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Deep sequencing after alcelaphine gammaherpesvirus 1 infection reveals the nature of CD8+ T cell expansion and identify an essential viral protein for fatal bovine malignant catarrhal fever [ATAC-seq]

ABSTRACT: Deep sequencing after alcelaphine gammaherpesvirus 1 infection reveals the nature of CD8+ T cell expansion and identify an essential viral protein for fatal bovine malignant catarrhal fever [ATAC-seq]

PROVIDER: PRJNA1066838 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27663600_1.fastq.gz	Fastqsanger.gz
	SRR27663600_2.fastq.gz	Fastqsanger.gz
	SRR27663601_1.fastq.gz	Fastqsanger.gz
	SRR27663601_2.fastq.gz	Fastqsanger.gz
	SRR27663602_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Deep sequencing after alcelaphine gammaherpesvirus 1 infection reveals the nature of CD8+ T cell expansion and identify an essential viral protein for fatal bovine malignant catarrhal fever

Project description:Deep sequencing after alcelaphine gammaherpesvirus 1 infection reveals the nature of CD8+ T cell expansion and identify an essential viral protein for fatal bovine malignant catarrhal fever

| PRJNA1066826 | ENA

Deep sequencing after alcelaphine gammaherpesvirus 1 infection reveals the nature of CD8+ T cell expansion and identify an essential viral protein for fatal bovine malignant catarrhal fever [scRNA-seq]

| PRJNA1066894 | ENA

Deep sequencing after alcelaphine gammaherpesvirus 1 infection reveals the nature of CD8+ T cell expansion and identify an essential viral protein for fatal bovine malignant catarrhal fever [RNA-seq]

| PRJNA1066836 | ENA

Project description:Alcelaphine gammaherpesvirus 1 (AlHV-1) is a member of the Gammaherpesvirinae subfamily and establishes asymptomatic latent infection in its natural host species, the wildebeest. Cross-species transmission to various ruminant species including cattle can occur, resulting in the induction of malignant catarrhal fever (MCF), a deadly peripheral T cell lymphoproliferative disease. Here, we experimentally infected calves to confirm that AlHV-1 latency-associated gene expression is essential for persistent infection of CD8+ T cells and MCF development. Then, deep sequencing of the T cell receptor repertoire revealed an oligoclonal expansion of peripheral CD8+ T cells during bovine MCF, associated with transcriptomic and epigenetic changes identified by (sc)RNA-seq and ATAC-seq analyses which indicated a mixed effector/memory and exhaustion phenotype of infected cells in vivo. Analysis of the viral genome transcription identified viral genomic regions being expressed in infected CD8+ T cells, such as the region predicted to encode the gene A10. A10 encodes a transmembrane signaling protein displaying multiple tyrosine residues, with predicted ITAM and SH3 motifs. We could demonstrate that impaired expression of A10 did not affect AlHV-1 replication in vitro but rendered AlHV-1 unable to induce MCF in the rabbit experimental model, and we showed that A10 is phosphorylated in T lymphocytes in vitro and affects T cell signaling. Finally, while AlHV-1 viruses expressing mutated forms of A10 devoid of ITAM and/or SH3 motifs could induce MCF, an A10 knock-in viral mutant unable to phosphorylate tyrosine residues resulted in the absence of MCF development. Overall, we identified AlHV-1-induced phenotypic changes in CD8+ T cells during MCF and demonstrated that A10 expression in infected CD8+ T lymphocytes results in the dysregulation of T cell signaling and MCF.

2024-05-01 | GSE253762 | GEO

Deep sequencing after alcelaphine gammaherpesvirus 1 infection reveals the nature of CD8+ T cell expansion and identify an essential viral protein for fatal bovine malignant catarrhal fever [RNA-seq]

2024-05-01 | GSE253728 | GEO

2024-05-01 | GSE253727 | GEO

Small RNA deep sequencing identifies viral microRNAs during malignant catarrhal fever induced by alcelaphine herpesvirus 1

