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ABSTRACT: 4SU-Seq of KSHV lytic reactivation in iSLK-BAC16 model

PROVIDER: PRJNA851589 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19792336_1.fastq.gz	Fastqsanger.gz
	SRR19792336_2.fastq.gz	Fastqsanger.gz
	SRR19792337_1.fastq.gz	Fastqsanger.gz
	SRR19792337_2.fastq.gz	Fastqsanger.gz
	SRR19792338_1.fastq.gz	Fastqsanger.gz

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Project description:ORF57 eCLIP of KSHV lytic reactivation in iSLK-BAC16 model

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Up-regulation of ATF4-LAMP3 axis by ORF45 facilitate lytic replication of Kaposi’s sarcoma-associated herpesvirus

Project description:To investigate the regulation of ER stress-related gene expression by KSHV-ORF45 during lytic replication, we performed RNA-sequencing analysis of iSLK-BAC16 vs. iSLK-STOP45 cells under lytic induction for 72h. When the differentially expressed genes were filtered and analyzed, we found that ER stress-related gene expression was much low in iSLK-STOP45 cells compared with iSLK-BAC16 cells, indicating that ORF45 expression is required for induction of ER stress.To further reveal the signal transduction of LAMP3 in KSHV lytic replication, RNA-sequencing analysis was performed to identify the differentially expressed genes (DEGs) in normal vs. LAMP3-silenced cells under lytic replication. A total of 35372 raw read targets were obtained and all DEG clusters were filtered and analyzed by KEGG pathway enrichment analysis. Eleven pathway were significantly enriched over 10 fold in LAMP3-depleted cells compared with control cells, including PI3K-Akt signaling pathway.Given that Akt and ERK activation play the important roles in KSHV lytic replication, we conclude that LAMP3 might promote Akt and ERK activation and then consequently facilitate KSHV lytic replication.

2022-11-09 | GSE192724 | GEO

Analyzing ceRNA networks involved in KSHV lytic replication mediated by vIRF1 or vFLIP.

Project description:Whole-transcriptome sequencing (RNA sequencing [RNA-seq]) was performed in the viral producer cell lines iSLK-RGB BAC16,iSLK-RGB-K9 mutant and iSLK-RGB-K13 mutant cells to uncover the global landscape of long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), mRNAs and microRNAs (miRNAs) in KSHV replication mediated by vIRF1 or vFLIP.

2022-02-24 | GSE180921 | GEO

Nuclesome Distribution data for KSHV reactivation

Project description:iSLK.219 cells at 0, 6, 12, 24, and 48 hours post KSHV reactivation. Nucleosome occupancy plays a key role in regulating access to the eukaryotic genomes. Although various chromatin regulatory complexes are known to regulate nucleosome occupancy, the role of DNA sequence in this regulation remains unclear, particularly in mammals. To address this problem, we measured nucleosome distribution at high temporal resolution in human cells at hundreds of genes during the reactivation of KaposiM-bM-^@M-^Ys sarcoma-associated herpesvirus (KSHV). We show that nucleosome redistribution peaks at 24 hours post KSHV reactivation and that the nucleosomal redistributions are widespread and transient. To clarify the role of DNA sequence in these nucleosomal redistributions, we compared the genes with altered nucleosome distribution to a sequence-based computer model and in vitro assembled nucleosomes. We demonstrate that both the predicted model and the assembled nucleosome distributions are concordant with the majority of nucleosome redistributions at 24 hours post KSHV reactivation. We suggest a model in which loci are held in unfavorable chromatin architecture and M-bM-^@M-^\springM-bM-^@M-^] to a transient intermediate state directed by DNA sequence information. We propose that DNA sequence plays a more considerable role in the regulation of nucleosome positions than was previously appreciated. The surprising findings that nucleosome redistributions are widespread, transient, and DNA-directed shift the current perspective regarding regulation of nucleosome distribution in humans. iSLK.219 cells at 0, 6, 12, 24, and 48 hours post KSHV reactivation.

2013-11-19 | E-GEOD-52453 | biostudies-arrayexpress

Mock, latent, and lytic rKSHV.219-infected iSLK cells [Expt3]

Project description:Expression profiling of stably infected epithelial cells using a custom tiling microarray. iSLK was infected with rKSHV.219 and selected with puromycin. Mock infected iSLK served as control for iSLK.219. Lytic reactivation of iSLK.219 was induced with 1 ug/mL doxycycline for 48 hours.

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ac4C-seq of cellular and KSHV transcripts in iSLK-Puro, iSLK-KSHV (i.e. iSLK-RGB), iSLK-KSHV (WT), iSLK-KSHV (ΔNAT10) cells

Project description:We used ac4C-seq to detedc cellular and KSHV transcripts in iSLK-Puro, iSLK-KSHV, iSLK-KSHV (WT), iSLK-KSHV (ΔNAT10) cells after after doxycycline and sodium butyrate treatment.

2023-09-27 | GSE174161 | GEO

Quantitative proteomics analysis of lytic KSHV infection in human endothelial cells reveals novel targets of viral immune modulation

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

Quantitative proteomics analysis of lytic KSHV infection in human endothelial cells reveals novel targets of viral immune modulation

2022-05-26 | PXD017365 | Pride

N6-methyladenosine modification in lytic viral gene expression during Kaposi's sarcoma-associated herpesvirus infection [MeRIP-seq]

Project description:Methylation at the N6 position of adenosine (m6A) is a highly prevalent reversible modification within eukaryotic mRNAs that has been linked to many stages of RNA processing and fate. Recent studies suggest that m6A deposition and proteins involved in the m6A pathway play a diverse set of roles in either restricting or modulating the lifecycles of select viruses. Here, we report that m6A levels are significantly increased in cells infected with the oncogenic human DNA virus Kaposi’s sarcoma-associated herpesvirus (KSHV). Transcriptome-wide m6A-sequencing of the KSHV-positive renal carcinoma cell line iSLK.219 during lytic reactivation revealed the presence of m6A across multiple kinetic classes of viral transcripts, and a concomitant decrease in m6A levels across much of the host transcriptome.

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Identification of symmetric methylation of histone H4 arginine 3 on KSHV genome (iSLKBac16WT ChIP-Seq)

Project description:The objective of this study was to identify the symmetric methylation sites on KSHV genome during latency and lytic reactivation

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