Ontology highlight
ABSTRACT:
PROVIDER: PRJNA851845 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20020757_1.fastq.gz | Fastqsanger.gz | |||
| SRR20020757_2.fastq.gz | Fastqsanger.gz | |||
| SRR20020758_1.fastq.gz | Fastqsanger.gz | |||
| SRR20020758_2.fastq.gz | Fastqsanger.gz | |||
| SRR20020759_1.fastq.gz | Fastqsanger.gz |
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Project description:Deregulation of host lncRNAs following infection with Kaposi’s sarcoma-associated herpesvirus (KSHV) was assessed. Total RNA was prepared from uninfected TIVE cells (telomerase-immortalized vein endothelial cells), and from TIVE cells latently infected with either wild-type KSHV or with a deletion mutant (Δcluster-KSHV) lacking ten of the twelve KSHV microRNA genes. The RNA was converted to labeled cRNA and used to probe a human lncRNA microarray. The goal was to investigate which host lncRNAs were either up- or down-regulated during latent infection with KSHV, and to determine if deregulation of host lncRNAs was dependent on KSHV miRNAs.
2017-07-12 | GSE89114 | GEO
Project description:We performed global host transcriptome analysis in human gingival epithelial cells upon Kaposi's sarcoma-associated herpesvirus (KSHV) infection to identify differentially expressed host genes. KSHV is a human oncogenic virus, which establishes persistent infection of the host. We collected mock as well as KSHV infected human gingival epithelial cells at 8 hours post-infection (hpi) in triplicate, and used the purified RNA for creating RNA-seq libraries for the analysis.
2023-01-25 | GSE223396 | GEO
Project description:Purpose: The goal of this study is to compare the small RNA expression profile in exosomes isolated from plasma samples from KSHV+/HIV- and KSHV+/HIV+ patients Methods: Total RNA was isolated from plasma exosomes obtained from Ugandan patients with different viral status. A small RNA fraction was gel purified and was used to make sequencing libraries. At least 14 million read sequences were obtained from each library. Non-redondant sequences were then aligned to genomic (hg19) and and mRNA sequence (hg19) using bowtie 2; sequences with perfect-match and 1bp mismatch alignments were retained for further analysis using DEseq2 Methods: Total RNA was isolated from plasma obtained from KSHV-infected patients with or without HIV co-infection. A small RNA fraction was gel purified and was used to make sequencing libraries. At least 14 million read sequences were obtained from each library. Non-redondant sequences were then aligned to genomic (hg19) and and mRNA sequence (hg19) using bowtie 2; sequences with perfect-match and 1bp mismatch alignments were retained for further analysis using DEseq2 Results:Plasma exosomes isolated from either KSHV-infected or KSHV/ HIV co-infected patients exposed to malaria are overwhelmingly populated with YRNAs instead of miRNAs Results: KSHV oral sheeding correlated with the detection of a pro-tumorigenic cellualr miRNA profile in plasma. KSHV plasma viremia is associated with the detec tion of KSHV encoded miRNA in plasma Conclusions: Ugandan patients exposed to Plasmodium falciparum show an unusual repertoire of small RNAs in plasma exosomes, as the exosomal RNA is mostly composed of small RNA from the YRNA biotype Conclusions: Our study represents the first detailed analysis of the small RNA biotypes present in plasma from KSHV infected and KSHV/HIV co-infected patients without clinical sign of KSHV associated malignancies.
2018-02-09 | GSE106238 | GEO
Project description:Kaposi’s Sarcoma associated herpesvirus (KSHV) is an oncogenic human virus and leading cause of mortality in HIV infection. Reactivation of KSHV from latent to lytic stage infection initiates a cascade of viral gene expression, and here we show how these changes remodel the host cell proteome to enable viral replication. By undertaking a systematic and unbiased analysis of changes to the endothelial cell proteome following lytic KSHV reactivation, we quantify >7000 cellular and 71 viral proteins. Lytic KSHV infection resulted in >2-fold downregulation of 291 cellular proteins, including PKR, the key cellular sensor of double-stranded RNA. A complementary KSHV genome-wide CRISPR genetic screen identified K5 as the viral gene responsible for the downregulation of two novel KSHV targets, Nectin-2 and CD155, both ligands of the NK cell DNAM-1 receptor. Despite the high episome copy number, we show that CRISPR Cas9 provides a remarkably efficient way to target KSHV genomes.
