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Bcl-xL is required to protect endothelial cells latently infected with KSHV from virus induced intrinsic apoptosis

ABSTRACT: An sgRNA sub-pool derived from hits and controls in a whole genome screen (PMID: 33122441) was used to investigate genes which are essential during latent KSHV infection of human endothelial cells. The initial pool of library transduced cells was used to confirm efficient transduction of the library and effective selection against sgRNAs targeting generally essential genes over the course of the 8 day experiment. Two replicate experiments were done and comparisons between mock infected and KSHV infected cells was used to identify KSHV infection-specific essential genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE226914 | GEO | 2023/05/04

REPOSITORIES: GEO

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Bcl-xL is required to protect endothelial cells latently infected with KSHV from virus induced intrinsic apoptosis

Project description:Bcl-xL is required to protect endothelial cells latently infected with KSHV from virus induced intrinsic apoptosis

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Mock or latently infected KSHV cells (BCBL, SLK and HFF)

Project description:[original title] Mock or latently infected KSHV cells (BCBL, SLK and HFF) vs common reference (mixture of RNA from both infected and uninfected cells). Expression profiling of latently infected cells using a custom tiling microarray. SLK and HFF cells were infected and selected for rKSHV.219. Mock infected SLK and HFF cells served as controls for each of these two stably infected cells, respectively. BJAB cells served as uninfected controls for the BCBL-1 cells. Biological replicates were harvested and analyzed.

2010-03-24 | GSE20443 | GEO

Bcl-XL, but not Bcl-2, can protect human B-lymphoma cell lines from parthenolide-induced apoptosis.

Project description:In this report, we investigated the effects of the natural product parthenolide on human B-lymphoma cell lines. We show that parthenolide inhibited NF-?B transcription factor c-Rel (REL). In addition, the sensitivity of several human B-lymphoma cell lines to parthenolide-induced apoptosis inversely correlated with their levels of anti-apoptosis protein Bcl-X(L). Furthermore, ectopic expression of Bcl-X(L) (but not Bcl-2) in two B-lymphoma cell lines decreased their sensitivity to parthenolide-induced apoptosis. Finally, over-expression of a transforming mutant of REL, which increased expression of endogenous Bcl-X(L), decreased the sensitivity of BJAB B-lymphoma cells to parthenolide-induced apoptosis. These results demonstrate that the NF-?B target gene products Bcl-X(L) and Bcl-2 can play different roles in protecting B-lymphoma cells from chemical-induced apoptosis.

| S-EPMC3288124 | biostudies-literature

Mock or latently infected KSHV cells (BCBL, SLK and HFF)

2010-06-05 | E-GEOD-20443 | biostudies-arrayexpress

Bcl-xl does not have to bind Bax to protect T cells from death.

Project description:Activated T cells die when antigen disappears from animals. This death is caused by proteins related to Bcl-2. Two hypotheses have been suggested to explain the actions of the different types of Bcl-2 proteins. One hypothesis suggests that, when T cells prepare to die, Bak and Bax, the proteins that actually kill activated T cells, are released from antiapoptotic proteins such as Bcl-2 and Bcl-xl. Another hypothesis suggests that Bak and Bax are normally free and are triggered to kill cells by release of messenger proteins, such as Bim, from Bcl-2 and Bcl-xl. Here, a form of Bcl-xl, which lacks a long unstructured loop, is used to show that the first hypothesis is not correct. Bcl-xl without its loop protects activated T cells from death, yet Bcl-xl without its loop cannot bind any form of Bak and Bax. Thus, binding of Bcl-xl to Bak or Bax is not involved in T cell life or death. The loop of Bcl-xl is also somewhat involved in Bcl-xl's binding of Bim because Bcl-xl without its loop binds Bim less well than wild-type Bcl-xl. Moreover, the loop may have additional, as yet unknown, functions because it changes its shape when Bcl-xl binds Bim.

| S-EPMC2118172 | biostudies-literature

microRNA Targetome Analysis of Latently KSHV-infected Primary Effusion Lymphoma Cell lines Using PAR-CLIP

