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Whole genome RNA-seq analysis of wild type or HIPK2-/- immortalized bone marrow-derived macrophages (iBMDM), with or without vesicular stomatitis virus (VSV) infection

ABSTRACT: Whole genome RNA-seq analysis of wild type or HIPK2-/- immortalized bone marrow-derived macrophages (iBMDM), with or without vesicular stomatitis virus (VSV) infection

PROVIDER: PRJNA422417 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6376690_1.fastq.gz	Fastqsanger.gz
	SRR6376690_2.fastq.gz	Fastqsanger.gz
	SRR6376691_1.fastq.gz	Fastqsanger.gz
	SRR6376691_2.fastq.gz	Fastqsanger.gz
	SRR6376692_1.fastq.gz	Fastqsanger.gz

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Whole genome RNA-seq analysis of wild type or HIPK2-/- immortalized bone marrow-derived macrophages (iBMDM), with or without vesicular stomatitis virus (VSV) infection

Project description:Wild type or HIPK2-/- immortalized bone marrow-derived macrophages (iBMDM) were infected with VSV for 6h, followed by whole genome RNA-seq analysis. Conclusions: HIPK2 deficiency aggravates viral infection and inhibited the production of IFNβ.

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mRNA-seq of immortailized bone marrow derived macrophages (iBMDM) after vesicular stomatitis virus (VSV) infection

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Genome-wide maps of chromatin state in iBMDM (immortalized bone-marrow-derived macrophages) cells without or with virus infection

Project description:iBMDM cells were infected with VSV (Vesicular Stomatitis Virus) or HSV-1 (Herpes Simplex Virus 1) for 8 hours, followed by CHIP-seq analysis with H3K27AC antibody. We find that chromatin state changed with virus infection, some enhacer and superenhancer were induced to promote anti-viral gene expression. Conclusions: virus infection induce enhancer and superenhancer activation.

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Genome-wide maps of chromatin state in iBMDM (immortalized bone-marrow-derived macrophages) cells without or with virus infection.

Project description:iBMDM cells were infected with VSV (Vesicular Stomatitis Virus) or HSV-1 (Herpes Simplex Virus 1) for 8 hours, followed by CHIP-seq analysis with H3K27AC antibody (Abcam, ab4729). We find that chromatin state changed with virus infection, some enhacer and superenhancer were induced to promote anti-viral gene expression. Conclusions: virus infection induce enhancer and superenhancer activation.

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Analysis of global gene expression profiles of hPAF1 deficient A549 cells during infection with H1N1 influenza A virus or vesicular stomatitis virus (VSV)

Project description:Viral infection is commonly associated with virus-driven hijacking of host proteins. We describe a novel mechanism by which influenza virus impacts host cells through the interaction of influenza NS1 protein with the infected cell epigenome. We show that the NS1 protein of influenza A H3N2 targets the transcription elongation PAF1 complex (hPAF1C). We demonstrate that binding of NS1 to hPAF1C results in suppression of hPAF1C-mediated transcriptional elongation. More importantly,in the following data sets, we show that hPAF1 plays a crucial role in the antiviral response. Loss of hPAF1C reduces antiviral gene expression and reduces inducible transcription of target genes after stimulation with viral RNA analogue poly(I:C), vesicular stomatitis virus (VSV), exogenous recombinant IFN(beta) and influenza virus (H1N1). This study underscores the importance of hPAF1C in controlling inducible antiviral gene expression. Untreated (no siRNA), control siRNA-treated and hPAF1 siRNA-treated A549 cells were stimulated with A/Puerto Rico/8/1934 influenza virus (H1N1) or vesicular stomatitis virus (VSV). Total RNA was isolated with the Qiagen RNeasy mini kit. 200ng of total RNA per sample was used to prepare biotin-labeled RNA using MessageAmp™ Premier RNA Amplification Kit (Applied Biosystems) and hybridized to HumanHT-12 v4 Expression BeadChips (Illumina). Data analysis was performed using the GeneSpring GX11.0 software (Agilent Technologies). 3 biological replicates per condition

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mRNA-seq of immortailized bone marrow derived macrophages (iBMDM) after vesicular stomatitis virus (VSV) infection

Project description:Analysis of mRNA-seq reveals how wild type immortalized bone marrow derived macrophages response to VSV infection

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