2021-08-23 | PXD021387 | Pride
Project description:Kaposi’s Sarcoma associated herpesvirus (KSHV) is an oncogenic human virus and leading cause of mortality in HIV infection. Reactivation of KSHV from latent to lytic stage infection initiates a cascade of viral gene expression, and here we show how these changes remodel the host cell proteome to enable viral replication. By undertaking a systematic and unbiased analysis of changes to the endothelial cell proteome following lytic KSHV reactivation, we quantify >7000 cellular and 71 viral proteins. Lytic KSHV infection resulted in >2-fold downregulation of 291 cellular proteins, including PKR, the key cellular sensor of double-stranded RNA. A complementary KSHV genome-wide CRISPR genetic screen identified K5 as the viral gene responsible for the downregulation of two novel KSHV targets, Nectin-2 and CD155, both ligands of the NK cell DNAM-1 receptor. Despite the high episome copy number, we show that CRISPR Cas9 provides a remarkably efficient way to target KSHV genomes.
2022-05-26 | PXD017365 | Pride
Project description:Latency-associated nuclear antigen (LANA), a multifunctional protein expressed by the Kaposi sarcoma-associated herpesvirus (KSHV) in latently-infected cells, is required for stable maintenance of the viral episome. This is mediated by two interactions: LANA binds to specific sequences (LBS1 and 2) on viral DNA, and also engages host histones, tethering the viral genome to host chromosomes in mitosis. LANA has also been suggested to affect host gene expression, but both the mechanism(s) and role of this dysregulation in KSHV biology remain unclear. Here we have examined LANA interactions with host chromatin on a genome-wide scale using ChIP-seq, and show that LANA predominantly targets human genes near their transcriptional start sites (TSSs). These host LANA-binding sites are generally found within transcriptionally active promoters and display striking overrepresentation of a consensus DNA sequence virtually identical to the LBS1 motif in KSHV DNA. Comparison of the ChIP-seq profile with whole transcriptome (RNA-seq) data reveals that few of the genes that are differentially regulated in latent infection are occupied by LANA at their promoters. This suggests that direct LANA binding to promoters is not the prime determinant of altered host transcription in KSHV-infected cells. Most surprisingly, the association of LANA to both host and viral DNA is strongly disrupted during the lytic cycle of KSHV. This disruption can be prevented by the inhibition of viral DNA synthesis, suggesting the existence of novel and potent regulatory mechanisms linked to either viral DNA replication or late gene expression. Profiling of KSHV LANA positioning on the host genome and examination of gene expression from promoters bound by KSHV LANA.
2014-04-01 | E-GEOD-56144 | biostudies-arrayexpress
Project description:KaposiM-bM-^@M-^Ys sarcoma-associated herpesvirus (KSHV) is an oncogenic gammaherpesvirus which establishes latent infection in endothelial and B cells, as well as in primary effusion lymphoma (PEL). During latency, the viral genome exists as a circular DNA minichromosome (episome) and is packaged into chromatin analogous to human chromosomes. Only a small subset of promoters, those which drive latent RNAs, are active in latent episomes. In general, nucleosome depletion (M-bM-^@M-^\open chromatinM-bM-^@M-^]) is a hallmark of eukaryotic regulatory elements such as promoters and transcriptional enhancers or insulators. We applied formaldehyde-assisted isolation of regulatory elements (FAIRE) followed by next-generation sequencing to identify regulatory elements in the KSHV genome and integrated these data with previously identified locations of histone modifications, RNA polymerase II occupancy, and CTCF binding sites. We found that (i) regions of open chromatin were not restricted to the transcriptionally defined latent loci; (ii) open chromatin was adjacent to regions harboring activating histone modifications, even at transcriptionally inactive loci; and (iii) CTCF binding sites fell within regions of open chromatin with few exceptions, including the constitutive LANA promoter and the vIL6 promoter. FAIRE-identified nucleosome depletion was similar among B and endothelial cell lineages, suggesting a common viral genome architecture in all forms of latency. Ten total samples analyzed by FAIRE-seq from latent KSHV-infected cell lines. Two replicates were performed for BC1, KSHV-BJAB, KSHV-HUVEC, and L1-TIVE cells using the Illumina HiSeq 2000 platform. For BCBL1 cells, 1 FAIRE-seq sample and 1 non-cross-linked control BCBL1 sample was analyzed using the Illumina GAIIx
2013-09-05 | E-GEOD-50581 | biostudies-arrayexpress