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A nucleosome switch primes Hepatitis B Virus infection [ChIP-Seq]

ABSTRACT: A nucleosome switch primes Hepatitis B Virus infection [ChIP-Seq]

PROVIDER: PRJNA1125296 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29452917_1.fastq.gz	Fastqsanger.gz
	SRR29452917_2.fastq.gz	Fastqsanger.gz
	SRR29452918_1.fastq.gz	Fastqsanger.gz
	SRR29452918_2.fastq.gz	Fastqsanger.gz
	SRR29452919_1.fastq.gz	Fastqsanger.gz

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A nucleosome switch primes Hepatitis B Virus infection

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A nucleosome switch primes Hepatitis B Virus infection [ChIP-Seq]

Project description:Chronic hepatitis B virus (HBV) infection is an incurable global health threat responsible for causing liver disease and hepatocellular carcinoma. During the genesis of infection, HBV establishes an independent minichromosome consisting of the viral covalently closed circular DNA (cccDNA) genome and host histones. The viral X gene must be expressed immediately upon infection to induce degradation of the host silencing factor, Smc5/6. However, the relationship between cccDNA chromatinization and X gene transcription remains poorly understood. Establishing a reconstituted viral minichromosome platform, we found that nucleosome occupancy in cccDNA drives X transcription. We corroborated these findings in cells and further showed that the chromatin destabilizing molecule CBL137 inhibits X transcription and HBV infection in hepatocytes. Our results shed light on a long-standing paradox and represent a potential new therapeutic avenue for the treatment of chronic HBV infection.

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Project description:Chronic hepatitis B virus (HBV) infection is an incurable global health threat capable of causing liver disease and hepatocellular carcinoma. During the genesis of infection, HBV establishes an independent chromosome, cccDNA, consisting of the circular viral genome and host histones. The first viral protein expressed, HBx, induces degradation of a host silencing factor to facilitate infection. However, the relationship between cccDNA’s chromatin and early HBx transcription state remains poorly understood. Using reconstituted viral chromosomes, we found that nucleosomes in cccDNA drive HBx transcription. We corroborated these findings in cells and further showed that chromatin destabilizing drugs inhibit viral transcription and antigen expression in hepatocytes. Our results shed new light on a long-standing paradox and represent a novel therapeutic avenue for the treatment of chronic HBV.

2023-03-03 | GSE225715 | GEO

A nucleosome switch primes Hepatitis B Virus infection [RNA-Seq]

2023-03-03 | GSE225714 | GEO

A nucleosome switch primes Hepatitis B Virus infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-03 | GSE225716 | GEO

Association Between Hepatitis C Infection and Renal Cell Carcinoma

Project description:The purpose of this study is to determine if there is an association between hepatitis C infection and kidney cancer. All patients who are diagnosed with kidney cancer and who will either have a biopsy or surgery will be offered to be tested for hepatitis C. The control group will be colon cancer patients. Both groups would be of recent diagnosis (6 months).

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Project description:The natural history of chronic hepatitis B virus (HBV) infection could be divided in different phases by transaminase and HBV replication levels. However, it remains unknown how the intrahepatic transcriptomes in patients are correlated with the clinical phases. Here, we determined the intrahepatic transcriptomes of chronic hepatitis B patients and examined the role of specific groups of genes, including immune-related genes, in the control of hepatitis B virus infection.

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Janus kinase-Inhibition modulates hepatitis E virus infection

Project description:Background: Human hepatitis E virus (HEV) usually causes a self-limiting disease, but especially immunocompromised individuals are at risk to develop a chronic and severe course of infection. Janus kinase (JAK) inhibitors (JAKi) are a novel drug class for the treatment of autoimmune inflammatory rheumatic disease (AIRD). As JAKs play a key role in innate immunity, viral infections and reactivations are frequently reported during JAKi treatment in AIRD patients. The aim of this study was to characterize the influence of JAKis on HEV replication in vivo and in authentic cell culture models ex vivo. Methods: We evaluated liver enzymes of an AIRD patient under JAKi therapy with hepatitis E and HEV infections in a cohort of AIRD patients. Experiments with HEV were performed by infection of primary human hepatocytes (PHHs) followed by immunofluorescence staining of viral markers and transcriptomic analysis. Results: Acute hepatitis was observed in a patient with AIRD and concomitant HEV infection. No acute infection could be detected in the AIRD cohort. Infection experiments in PHHs displayed an up to 50-fold increase of progeny virus production during JAKi treatment and transcriptomic analysis revealed induction of antiviral programs during infection. This induction was perturbed in the presence of JAKis, concomitant with elevated HEV RNA levels. Conclusion: Therapeutic JAK inhibition increases HEV replication by modulating the HEV-triggered immune response. Therefore, clinical monitoring of HEV infection during JAKi treatment and in case of elevated liver enzymes should be considered.

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