Project description:Alcelaphine herpesvirus 1 (AlHV-1) is a ?-herpesvirus (?-HV) carried asymptomatically by wildebeest. Upon cross-species transmission, AlHV-1 induces an acute and fatal lymphoproliferative disease named malignant catarrhal fever (MCF) in many ruminants, including cattle and the rabbit model. Latency has been shown to be essential for MCF induction. However, the mechanisms causing the activation and proliferation of infected CD8+ T cells are unknown. Many ?-HVs express microRNAs (miRNAs). These small noncoding RNAs can suppress host or viral target genes involved in various pathways and are thought to facilitate viral infection and/or mediate activation and proliferation of infected lymphocytes. AlHV-1 genome has been predicted to encode a large number of miRNAs. However, their precise contribution in viral infection and pathogenesis in vivo remains unknown. Here, we have cloned small RNAs and sequenced 36 potential miRNAs expressed in a lymphoblastoid cell line propagated from a calf infected with AlHV-1 and developing MCF. Among the sequenced candidate miRNAs, 32 were expressed on the reverse strand of the genome in two main clusters. The expression of these 32 viral miRNAs was further validated using Northern blot and qRT-PCR in lymphoid organs of MCF-developing calves or rabbits. To determine the concerted contribution in MCF of 28 viral miRNAs clustered in the non-protein-coding region of the AlHV-1 genome, a recombinant virus was produced. The absence of these 28 miRNAs did not affect viral growth in vitro nor MCF induction in rabbits, demonstrating that AlHV-1 miRNAs clustered in the non-protein-coding genomic region are not essential for MCF induction. Small RNA sequencing from total RNA from AlHV-1-infected bovine lymphoblastoid cell line propagated with interleukin 2

2015-08-27 | E-GEOD-71056 | biostudies-arrayexpress

Small RNA deep sequencing identifies viral microRNAs during malignant catarrhal fever induced by alcelaphine herpesvirus 1

Project description:Alcelaphine herpesvirus 1 (AlHV-1) is a γ-herpesvirus (γ-HV) carried asymptomatically by wildebeest. Upon cross-species transmission, AlHV-1 induces an acute and fatal lymphoproliferative disease named malignant catarrhal fever (MCF) in many ruminants, including cattle and the rabbit model. Latency has been shown to be essential for MCF induction. However, the mechanisms causing the activation and proliferation of infected CD8+ T cells are unknown. Many γ-HVs express microRNAs (miRNAs). These small noncoding RNAs can suppress host or viral target genes involved in various pathways and are thought to facilitate viral infection and/or mediate activation and proliferation of infected lymphocytes. AlHV-1 genome has been predicted to encode a large number of miRNAs. However, their precise contribution in viral infection and pathogenesis in vivo remains unknown. Here, we have cloned small RNAs and sequenced 36 potential miRNAs expressed in a lymphoblastoid cell line propagated from a calf infected with AlHV-1 and developing MCF. Among the sequenced candidate miRNAs, 32 were expressed on the reverse strand of the genome in two main clusters. The expression of these 32 viral miRNAs was further validated using Northern blot and qRT-PCR in lymphoid organs of MCF-developing calves or rabbits. To determine the concerted contribution in MCF of 28 viral miRNAs clustered in the non-protein-coding region of the AlHV-1 genome, a recombinant virus was produced. The absence of these 28 miRNAs did not affect viral growth in vitro nor MCF induction in rabbits, demonstrating that AlHV-1 miRNAs clustered in the non-protein-coding genomic region are not essential for MCF induction.

2015-08-27 | GSE71056 | GEO

Analysis of antigenic polypeptides of malignant catarrhal fever viruses

Project description:Analysis of malignant catarrhal fever virus antigens for diagnostic and therapeutic purposes

| PRJEB40305 | ENA

Transcription profiling by array of bovine gene expression changes during inflammatory gamma-herpesvirus infection

Project description:Changes in gene expression in lymph node and kidney of cattle infected with alcelaphine herpesvirus-1. All animals in the group infected with AlHV-1 showed clinical signs of Malignant catarrhal fever (MCF) within one month. Diagnosis of MCF in these animals was confirmed by diagnostic PCR. No clinical signs were seen in the control animals, which were subject to post-mortem examination separately from the MCF-affected animals. RNA samples from kidney and lymph node of 4 MCF-affected and 4 control animals that passed the RNA quality criteria were used for array analysis. Quality assessments of probe-level Affymetrix chip data and normalised data were carried out using statistical and graphical methods including MA plots and smoothed histogram plots. The MA-plots showed normalisation was effective; while smoothed histograms indicated there was no systematic bias in the data.

2012-10-26 | E-MEXP-3497 | biostudies-arrayexpress

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