Murid herpesvirus 68
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA232261 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1068250.fastq.gz | Fastqsanger.gz | |||
| SRR1068251.fastq.gz | Fastqsanger.gz | |||
| SRR1068361.fastq.gz | Fastqsanger.gz | |||
| SRR1068252.fastq.gz | Fastqsanger.gz | |||
| SRR1068253.fastq.gz | Fastqsanger.gz |
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Project description:Murine gammaherpesvirus 68 (MHV-68) is closely related to Epstein-Barr virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV) and provides a small animal model to study the pathogenesis of gammaherpesvirus (γHV) infections. To completely explore the potential of the MHV-68 system for the investigation of gHV miRNAs, it would be desirable to know the number and expression patterns of all miRNAs encoded by MHV-68. By using small RNA deep sequencing, we systematically investigated the MHV-68 miRNA expression profiles in both lytically and persistently infected cells. In addition to the known nine MHV-68 miRNAs, we identified six novel MHV-68 miRNA genes and analyzed the expression levels of all MHV-68 miRNAs. Furthermore, we also characterized the cellular miRNA expression signatures in MHV-68 infected versus non-infected NIH3T3 fibroblasts and in TPA-treated versus non-treated S11 cells. We found that mmu-mir-15b and mmu-mir-16 are highly upregulated upon MHV-68 infection of NIH3T3 cells, indicating a potential role of cellular miRNAs during MHV-68 infection. Our data will aid to fully explore the functions of gHV miRNAs.
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Project description:Mus musculus strain:Murid herpesvirus 4 Raw sequence reads
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Project description:Murine gammaherpesvirus 68 (MHV-68) is closely related to Epstein-Barr virus (EBV) and KaposiM-bM-^@M-^Ys sarcoma-associated herpesvirus (KSHV) and provides a small animal model to study the pathogenesis of gammaherpesvirus (M-NM-3HV) infections. To completely explore the potential of the MHV-68 system for the investigation of gHV miRNAs, it would be desirable to know the number and expression patterns of all miRNAs encoded by MHV-68. By using small RNA deep sequencing, we systematically investigated the MHV-68 miRNA expression profiles in both lytically and persistently infected cells. In addition to the known nine MHV-68 miRNAs, we identified six novel MHV-68 miRNA genes and analyzed the expression levels of all MHV-68 miRNAs. Furthermore, we also characterized the cellular miRNA expression signatures in MHV-68 infected versus non-infected NIH3T3 fibroblasts and in TPA-treated versus non-treated S11 cells. We found that mmu-mir-15b and mmu-mir-16 are highly upregulated upon MHV-68 infection of NIH3T3 cells, indicating a potential role of cellular miRNAs during MHV-68 infection. Our data will aid to fully explore the functions of gHV miRNAs. A mouse fibroblast cell line infected with/without MHV-68 and a MHV-68 infected mouse B lymphoma cell line treated with/without TPA (4 samples in total) were examined.
2010-07-15 | E-GEOD-22938 | biostudies-arrayexpress
Project description:Zoysia japonica cultivar:68 Transcriptome or Gene expression
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Project description:Mentha canadensis cultivar:68-7 Transcriptome or Gene expression
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Project description:Previous studies identified a role for latent herpesvirus infection in cross-protection to infection and exacerbation of chronic inflammatory diseases. Here, we compared the gene expression signature from livers, spleens and brains of mice infected with wild-type gammaherpesvirus 68 (MHV68), a mutant virus defective in the establishment of latency (ORF73.stop) or mockulum. We identified over 600 genes differentially expressed in organs of mice latently infected with MHV68 and found distinct sets of genes linked to different pathways were altered in spleen compared to liver. Several of the most differentially expressed latency-specific genes (e.g. IFNγ, Cxcl9, Ccl5) are associated with known latency-specific phenotypes. RNA was extracted from livers, spleens and brains of 7-9 week old male C57Bl/6 mice infected with gammaherpesvirus 68 (MHV68), a virus defective in establishment of latency (ORF73.stop) or mockulum. RNA from 3-4 mice per treatment was pooled and analyzed by M430 2.0 Affymetrix Gene Chip. Three biologic replicates were analyzed for all conditions, except mock livers, for which four biologic replicates were analyzed.
2013-10-18 | E-GEOD-51365 | biostudies-arrayexpress
Project description:Previous studies identified a role for latent herpesvirus infection in cross-protection to infection and exacerbation of chronic inflammatory diseases. Here, we compared the gene expression signature from livers, spleens and brains of mice infected with wild-type gammaherpesvirus 68 (MHV68), a mutant virus defective in the establishment of latency (ORF73.stop) or mockulum. We identified over 600 genes differentially expressed in organs of mice latently infected with MHV68 and found distinct sets of genes linked to different pathways were altered in spleen compared to liver. Several of the most differentially expressed latency-specific genes (e.g. IFNγ, Cxcl9, Ccl5) are associated with known latency-specific phenotypes.
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Project description:Gammaherpesvirinae, such as the human Epstein-Barr virus (EBV) and the Kaposi's sarcoma associated herpesvirus (KSHV) are highly prevalent pathogens that have been associated with several neoplastic diseases. As EBV and KSHV are host-range specific and replicate poorly in vitro, animal counterparts such as Murid herpesvirus-4 (MuHV-4) have been widely used as models. In this study, we used MuHV-4 in order to improve the knowledge about proteins that compose gammaherpesviruses virions. To this end, MuHV-4 extracellular virions were isolated and structural proteins were identified using liquid chromatography tandem mass spectrometry-based proteomic approaches. These analyses allowed the identification of 31 structural proteins encoded by the MuHV-4 genome which were classified as capsid (8), envelope (9), tegument (13) and unclassified (1) structural proteins. In addition, we estimated the relative abundance of the identified proteins in MuHV-4 virions by using exponentially modified protein abundance index analyses. In parallel, several host proteins were found in purified MuHV-4 virions including Annexin A2. Although Annexin A2 has previously been detected in different virions from various families, its role in the virion remains controversial. Interestingly, despite its relatively high abundance in virions, Annexin A2 was not essential for the growth of MuHV-4 in vitro. Altogether, these results extend previous work aimed at determining the composition of gammaherpesvirus virions and provide novel insights for understanding MuHV-4 biology.
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