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ABSTRACT: ChIP-Seq of HSV-1 (tsKos) Productive Infection

PROVIDER: PRJNA508791 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8288210.fastq.gz	Fastqsanger.gz
	SRR8288205.fastq.gz	Fastqsanger.gz
	SRR8288206.fastq.gz	Fastqsanger.gz
	SRR8288207.fastq.gz	Fastqsanger.gz
	SRR8288208.fastq.gz	Fastqsanger.gz

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Project description:ChIP-Seq of HSV-1 Productive Infection

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Project description:The goal of this study was to determine how RNA poymerase II (Pol II) occupancy changed in response to herpes simplex virus-1 (HSV-1) infection using ChIP-seq of Pol II. ChIP assays were performed 4 hours after cells were infected (or mock infected) with HSV-1. Because host cell Pol II transcribes the HSV-1 genome, the ChIP-seq data also reveal polymerase occupancy on the viral genome.

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Project description:GTF ChIP-Seq of WT (KOS) and ICP4 null (n12) HSV-1 Productive Infection in MRC5 cells

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Project description:Histone ChIP-Seq of WT (KOS) and ICP4 null (n12) HSV-1 Productive Infection in MRC5 cells

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HSV-1 infection induces a delay of promoter-proximal pausing linked to a shift of H2A.Z-containing +1 nucleosomes (ATAC-seq)

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Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ChIP-seq, we found that the enrichment of P65 in proinflammatory cytokines(Il1b, Il6, Il12b, etc.) promoter regions was decreased due to Rpsa deficiency.

2023-11-12 | GSE204891 | GEO

Deficiency of Rpsa results in reduced levels of H3K4me3 in inflammatory cytokines promoter regions

Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ChIP-seq, we found that the level of H3K4me3 in proinflammatory cytokines(Il1b, Il6, Il12b, etc.) promoter regions was decreased due to Rpsa deficiency.

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Mass spectrometric characterization of HSV-1 L-particles from human dendritic cells and BHK21 cells and analysis of their functional role Part B

Project description:Herpes simplex virus type 1 (HSV-1) is a very common human pathogenic virus among the world’s 12 population. The lytic replication cycle of HSV-1 is, amongst others, characterized by a tripartite viral 13 gene expression cascade, the assembly of nucleocapsids involving their subsequent nuclear egress, 14 tegumentation, re-envelopment and the final release of progeny viral particles. During productive 15 infection of a multitude of different cell types, HSV-1 generates not only infectious heavy (H-) 16 particles, but also non-infectious light (L-) particles, lacking the capsid. In monocyte-derived mature 17 dendritic cells (mDCs), HSV-1 causes a non-productive infection with the predominant release of L-18 particles. Until now, the generation and function of L-particles is not well understood, however, they 19 are described as factors transferring viral components to the cellular microenvironment. To obtain 20 deeper insights into the L-particle composition, we performed a mass-spectrometry-based analysis of 21 L-particles derived from HSV-1-infected mDCs or BHK21 cells and H-particles from the latter one. 22 In total, we detected 63 viral proteins in both H- and L-particle preparations derived from HSV-1-23 infected BHK21 cells. In L-particles from HSV-1-infected mDCs we identified 41 viral proteins 24 which are differentially distributed compared to L-particles from BHK21 cells. In this study, we 25 present data suggesting that L-particles modify mDCs and suppress their T cell stimulatory capacity. 26 Due to the plethora of specific viral proteins incorporated into and transmitted by L-particles, it is 27 tempting to speculate that L-particles manipulate non-infected bystander cells for the benefit of the 28 virus.

2021-09-09 | PXD020846 | Pride

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