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Real-time quantitative PCR analysis of human HepaRG cells infected with hepatitis E virus (HEV) [pre-array]

ABSTRACT: Real-time quantitative PCR analysis of human HepaRG cells infected with hepatitis E virus (HEV) [pre-array]

PROVIDER: PRJNA1020171 | ENA |

REPOSITORIES: ENA

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Real-time quantitative PCR analysis of human HepaRG cells infected with hepatitis E virus (HEV) [pre-array]

Project description:We aimed to identify interferon (IFN)-regulated genes that are differentially expressed during chronic HEV infection in human hepatocytes, the main site of HEV replication, using HepaRG cells. We have performed a preliminary screen using whole-cell RNA extracts prepared from HepaRG mock-infected or infected cells to determine whether HEV was able to trigger an IFN response. Different multiplicities of infection (MOI) (10 and 100 genome equivalent (GE)/cell) and time points (D+7, D+14, D+26, D+40, D+72 and D+100) were analyzed using the PCR array. We have also treated HepaRG cells after overnight treatment with IFN-β to confirm the ability of HepaRG to respond to IFN-I treatment.

2023-11-08 | GSE243855 | GEO

Real-time quantitative PCR analysis of human HepaRG cells infected with hepatitis E virus (HEV) [D100 plaque 2]

2023-11-08 | GSE243860 | GEO

Real-time quantitative PCR analysis of human HepaRG cells infected with hepatitis E virus (HEV) [D100 plaque 1]

2023-11-08 | GSE243856 | GEO

Real-time quantitative PCR analysis of human HepaRG cells infected with hepatitis E virus (HEV) [D100 plaque 1]

Project description:Real-time quantitative PCR analysis of human HepaRG cells infected with hepatitis E virus (HEV) [D100 plaque 1]

| PRJNA1020176 | ENA

Real-time quantitative PCR analysis of human HepaRG cells infected with hepatitis E virus (HEV) [D100 plaque 2]

Project description:Real-time quantitative PCR analysis of human HepaRG cells infected with hepatitis E virus (HEV) [D100 plaque 2]

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Real-time quantitative PCR analysis of liver tissue from pigs infected experimentally with hepatitis E virus (HEV) [pig liver]

Project description:We aimed to identify interferon (IFN)-regulated genes that are differentially expressed during HEV infection in swine liver tissues.

2023-11-08 | GSE243862 | GEO

Real-time quantitative PCR analysis of liver tissue from pigs infected experimentally with hepatitis E virus (HEV)

Project description:Real-time quantitative PCR analysis of liver tissue from pigs infected experimentally with hepatitis E virus (HEV)

| PRJNA1020180 | ENA

Real-time quantitative PCR analysis of liver tissue from pigs infected experimentally with hepatitis E virus (HEV) [pig liver]

Project description:Real-time quantitative PCR analysis of liver tissue from pigs infected experimentally with hepatitis E virus (HEV) [pig liver]

| PRJNA1020183 | ENA

Cellular response to hepatitis E virus (HEV) infection

Project description:What happens in cells infected with HEV is largely unknown. We used a recently established genotype 3 HEV cell culture system and profiled the host responses by RNA-seq.

2019-10-31 | GSE88731 | GEO

The unique proteasomal processing of viral ORF1 drives HEV-induced liver fibrosis

Project description:Hepatitis E virus (HEV) is a globally prevalent pathogen that causes 20 million infections and 60,000 fatalities annually, endangering particularly pregnant women and immunosuppressed individuals. Liver cirrhosis, which results from advanced fibrosis, is the primary symptom and leading mortality cause in chronic hepatitis E patients. However, the causation and process of liver fibrosis triggered by chronic HEV infection remain poorly understood. Here, we unexpectedly discovered that the viral multiple-domain replicase (ORF1) undergoes unique ubiquitin-proteasomal processing in HEV replicon hepatocytes, HEV-infected gerbil livers, and HEV-infected patient livers, which follows a CHIP-mediated K48 ubiquitination and produces the HEV-Derived Smad Activator (HDSA). Lacking putative helicase and RNA polymerase domains, this enriched viral polypeptide in hepatocytes and gerbil livers is non-HSP90-bound, stable, and exhibits exclusively nuclear localization. Surprisingly, HDSA markedly potentiates the fibrogenic TGF-β/Smad pathway in livers by facilitating promoter binding and coactivator recruitment of SMAD3, leading to profound liver fibrotic symptoms and damage. Thus, we have identified the first viral protein derived from the unique proteasomal processing of the host, defined its notable role in liver fibrosis, and highlighted the nature of complex host-HEV interactions that drives HEV pathogenesis.

2024-08-01 | GSE251924 | GEO

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