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Expression data in KSHV-infected primary rat mesenchymal precursor (MM) cells

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE50381 | GEO | 2013/08/28

SECONDARY ACCESSION(S): PRJNA217372

REPOSITORIES: GEO

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Expression data in KSHV-infected primary rat mesenchymal precursor (MM) cells

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

CD109 is novel KSHV entry receptor in human endothelial cells and enhances infection during cellular senescence

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

HIF1α enrichment on KSHV genome in normoxia and hypoxia

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

Genome-wide mapping of RTA binding sites in KSHV+ PEL cells during KSHV reactivation.

Project description:Chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) analysis was performed during Kaposi's sarcoma-associated herpesvirus (KSHV) reactivation in KSHV+ recombinant primary effusion B-cell lymphoma cells (PEL). RTA binding sites were identified genome-wide in a recombinant PEL cell line called TRExBCBL1-3xFLAG-RTA cells at 12 hours post-induction (hpi) of RTA expression.

2019-01-09 | GSE123897 | GEO

Viral RNA-binding protein KSHV ORF57 and host transcriptome

Project description:Kaposi's sarcoma-associated herpesvirus (KSHV) encodes a viral RNA-binding protein ORF57 that plays an essential role in posttranscriptional regulation of viral gene expression. Ectopice expression of KSHV ORF57 in HEK293T cells was evaluated on its effect on host gene expression in the study, with the cells transfected with an empty vector serving as a control.

2023-02-13 | GSE179728 | GEO

RNA-seq analysis of KSHV-infected BCBL-1 cells, a primary effusion lymphoma cell line

Project description:Primari effusion lymphoma are (PEL) patient-derived transformed B-cells harboring latent Kaposi's sarcoma-associated herpesvirus (KSHV). The treatment of PEL cells with valproic acid (VA) leads to reactivation of KSHV and viral lytic replication. The aim of this project is to evaluate the effect of KSHV lytic infection on expression of the host transcriptome.

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RIG-I and MDA5 fRIP during KSHV lytic reactivation

Project description:The RIG-I like receptors (RLRs) RIG-I and MDA5 are cytosolic RNA helicases best characterized as restriction factors for RNA viruses. However, evidence suggests RLRs participate in innate immune recognition of other pathogens, including DNA viruses. Kaposi's sarcoma-associated herpesvirus (KSHV) is a human gammaherpesvirus and the etiological agent of Kaposi's sarcoma and primary effusion lymphoma (PEL). We demonstrate that RIG-I and MDA5 restrict KSHV lytic reactivation in PEL. By performing fRIP-Seq, we define the in vivo RLR substrates and demonstrate that RIG-I and MDA5-mediated restriction is facilitated exclusively by the recognition of host-derived RNAs.

2018-10-11 | GSE116650 | GEO

Effect of LANA deletion on the host gene expression during de novo KSHV infection of SLK cells.

2016-08-01 | GSE78282 | GEO

Host gene expression analysis in oral epithelial cells upon KSHV infection

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

Effect of LANA deletion on the host gene expression during de novo KSHV infection of SLK cells.

Project description:Human SLK cells were infected with wildtype (wt) and LANA knockout (KO) Kaposi's sarcoma-associated herpesvirus (KSHV), separately for 3 days. Cellular gene expression changes were identified upon the wild type and LANA KO KSHV virus infection compared to the uninfected SLK cells using the human gene expression microarray U133plus2.0. 2 independent biological replicates from uninfected SLK cells, wild type KSHV infected SLK cells at 72hrs post-infection (hpi) , and LANA KO infected SLK cells at 72 hrs post-infection were collected and RNA was prepared for microarray analysis.

2016-08-01 | E-GEOD-78282 | biostudies-arrayexpress

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