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Response of IRF7-deficient peripheral blood mononuclear cells to pH1N1 influenza virus infection

ABSTRACT: IRF7 plays a critical role in the production and amplification of the antiviral type I and III interferon response. Autosomal recessive IRF7-deficiency resulted in life-threatening influenza disease in a 3-year-old child. We studied the impact of IRF7-deficiency in non-hematopoietic tissues (fibroblasts and lung epithelial cells) as well in hematopoietic cells (peripheral blood mononuclear cells (PBMCs)). Genome-wide gene expression analysis demonstrated a profound loss of type I and III IFNs in PBMCs infected with influenza virus.

ORGANISM(S): Homo sapiens

PROVIDER: GSE66486 | GEO | 2015/04/07

SECONDARY ACCESSION(S): PRJNA277057

REPOSITORIES: GEO

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Response of IRF7-deficient peripheral blood mononuclear cells to pH1N1 influenza virus infection

Project description:IRF7 plays a critical role in the production and amplification of the antiviral type I and III interferon response. Autosomal recessive IRF7-deficiency resulted in life-threatening influenza disease in a 3-year-old child. We studied the impact of IRF7-deficiency in non-hematopoietic tissues (fibroblasts and lung epithelial cells) as well in hematopoietic cells (peripheral blood mononuclear cells (PBMCs)). Genome-wide gene expression analysis demonstrated a profound loss of type I and III IFNs in PBMCs infected with influenza virus. PBMCs were isolated from 4 healthy donors and patients with deficiencies for IRF7 and UNC93B. The cells were infected with influenza virus A/CA/4/2009 at a multiplicity of infection (MOI) of 2 for 8 and 16 hours. Uninfected cells were cultured for 16 hours.

2015-04-07 | E-GEOD-66486 | biostudies-arrayexpress

Life-threatening influenza pneumonitis in a child with inherited IRF9 deficiency

Project description:Life-threatening influenza pneumonitis in a child with inherited IRF9 deficiency

| PRJNA482784 | ENA

Chicken IRF7 knockout by CRISPR-Cas9 in DF-1 and in vitro H6N2 infection followed by RNA-seq

Project description:To elucidate the functional role of chicken IRF7 against avian influenza virus (AIV) infection, we generated inducible IRF7 knockout DF-1 cell lines and performed in vitro infection using low pathogenic AIVs (LPAIVs) followed by RNA-seq.

2018-10-01 | GSE119590 | GEO

Life-threatening influenza pneumonitis in a child with inherited IRF9 deficiency

Project description:Life-threatening pulmonary influenza can be caused by inborn errors of type I and III IFN immunity. We report a 5 year-old child with severe pulmonary influenza at 2 years. She is homozygous for a loss-of-function IRF9 allele. Her cells activate gamma-activated factor (GAF) STAT1 homodimers but not interferon-stimulated gene factor 3 (ISGF3) trimers (STAT1/STAT2/IRF9) in response to IFN-α2b. The transcriptome induced by IFN-α2b in the patient’s cells is much narrower than that of control cells; however, induction of a subset of interferon-stimulated gene transcripts remains detectable. In vitro, the patient’s cells do not control three respiratory viruses, influenza A virus (IAV), parainfluenza virus, and respiratory syncytial virus. These phenotypes are rescued by wild-type IRF9, whereas silencing IRF9 expression in control cells increases viral replication. However, the child has controlled various common viruses in vivo, including respiratory viruses other than IAV. Our findings show that human IRF9- and ISGF3-dependent type I and III IFN responsive pathways are essential for controlling IAV.

