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Heat Shock Protein Family A Member 1 Promotes Intracellular Amplification of Hepatitis B Virus Covalently Closed Circular DNA

ABSTRACT: Heat Shock Protein Family A Member 1 Promotes Intracellular Amplification of Hepatitis B Virus Covalently Closed Circular DNA

PROVIDER: PRJNA862739 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20665241_1.fastq.gz	Fastqsanger.gz
	SRR20665241_2.fastq.gz	Fastqsanger.gz
	SRR20665242_1.fastq.gz	Fastqsanger.gz
	SRR20665242_2.fastq.gz	Fastqsanger.gz
	SRR20665243_1.fastq.gz	Fastqsanger.gz

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Heat Shock Protein Family A Member 1 Promotes Intracellular Amplification of Hepatitis B Virus Covalently Closed Circular DNA

Project description:Hepatitis B virus (HBV) contains a partially double-stranded relaxed circular DNA (rcDNA) genome that is converted into a covalently closed circular DNA (cccDNA) in the nucleus of infected hepatocyte by cellular DNA repair machinery. cccDNA associates with nucleosomes to form a minichromosome that transcribes RNA to support the expression of viral proteins and reverse transcriptional replication of viral DNA. In addition to the de novo synthesis from incoming virion rcDNA, cccDNA can also been synthesized from rcDNA in the progeny nucleocapsids in the cytoplasm of infected hepatocytes via the intracellular amplification pathway. In our efforts to identify cellular DNA repair proteins required for cccDNA synthesis by a chemogenetic screen, we found that B02, a small molecular inhibitor of DNA homologous recombination repair protein RAD51, significantly enhanced the synthesis of cccDNA via intracellular amplification pathway in human hepatoma cells. Ironically, neither siRNA knockdown of RAD51 expression nor treatment with another structurally distinct RAD51 inhibitor or activator altered cccDNA amplification. However, further mechanistic studies revealed that B02 treatment significantly elevated the levels of multiple heat shock protein mRNA and siRNA knockdown of HSPA1A expression or treatment with HSPA1 inhibitors significantly attenuated B02 enhancement of cccDNA amplification. Moreover, B02 enhanced cccDNA amplification was efficiently inhibited by compounds that selectively inhibit DNA polymerase α or topoisomerase II, the enzymes required for cccDNA intracellular amplification. Our results thus indicate that B02 treatment induces a heat shock protein-mediated cellular response that positively regulates the conversion of rcDNA into cccDNA via the authentic intracellular amplification pathway

2022-12-08 | GSE209863 | GEO

Heat Shock Protein Family A Member 1 Promotes Intracellular Amplification of Hepatitis B Virus Covalently Closed Circular DNA.

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DNA Polymerase alpha is essential for intracellular amplification of hepatitis B virus covalently closed circular DNA.

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Development of a single domain antibody to target a G-quadruplex located on the hepatitis B virus covalently closed circular DNA Genome

Project description:Guanine-quadruplexes (G4s) are a secondary structure that can be adopted by DNA and have recently been shown to play an important role in regulating viral replication, transcription, and translation. Here we describe the development of a humanized single-domain antibody (S10) that can target a G4 located in the PreCore/Core (PreC) promoter region on the hepatitis B virus (HBV) covalently closed circular DNA (cccDNA) genome. Using cross-linking chromatin immunoprecipitation (ChIP) coupled with qPCR and next-generation sequencing, we show that S10 binds to HBV’s PreC locus and cccDNA, showing target specificity. Herein, we demonstrate that a single domain antibody can be designed to probe the existence of a G4 in vitro and intracellularly within the HBV cccDNA genome.

2026-02-02 | GSE254033 | GEO

ZNF638 represses HBV covalently closed circular DNA transcription involving HUSH complex epigenetic silencing

Project description:ZNF638 represses HBV covalently closed circular DNA transcription involving HUSH complex epigenetic silencing

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Interferon Alpha Induces Multiple Cellular Proteins That Coordinately Suppress Hepadnaviral Covalently Closed Circular DNA Transcription

Project description:Interferon Alpha Induces Multiple Cellular Proteins That Coordinately Suppress Hepadnaviral Covalently Closed Circular DNA Transcription

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ZNF638 represses HBV covalently closed circular DNA transcription involving HUSH complex epigenetic silencing

Project description:Hepatitis B virus (HBV) infection represents a significant public health burden worldwide. Covalently closed circular DNA (cccDNA) is the transcriptional template of HBV, which interacts with both host and viral proteins to form minichromosome in the nucleus and exhibits resistance to antiviral agents. Here, we provide evidence that ZNF638 mediates transcriptional silencing of HBV cccDNA. Mechanically, ZNF638 bound to HBV cccDNA, increasing the occupancy of HUSH complex to target loci, which subsequently recruited SETDB1, leading to enhanced H3K9me3 modification, thereby repressing cccDNA transcription. Our research findings improved the existing understanding of ZNF638- and HUSH-mediated epigenetic silencing on viral DNA, that (1) ZNF638 and HUSH complex inhibited HBV transcription, not only by epigenetic silencing extrachromosome cccDNA but also silencing the integrate viral DNA, and (2) ZNF638- and HUSH-mediated repression appeared to function as an epigenetic rheostat: occupancy of HUSH components at the locus inhibited transcription; release from the target locus activated transcription. In summary, the study demonstrates a novel epigenetic role of ZNF638 and HUSH complex in negatively regulating HBV cccDNA transcription by deposit repressive H3K9me3 histone marks and highlights the importance of epigenetic therapy targeting cccDNA, suggesting that ZNF638 could be a potential target for epigenetic therapy of viral diseases.

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