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Host genetic variation guides hepacivirus clearance, chronicity, and liver fibrosis in mice

ABSTRACT: Host genetic variation guides hepacivirus clearance, chronicity, and liver fibrosis in mice

PROVIDER: PRJNA961176 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24293541.fastq.gz	Fastqsanger.gz
	SRR24293542.fastq.gz	Fastqsanger.gz
	SRR24293543.fastq.gz	Fastqsanger.gz
	SRR24293544.fastq.gz	Fastqsanger.gz
	SRR24293545.fastq.gz	Fastqsanger.gz

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Host genetic variation guides hepacivirus clearance, chronicity, and liver fibrosis in mice

Project description:The dataset describes the host transcriptional response in WT and Collaborative Cross lines infected with Norway rat hepacivirus.

2023-04-25 | GSE230468 | GEO

Host genetic variation guides hepacivirus clearance, chronicity, and liver fibrosis in mice.

Project description:Background aimsHuman genetic variation is thought to guide the outcome of HCV infection, but model systems within which to dissect these host genetic mechanisms are limited. Norway rat hepacivirus, closely related to HCV, causes chronic liver infection in rats but causes acute self-limiting hepatitis in typical strains of laboratory mice, which resolves in 2 weeks. The Collaborative Cross (CC) is a robust mouse genetics resource comprised of a panel of recombinant inbred strains, which model the complexity of the human genome and provide a system within which to understand diseases driven by complex allelic variation.Approach resultsWe infected a panel of CC strains with Norway rat hepacivirus and identified several that failed to clear the virus after 4 weeks. Strains displayed an array of virologic phenotypes ranging from delayed clearance (CC046) to chronicity (CC071, CC080) with viremia for at least 10 months. Body weight loss, hepatocyte infection frequency, viral evolution, T-cell recruitment to the liver, liver inflammation, and the capacity to develop liver fibrosis varied among infected CC strains.ConclusionsThese models recapitulate many aspects of HCV infection in humans and demonstrate that host genetic variation affects a multitude of viruses and host phenotypes. These models can be used to better understand the molecular mechanisms that drive hepacivirus clearance and chronicity, the virus and host interactions that promote chronic disease manifestations like liver fibrosis, therapeutic and vaccine performance, and how these factors are affected by host genetic variation.

| S-EPMC10718216 | biostudies-literature

Pathogenesis, miR-122 gene-regulation, and protective immune responses after acute equine hepacivirus infection

Project description:Equine hepacivirus (EqHV) is phylogenetically the closest relative of hepatitis C virus (HCV) and shares genome organization, hepatotropism, transient or persistent infection outcome, and the ability to cause hepatitis. Thus, EqHV studies are important to understand equine liver disease, and further as an outbred surrogate animal model for HCV pathogenesis and protective immune responses. Here, we aimed to characterize the course of EqHV infection and associated protective immune responses. Approach & Results: Seven horses were experimentally inoculated with EqHV, monitored for 6 months, and rechallenged with the same, and subsequently a heterologous EqHV. Clearance was the primary outcome (6 of 7) and was associated with subclinical hepatitis characterized by lymphocytic infiltrate and individual hepatocyte necrosis. Seroconversion was delayed and antibody titers waned slowly. Clearance of primary infection conferred non-sterilizing immunity resulting in shortened duration of viremia after rechallenge. Peripheral blood mononuclear cell responses in horses were minimal, although EqHV specific T cells were identified. Additionally, an interferon stimulated gene signature was detected in the liver during EqHV infection, similar to acute HCV in humans. EqHV, as HCV, is stimulated by direct binding of the liver-specific microRNA, miR-122. Interestingly, we found that EqHV infection sequesters enough miR-122 to functionally affect gene regulation in the liver. This RNA-based mechanism thus could have consequences for pathology. Conclusions: EqHV infection in horses typically has an acute resolving course, and the protective immune response lasts for at least a year and broadly attenuates subsequent infections. This could have important implications to achieve the primary goal of an HCV vaccine; to prevent chronicity while accepting acute resolving infection after virus exposure.

2021-06-01 | GSE167260 | GEO

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