2018-08-06 | GSE117637 | GEO

Identification of novel gene signatures in patients with atopic dermatitis complicated by eczema herpeticum

Project description:Background: A subset of patients with atopic dermatitis (AD) is prone to disseminated herpes simplex virus (HSV) infection, i.e. eczema herpeticum (ADEH+). Biomarkers that identify ADEH+ are lacking. Objective: To search for novel ADEH+ gene signatures in peripheral blood mononuclear cells (PBMCs). Methods: A RNA-sequencing (RNA-seq) approach was applied to evaluate global transcriptional changes using PBMCs from ADEH+ and AD without a history of EH (ADEH-). Candidate genes were confirmed by qPCR or ELISA. Results: ADEH+ PBMCs had distinct changes to the transcriptome when compared to ADEH- PBMCs following HSV-1 stimulation: 792 genes were differentially expressed at a false discovery rate (FDR) < 0.05 (ANOVA), and 15 type I and type III interferon (IFN) genes were among the top 20 most down-regulated genes in ADEH+. We further validated that IFN-α and IL-29 mRNA and protein levels were significantly decreased in HSV-1 stimulated PBMCs from ADEH+ compared to ADEH- and normal. Ingenuity pathway analysis (IPA) demonstrated that the up-stream regulators of type I and type III IFNs, IRF3 and IRF7 was significantly inhibited in ADEH+ based on the down-regulation of their target genes. Furthermore, we found that gene expression of IRF3 and IRF7 were significantly decreased in HSV-1 stimulated PBMC from ADEH+ subjects. Conclusions: PBMCs from ADEH+ have a distinct immune response following HSV-1 exposure compared to ADEH- . Inhibition of the IRF3 and IRF7 innate immune pathways in ADEH+ may be the important mechanisms for increased susceptibility to disseminated viral infection.

2015-08-18 | GSE60481 | GEO

Irf3 phenotyping

Project description:The interferon regulatory factors IRF3 and IRF7 are key players in the regulation of type I and III IFN genes. In this study, we analyzed the role of IRF3 and IRF7 for the host response to influenza A virus infections in Irf3-/-, Irf7-/- and Irf3-/-Irf7-/- knock-out mice.

2016-11-02 | GSE77600 | GEO

RNA profiling of IRF7 knockout acute myeloid leukemia (AML) cells

Project description:Acute myeloid leukemia (AML) is an aggressive hematopoietic malignant. In our study, we found that knockout of IRF7 in AML cells accelerates the AML progression and shorten the mice survival, which is medicated by LSC level. The goals of this study aim to reveal the mechanism mediated by IRF7 knockout, we performed the RNAseq profiling of WT c-kit-, WT c-kit+ and IRF7-/- c-kit+ AML cells

2021-06-30 | GSE178560 | GEO

Overexpression of chicken IRF7 increased viral replication and programmed cell death to the avian influenza virus infection through TGF-beta/FoxO signaling axis in DF-1

Project description:To elucidate the functional role of chicken IRF7 against avian influenza virus (AIV) infection, we generated inducible IRF7 overexpression DF-1 cell lines that could fine control the IRF7 expression level and performed in vitro infection using low pathogenic AIVs (LPAIVs) followed by RNA-seq.

2018-06-01 | GSE115131 | GEO

ChIP-seq for IRF7

Project description:We performed ChiP-Seq for IRF7 in GM-CSF induced bone-marrow cells. IRF7 ChIP-Seq in myeloid cells

2014-12-03 | E-GEOD-62697 | biostudies-arrayexpress

Bud13 Promotes a Type I Interferon Response by Countering Intron Retention in Irf7

Project description:Intron retention (IR) has emerged as an important mechanism of gene expression control. Despite this, the factors that control IR events remain poorly understood. We observed consistent IR in one intron of the Irf7 gene and identified Bud13 as an RNA-binding protein that acts at this intron to increase the amount of successful splicing. Deficiency in Bud13 led to increased IR, decreased mature Irf7 transcript and protein levels, and consequently to a dampened type I interferon response. This impairment of Irf7 production in Bud13 deficient cells compromised their ability to withstand VSV infection. Global analysis of Bud13 knockdown and BUD13 cross-linking to RNA revealed a subset of introns that share many characteristics with the one found in Irf7 and are spliced in a Bud13-dependent manner. Deficiency of Bud13 led to decreased mature transcript from genes containing such introns. Thus, by acting as an antagonist to IR, Bud13 facilitates the expression of genes at which IR occurs.

2018-11-15 | GSE122543 | GEO

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