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RNA-seq of HBV-infected Primary Human Hepatocytes treatment by Tazarotene

ABSTRACT: RNA-seq of HBV-infected Primary Human Hepatocytes treatment by Tazarotene

PROVIDER: PRJNA454860 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7106430_1.fastq.gz	Fastqsanger.gz
	SRR7106430_2.fastq.gz	Fastqsanger.gz
	SRR7106431_1.fastq.gz	Fastqsanger.gz
	SRR7106431_2.fastq.gz	Fastqsanger.gz
	SRR7106432_1.fastq.gz	Fastqsanger.gz

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Project description:Monitor HBV mRNA reduction in response to Tazarotene and to identify global transcriptome-wide gene expression associated with Tazarotene treatment in HBV infected PHH using RNA-Seq

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

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

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

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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

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