Episomal HBV persistence within transcribed host nuclear chromatin compartments involves HBx
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA391572 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5749380_1.fastq.gz | Fastqsanger.gz | |||
| SRR5749380_2.fastq.gz | Fastqsanger.gz | |||
| SRR5749390.fastq.gz | Fastqsanger.gz | |||
| SRR5749400_1.fastq.gz | Fastqsanger.gz | |||
| SRR5749400_2.fastq.gz | Fastqsanger.gz |
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Project description:In hepatocyte nuclei, hepatitis B virus (HBV) genomes occur episomally as covalently closed circular DNA (cccDNA). The HBV X protein (HBx) is required to initiate and maintain HBV replication and acts as host gene trans-regulator. However, functionally relevant spatiotemporal localization and interactions of cccDNA and HBx remain to be understood. This is the first study utilizing circularized chromosome conformation capture (4C) to identify regional virus-host genome interactions. We combined 4C with RNA-seq and ChIP-seq to illuminate the nuclear landscape associated with HBV episomes and HBx. Moreover, we functionally studied HBx-binding to episomal HBV DNA. In human HBV-positive HepaRG hepatocytes, 4C and ChIP revealed specific nuclear localization of HBV episomes and HBx associated with actively transcribed nuclear domains correlating well in size with constrained topological units built up by chromatin fibre loops, which are believed to constitute fundamental cell nuclear architectural units. Interestingly, HBx alone occupied transcribed chromatin domains, and its binding to HBV episomes depended on its C-terminus in vitro. In conclusion, HBx and HBV DNA similarly follow higher-order nuclear assembly patterns, specifically favoring transcriptionally active nuclear compartments. These novel observations may shed light on important unsolved problems: to understand the long-term episomal stability and the facilitation of viral persistence.
2018-04-30 | GSE100400 | GEO
Project description:BackgroundIn hepatocyte nuclei, hepatitis B virus (HBV) genomes occur episomally as covalently closed circular DNA (cccDNA). The HBV X protein (HBx) is required to initiate and maintain HBV replication. The functional nuclear localization of cccDNA and HBx remains unexplored.ResultsTo identify virus-host genome interactions and the underlying nuclear landscape for the first time, we combined circular chromosome conformation capture (4C) with RNA-seq and ChIP-seq. Moreover, we studied HBx-binding to HBV episomes. In HBV-positive HepaRG hepatocytes, we observed preferential association of HBV episomes and HBx with actively transcribed nuclear domains on the host genome correlating in size with constrained topological units of chromatin. Interestingly, HBx alone occupied transcribed chromatin domains. Silencing of native HBx caused reduced episomal HBV stability.ConclusionsAs part of the HBV episome, HBx might stabilize HBV episomal nuclear localization. Our observations may contribute to the understanding of long-term episomal stability and the facilitation of viral persistence. The exact mechanism by which HBx contributes to HBV nuclear persistence warrants further investigations.
| S-EPMC6015472 | biostudies-literature
Project description:Hepatitis B Virus (HBV) remains a major public health problem, and is a major cause liver cancer worldwide. HBV infection in vivo requires the function of the HBx protein, which facilitates expression of viral genes from the episomal genome by an unknown mechanism. Evidence suggests that HBx functions as a targeting subunit for the CRL4 E3 ubiquitin ligase, redirecting the complex to target and degrade an unknown host restriction factor. We used substrate trapping proteomics to search for ubiquitylation substrates of HBx. We used MLN4924 to block CRL activity and stabilize interactions between HBx and its substrates. We then performed APMS to identify bound proteins and potential substrates.
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Project description:Mature microRNA expression profiling of HBx-expressing HepG2 cells versus Control cells under UV stress
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Project description:A genome-wide integrated DNA methylation analysis of the early stage of hepatocellular carcinoma development that induced by HBx. The HBV x (HBx) protein, which plays a critical role in the development of HCC, was shown to interact with several epigenetic factors, such as DNMT3A and HDAC1. Most HBx transgenic (TG) mice spontaneously develop HCC at about 1 year of age, providing genetic validation of the oncogenic potential of HBx even in the absence of viral integration and chronic inflammation. Therefore, it would be intriguing to study the regulatory role of HBx in the epigenome and its impact on HCC development. We performed a genome-wide analysis to examine the differences in DNA methylation enrichment pattern between cancer and normal liver cells.
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