Project description:This SuperSeries is composed of the following subset Series: GSE31745: Primary effusion lymphoma cell lines BC-1 and BC-3 GSE31746: BJAB Cell Lines Transduced with lentiviral vector pNL-SIN-CMV-AcGFP expressing KSHV miRNAs miR-K1, miR-K12-11, or miR-K4-3p GSE32109: microRNA Targetome Analysis of Latently KSHV-infected Primary Effusion Lymphoma Cell lines Using PAR-CLIP [Illumina] Refer to individual Series

2011-11-16 | E-GEOD-32113 | biostudies-arrayexpress

KSHV oral shedding and plasma viremia result in significant changes in the extracellular tumorigenic miRNA expression profile in patients exposed to malaria

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

Synthetic Lethal Interaction Between Loss of Function of OGDH and Bcl-xL in Glioblastoma

Project description:Glioblastoma (GBM) remains an incurable disease, requiring more effective therapies. Through CRISPR and RNAi library screening interrogation we identified several TCA-cycle enzymes as essential for GBM growth. By combining a transcriptome and metabolite screening analyses we discovered that loss of function of OGDH by the clinically validated drug compound, CPI-613, is synthetically lethal with Bcl-xL inhibition (genetically and through the clinically validated BH3-mimetic, ABT263) in patient-derived xenograft as well neurosphere GBM cultures. CPI-613 mediated energy deprivation drives an integrated stress response with an up-regulation of the BH3-only domain protein, Noxa in an ATF4 dependent manner as demonstrated by genetic loss of function experiments. Consistently, silencing of Noxa rescued from cell death induced by CPI-613 in model systems of GBM. In patient-derived xenograft models of GBM in mice, the combination treatment of ABT263 and CPI613 suppressed tumor growth more potently than each compound on its own. Therefore, combined inhibition of Bcl-xL along with interference of the TCA-cycle might be a novel treatment strategy for GBM.

2023-09-01 | GSE223297 | GEO

scRNAseq analysis of lytically and latently infected KSHV-infected iSLK.219 cells with and without caspase inhibitor treatment

Project description:The goal of this analysis was to examine the cell-to-cell variation in Kaposi's sarcoma-associated herpesvirus (KSHV) reactivation and type I interferon response after caspase inhibitor treatment. We profiled the levels of host and viral mRNAs at a single-cell level using the iSLK.219 tissue culture model system (Myoung and Ganem, 2011). We examined gene expression in lytically reactivating cells, lytically reactivating cells treated with caspase inhibitors, and lytically reactivating cells treated with casapse inhibitors and neutralizing antibodies against interferons. (we previously described that caspase inhibitors elicit an interferion response in KSHV-infected cells, Tabtieng et al., 2018). We also examined gene expression in a mixture of latently infected cells and uninfected cells as a control.

2022-09-29 | GSE190558 | GEO

KSHV uses viral IL6 to expand infected immunosuppressive macrophages (scRNA-seq)

Project description:Kaposi’s sarcoma-associated herpesvirus (KSHV) is an oncogenic double-stranded DNA virus and the etiologic agent of Kaposi’s sarcoma and hyperinflammatory lymphoproliferative disorders. Understanding the mechanism by which KSHV increases infected cell populations is crucial for curing KSHV-associated diseases. Here, we demonstrate that KSHV preferentially infects CD14+ monocytes and sustains viral replication through the viral interleukin-6 (vIL-6)-mediated activation of STAT1 and 3. Using vIL6-sufficient and vIL6-deficient recombinant KSHV, we demonstrated that vIL6 plays a critical role in promoting the proliferation and differentiation of KSHV-infected monocytes into macrophages. The macrophages derived from vIL6-sufficient (wild type) KSHV infection showed a distinct transcriptional profile of elevated IFN-pathway activation with immune suppression and were compromised in T-cell stimulation function compared to those from vIL6-deficient KSHV infection or uninfected control. These results highlight a clever strategy, in which KSHV utilizes vIL6 to secure its initial viral pool by expanding infected dysfunctional macrophages. This mechanism also facilitates KSHV to escape from host immune surveillance and to establish a lifelong infection.

2023-08-30 | GSE227166 | GEO

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