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ABSTRACT: Total RNA-Seq in KSHV lytic reactivation with spliceosome inhibition

PROVIDER: PRJNA851982 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19793314_1.fastq.gz	Fastqsanger.gz
	SRR19793314_2.fastq.gz	Fastqsanger.gz
	SRR19793315_1.fastq.gz	Fastqsanger.gz
	SRR19793315_2.fastq.gz	Fastqsanger.gz
	SRR19793316_1.fastq.gz	Fastqsanger.gz

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Project description:Total RNA-Seq in KSHV lytic reactivation model with RNA ligase depletion

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The Integrator complex is required for optimal lytic lifecycle of Kaposi’s Sarcoma-Associated Herpesvirus [ChIP-seq]

Project description:The Integrator complex (INT) is an essential regulator of RNA biogenesis across evolution. Most current findings describe INT’s function in states of equilibrium, presenting a research gap in INT’s role in dynamic states, such as in infections and cancers. Viruses hijack cellular RNA machinery to transcribe their genes and produce viral progeny, presenting a unique condition to investigate INT-dependent RNA regulation under perturbation. Kaposi’s sarcoma-associated herpesvirus (KSHV) is an oncogenic DNA virus that causes two deadly cancers, Kaposi’s sarcoma and primary effusion lymphoma. KSHV undergoes a highly regulated and robust transcription of viral genes upon lytic reactivation, providing a complex and dynamic system to investigate Integrator-mediated viral/host RNA metabolism. We find that Integrator subunit 11 (INTS11), the enzymatic core of INT, is required for an optimal KSHV lytic lifecycle following reactivation from latency or after primary infection. While INTS11 knockdown’s impact on the human transcriptome remains bi-directional, it almost exclusively represses the KSHV transcriptome throughout the lytic stages. This inhibits viral protein expression, viral genome replication, and virion production. Integrator subunits 9 and 6 are also important for the KSHV lytic lifecycle. RNA-seq analyses revealed dynamic and unique signatures of human transcriptomes during each latent or lytic stage. Mechanistically, ChIP-seq analysis showed that INTS11 is broadly and increasingly recruited to the KSHV genome with unique binding site specificities as the lytic cycle progresses, suggesting that KSHV hijacks INTS11 to facilitate its lytic lifecycle. These findings reveal unexpected and critical roles of the Integrator complex in the lytic phase of KSHV infection.

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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.

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

2021-08-23 | PXD021387 | Pride

The Integrator complex is required for optimal lytic lifecycle of Kaposi’s Sarcoma-Associated Herpesvirus [RNA-seq]

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Next Generation Sequencing analysis of KSHV lytic replication in TREx-BCBL1-RTA cells

Project description:Purpose: miR-Seq was utilised to identify miRNAs which are altered during the course of KSHV lytic replication at 0, 16 and 24 hours post reactivation in TREx-BCBL1-RTA cells. Methods: Virus lytic replication was induced via addition of 2 µg/mL doxycycline hyclate (Sigma-Aldrich). Total RNA was extracted from TREx-BCBL-1s at 0, 16 and 24 hours post lytic induction. Small RNA libraries were prepared using the TruSeq Small RNA Library Prep Kit (Illumina). Quality filtered (Q < 20), and adapter trimmed reads (Trimmomatic v0.39) [59] were aligned to the GRCh38/hg38 assembly of the human genome using Bowtie2 (V 2.4.2).

2022-02-09 | GSE186652 | GEO

Effect of KSHV lytic reactivation on host mRNA m5C modification landscape in lymphoma B cell

Project description:Herpesviruses are a group of double-stranded DNA viruses known to develop versatile viral strategies to escape host immune surveillance for promoting their replication and propagation. This is illustrated by Kaposi’s sarcoma-associated herpesvirus (KSHV), an oncogenic gamma-herpesvirus that overcomes host immune suppression by multiple mechanisms. In this study, we reported that KSHV dysregulates 5-methylcytosine (m5C) modification and mRNA stability of host antiviral factors to benefit its lytic replication. KSHV lytic reactivation or de novo challenge led to downregulation of m5C RNA methyltransferases, NSUN2 and NSUN1 (NSUN2/1), while NSUN2/1 depletion promoted KSHV lytic replication. We further performed the RNA bisulfite sequencing (RNA-BS-seq) to identify KSHV-dependent m5C modification of host mRNAs. Overall, our results highlighted a new strategy for human gamma-herpesviruses to counteract host antiviral factors and promote their lytic replication by manipulating host m5C RNA methylation.

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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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Identification of symmetric methylation of histone H4 arginine 3 on KSHV genome (H4R3me2s 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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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

2017-04-24 | GSE98087 | GEO

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