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H3K4me3 ChIPmentation on HSV-1 infected primary human fibroblasts

ABSTRACT: H3K4me3 ChIPmentation on HSV-1 infected primary human fibroblasts

PROVIDER: PRJNA549467 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9320373_1.fastq.gz	Fastqsanger.gz
	SRR9320373_2.fastq.gz	Fastqsanger.gz
	SRR9320374_1.fastq.gz	Fastqsanger.gz
	SRR9320374_2.fastq.gz	Fastqsanger.gz
	SRR9320375_1.fastq.gz	Fastqsanger.gz

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H3K4me3 ChIPmentation on HSV-1 infected primary human fibroblasts

Project description:Primary human fetal foreskin fibroblasts (HFFFs) were infected with wild-type simplex virus 1 (HSV-1) strain 17 at a multiplicity of infection (MOI) of 10. ChIPmentation libraries were prepared starting with 500,000 cells per condition following the protocol described by Christian Schmidl et al, Nature Methods 2015

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Project description:Primary human foreskin fibroblasts (HFF) were infected with wild-type herpes simplex virus 1 (HSV-1) strain 17 or its vhs null mutant, or with BAC-derived viruses expressing either a wild-type or catalytically inactive vhs with the D195N mutation at a multiplicity of infection (MOI) of 10. Chromatin-associated RNA was prepared and subjected to RNA-seq.

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Project description:Primary human foreskin fibroblasts (HFF) were infected with wild-type simplex virus 1 (HSV-1) strain 17 or its vhs null mutant at a multiplicity of infection (MOI) of 10. Subcellular RNA fractions including total RNA, cytoplasmic RNA, nucleoplasmic RNA and chromatin-associated RNA were prepared and subjected to RNA-seq.

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Raw RNAseq data of HSV-1-infected mouse skin fibroblasts

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Raw RNAseq data of HSV-1-infected mouse skin fibroblasts

Project description:Herpes simplex viruses (HSV) are responsible for a broad variety of human diseases, including cold sores, ocular herpes and herpetic encephalitis, leading to a great burden worldwide. However, the role for sex in herpes infection is controversial and unclear due to the complexity of factors involving in the formation of HSV diseases. Herein, we ask whether there is a sexual dimorphism based on the chromosomal rather than hormonal differences in the primary skin cells during low exposure of HSV. Profiling of male and female transcriptional programs reveals that cytosolic sensing pathway is induced to a greater degree in female cells, correlated with higher yields of infectious virions in male counterparts. Female skin cells distinctively reactivate Xist, a critical component of X inactivation, to silence the expression of the transcriptional repressor on X chromosome, which thereby maintains higher viperin level and further explains the different growth phenotypes between two sexes. Collectively, we propose a model that HSV-1 triggers a sex-specific regulation of antiviral response in the cytosolic sensing signaling via the control of Xist.

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