RNA sequencing analysis to identify gene targets of Kaposi's sarcoma herpesvirus (KSHV) ORF24
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ABSTRACT:
PROVIDER: PRJNA522743 | ENA |
REPOSITORIES: ENA
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Project description:Transfection of a Kaposi's sarcoma (KS) herpesvirus (KSHV) Bacterial Artificial Chromosome (KSHVBac36) into mouse bone marrow endothelial lineage cells generated a cell (mECK36) that induced KS-like tumors in mice. mECK36 formed KSHV-harboring vascularized spindle-cell sarcomas that were LANA+ and displayed a KSHV and host transcriptomes reminiscent of KS tumors. Keywords: Cell type comparison
2007-01-01 | GSE6482 | GEO
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:Chromatin Immuno-precipitaion sequencing was performed using H3-Ac, H3K4Me3, H3K9Me3, H3K27Me3, LANA, RTA and DNA Polymerase 1 alpha antibodies to investigate its enrichment on Kaposi's sarcoma associated herpesvirus (KSHV) genome in BC3 cells under normoxic or hypoxic conditions
2022-08-15 | GSE202670 | GEO
Project description:The aging process is characterized by cellular functional decline and increased susceptibility to infections. Understanding the association between virus infection and aging is crucial for developing effective strategies against viral infections in older individuals. Kaposi's sarcoma-associated herpesvirus (KSHV) infection increases the risk of Kaposi's sarcoma, a vascular cancer prevalent among the elderly without HIV infection. However, the relationship between KSHV pathogenesis and cellular senescence remains unknown. Here, we demonstrate that KSHV infectivity is significantly increased in senescent human endothelial cells due to enhanced binding of virions to cell surface. Proteomic analysis identified caveolin-1 and CD109 that promote KSHV infection and were significantly upregulated in senescent cells. In particular, CD109 is expressed on cell surface and directly interacts with KSHV virions to enhance KSHV infection. Knockout of CD109 abolished while overexpression of CD109 promote KSHV binding to cell surface, and infectivity. These results identify CD109 as a novel KSHV entry receptor that enhances KSHV infection in senescent cells, which might in part explain the higher sensitivity of elder subjects to KSHV infection and Kaposi's sarcoma.
2024-04-17 | PXD048212 | Pride
Project description:Genome-wide map of viral transcription factor ORF34 binding in Kaposi's Sarcoma Herpesvirus (KSHV)
| PRJNA522742 | ENA
Project description:The Kaposi's sarcoma associated herpesvirus (KSHV) is an oncogenic virus that causes Kaposi's sarcoma, primary effusion lymphoma (PEL), and some forms of multicentric Castleman's disease. The KSHV ORF57 protein is a conserved posttranscriptional regulator of gene expression that is essential for virus replication. ORF57 is multifunctional, but most of its activities are directly linked to its ability to bind RNA. We globally identified virus and host RNAs bound by ORF57 during lytic reactivation in PEL cells using high-throughput sequencing of RNA isolated by crosslinking immunoprecipitation (HITS-CLIP). As expected, ORF57-bound RNA fragments mapped throughout the KSHV genome, including the known ORF57 ligand PAN RNA. In agreement with previously published ChIP results, we observed that ORF57 bound RNAs near the oriLyt regions of the genome. Examination of the host RNA fragments revealed that a subset of the ORF57-bound RNAs was derived from transcript 5´ ends. The position of these 5´-bound fragments correlated closely with the 5´-most exonintron junction of the pre-mRNA. We selected four candidates (BTG1, EGR1, ZFP36, and TNFSF9) and analyzed their pre-mRNA and mRNA levels during lytic phase. Analysis of both steady-state and newly made RNAs revealed that these candidate ORF57-bound pre-mRNAs persisted for longer periods of time throughout infection than control RNAs, consistent with a role for ORF57 in pre-mRNA metabolism. In addition, exogenous expression of ORF57 was sufficient to increase the pre-mRNA levels and, in one case, the mRNA levels of the putative ORF57 targets. These results demonstrate that ORF57 interacts with specific host pre-mRNAs during lytic reactivation and alters their processing, likely by stabilizing pre-mRNAs. These data suggest that ORF57 is involved in modulating host gene expression in addition to KSHV gene expression during lytic reactivation. HITS-CLIP was performed on TREx BCBL-Rta cells 20 hpi using antibodies against ORF57. Three biological replicates were performed.
2015-02-01 | E-GEOD-64413 | biostudies-arrayexpress
Project description:Kaposi's sarcoma-associated herpesvirus (KSHV) can efficiently infect and transform primary rat mesenchymal precursor (MM) cells. Regulation of cell cycle progression and apoptosis by KSHV-encoded microRNAs is required for KSHV-induced cellular transformation and tumorigenesis.
2013-08-28 | GSE50381 | GEO
Project description:Chromatin Immuno-precipitaion sequencing was performed using HIF1 alpha antibodies to investigate its enrichment on Kaposi's sarcoma associated herpesvirus (KSHV) genome in BC3 cells and purified KSHV infected PBMCs under normoxic or hypoxic conditions
2020-11-01 | GSE149401 | GEO
Project description:Kaposi's sarcoma-associated herpesvirus (KSHV) can efficiently infect and transform primary rat mesenchymal precursor (MM) cells. Regulation of cell cycle progression and apoptosis by KSHV-encoded microRNAs is required for KSHV-induced cellular transformation and tumorigenesis. To determine the roles of KSHV miRs in growth deregulation, we infected MM cells with the KSHV miR cluster deletion mutant and monitored infection by examining green fluorescence protein expression from a cassette inserted in the KSHV genome.
2013-08-28 | E-GEOD-50381 | biostudies-arrayexpress
Project description:ORF24 is the core component of a virally encoded transcription complex in KSHV that is active during later stages of infection. ORF24 makes interactions with both promoter DNA and host RNA polymerase II. The aim of this study was to identify the targets of the virally encoded transcription complex by sequencing total RNA from cells that express a mutant ORF24 that does not interact with RNA polymerase II and compare it to RNA from a mutant rescue cell line (WT). We observed that most viral genes were down regulated in the absence of the ORF24-Pol II interaction and as expected, majority of them were late genes.
2019-02-16 | GSE126602 | GEO