes

Project description:Background and Aims: Recent identification of intracellular DNA sensing pathways and involvement in numerous diverse disease processes including viral pathogenesis and autoimmunity suggests a role for these processes in liver pathology. The presence of these pathways in the liver and their role in HBV infection is unknown. Methods: In order to characterize the role of DNA sensing pathways in the liver, we utilized in vitro models. Microarray was performed on DNA treated and HBV infected hepatoma primary human hepatocytes. Results: Here we show that HBV infection and foreign DNA results in a significant innate immune response characterized by the production of inflammatory chemokines. The goal of this study is to characterize the changes in gene expression triggered by HBV and foreign DNA in primary human hepatocytes. PHHs were infected with HBV (MO.I = 50) for 40 hours. PHHs were transfected with 1Î¼g/mL of ISD/dsDNA90 for 12 or 24 hours. Three replicates were performed for each condition.

2016-08-09 | E-GEOD-69590 | biostudies-arrayexpress

SENP3-mediated host defense response contains HBV replication and restores protein synthesis

Project description:Certain organs are capable of containing the replication of various types of viruses. In the liver, infection of Hepatitis B virus (HBV), the etiological factor of Hepatitis B and hepatocellular carcinoma (HCC), often remains asymptomatic and leads to a chronic carrier state. Here we investigated how hepatocytes contain HBV replication and promote their own survival by orchestrating a translational defense mechanism via the stress-sensitive SUMO-2/3-specific peptidase SENP3. We found that SENP3 expression level decreased in HBV-infected hepatocytes in various models including HepG2-NTCP cell lines and a humanized mouse model. Downregulation of SENP3 reduced HBV replication and boosted host protein translation. We also discovered that IQGAP2, a Ras GTPase-activating-like protein, is a key substrate for SENP3-mediated de-SUMOylation. Downregulation of SENP3 in HBV infected cells facilitated IQGAP2 SUMOylation and degradation, which leads to suppression of HBV gene expression and restoration of global translation of host genes via modulation of AKT phosphorylation. Thus, The SENP3-IQGAP2 de-SUMOylation axis is a host defense mechanism of hepatocytes that restores host protein translation and suppresses HBV gene expression.

2018-11-14 | GSE122461 | GEO

Changes of microRNA expression levels in HBV-infected human primary hepatocytes

Project description:Human primary hepatocytes isolated from chimeric mice were infected with HBV for 7 days. The comprehensive changes of miRNA levels were determined by miRNA array.

2014-03-15 | GSE55929 | GEO

Transcriptional profiling of hepatocytes isolated from chronically HBV-infected human liver chimeric mice

Project description:We generated human liver chimeric mice that were repopulated with human hepatocytes and we infected them for 11 weeks with Hepatitis B virus (HBV). Hepatocytes were isolated from the infected chimeric mouse livers and their gene expressions were compared with those from uninfected chimeric mice using RNA-sequencing.

2020-05-22 | GSE145835 | GEO

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