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

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

PROVIDER: PRJNA703994 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13764574.fastq.gz	Fastqsanger.gz
	SRR13764575.fastq.gz	Fastqsanger.gz
	SRR13764576.fastq.gz	Fastqsanger.gz
	SRR13764577.fastq.gz	Fastqsanger.gz
	SRR13764578.fastq.gz	Fastqsanger.gz

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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

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

Project description:Equine hepacivirus (EqHV) is the closest genetic relative of hepatitis C virus (HCV) and shares features of genome organization, hepatotropism, persistent infection, and the ability to cause liver disease. As such, EqHV studies are important both in order to understand equine liver disease, and as an outbred animal model for HCV pathogenesis and immune responses. Here, we characterize the natural history and immune response to EqHV infection. Seven horses were experimentally inoculated with EqHV, monitored for 6 months, and challenge inoculated with the same, and subsequently a divergent EqHV inoculum. 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. Resolving horses developed non-sterilizing immunity resulting in short duration of infection upon challenge. Unlike those observed in acutely HCV-infected patients, peripheral blood mononuclear cell responses in horses were minimal, although EqHV specific T-cells were identified. In contrast, an interferon stimulated gene signature was detected in the liver during EqHV infection, which is similar to acute HCV in humans. EqHV, similarly to HCV, is stimulated by direct binding of the liver-specific microRNA, miR-122. Surprisingly, 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. Conclusion: EqHV infection in horses typically has an acute resolving course, and the immune response attenuates subsequent infections lasting for at least a year. This could have important implications to achieve the first goal of an HCV vaccine; to prevent chronicity while accepting acute resolving infection after challenge.

2020-09-30 | GSE158753 | GEO

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

Project description:Pathogenesis, miR-122 gene-regulation, and protective immune responses after acute infection of horses with equine hepacivirus

| PRJNA666423 | ENA

Pathogenesis, MicroRNA-122 Gene-Regulation, and Protective Immune Responses After Acute Equine Hepacivirus Infection.

Project description:Background and aimsEquine hepacivirus (EqHV) is phylogenetically the closest relative of 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 and resultsSeven 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 nonsterilizing 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), 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.ConclusionsEqHV 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.

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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

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