Kaposi's sarcoma-associated herpes virus
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE1377 | GEO | 2004/05/08
SECONDARY ACCESSION(S): PRJNA90025
REPOSITORIES: GEO
Similar Datasets
Project description:Primary human dermal endothelial cells were infected or NOT infected with isolated Kaposi's sarcoma associated herpes virus for 7 days. Total RNA was isolated using Trireagent and subjected to microarray.
2008-06-12 | E-GEOD-1377 | biostudies-arrayexpress
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:Identification of the relationships of Kaposi sarcoma (KS), normal skin to various cell cultures. The effects of KS herpes virus, the infectious cause of KS, on infected endothelial cells are also investigated.
2004-08-01 | E-MEXP-66 | biostudies-arrayexpress
Project description:Kaposi's Sarcoma (KS) is a proliferation of aberrant vascular structures lined by spindle cells, and is caused by a gammaherpes virus (HHV8/KSHV). Its course is aggravated by co-infection with HIV-1, where the timing of infection with HIV-1 and HHV8 is important for the clinical outcome. METHODS: In order to better understand the pathogenesis of KS, we have analysed tissue from two AIDS-KS lesions, and from normal skin by serial analysis of gene expression (SAGE). Semi-quantitative RT-PCR was then used to validate the results. RESULTS: The expression profile of AIDS-related KS (AIDS-KS) reflects an active process in the skin. Transcripts of HHV8 were found to be very low, and HIV-1 mRNA was not detected by SAGE, although it could be found using RT-PCR. Comparing the expression profile of AIDS-KS tissue with publicly available SAGE libraries suggested that AIDS-KS mRNA levels are most similar to those in an artificially mixed library of endothelial cells and leukocytes, in line with the description of KS lesions as containing spindle cells with endothelial characteristics, and an inflammatory infiltrate. At least 64 transcripts were found to be significantly elevated, and 28 were statistically downregulated in AIDS-KS compared to normal skin. Five of the upregulated mRNAs, including Tie 1 and sialoadhesin/CD169, were confirmed by semi-quantitative PCR to be elevated in additional AIDS-KS biopsies. Antibodies to sialoadhesin/CD169, a known marker of activated macrophages, were shown to specifically label tumour macrophages. CONCLUSION: The expression profile of AIDS-KS showed 64 genes to be significantly upregulated, and 28 genes downregulated, compared with normal skin. One of the genes with increased expression was sialoadhesin (CD169). Antibodies to sialoadhesin/CD169 specifically labelled tumour-associated macrophages, suggesting that macrophages present in AIDS-KS lesions belong to a subset of human CD169+ macrophages. Keywords: other
2003-07-16 | GSE514 | GEO
Project description:Metabolic reprogramming of Kaposi’s sarcoma associated herpes virus infected B-cells in hypoxia
| PRJNA471994 | 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:LMP2A of Epstein-Barr virus is a receptor that mimics an activated B cell receptor, BCR. K1 and K15, related receptors of Kaposi sarcoma-associated herpes virus, KSHV, are expressed in virus-associated tumors but their functions are less obvious. We addressed this uncertainty with mutant EBVs encoding the KSHV genes K1 or K15 in lieu of LMP2A and infected primary human B cells with them. K1 and K15 encoded proteins appear to have noncomplementing redundant functions in this model but our findings suggest that both KSHV proteins can replace LMP2A’s key activities contributing to the survival, activation and proliferation of B cells.
2014-04-01 | GSE53914 | GEO
Project description:LMP2A of Epstein-Barr virus is a receptor that mimics an activated B cell receptor, BCR. K1 and K15, related receptors of Kaposi sarcoma-associated herpes virus, KSHV, are expressed in virus-associated tumors but their functions are less obvious. We addressed this uncertainty with mutant EBVs encoding the KSHV genes K1 or K15 in lieu of LMP2A and infected primary human B cells with them. K1 and K15 encoded proteins appear to have noncomplementing redundant functions in this model but our findings suggest that both KSHV proteins can replace LMP2AM-bM-^@M-^Ys key activities contributing to the survival, activation and proliferation of B cells. We infected unsorted B cells with the four virus stocks, wt EBV, K1 EBV, K15 EBV or M-NM-^TLMP2A EBV, adjusted to yield similar rates of EBV-activated and growth transformed B cells. Eight days p.i. activated B cells in the lymphocyte gate were collected by FACS sorting and their RNAs analyzed with the aid of the Affymetrix GeneChip Human Gene 1.0 ST Array covering the whole transcriptome of approx. 29,000 annotated human genes. B cell preparations from four different donors were infected and analyzed accordingly.
2014-04-01 | E-GEOD-53914 | biostudies-arrayexpress
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