RNA-Sequencing data of Varicella Zoster Virus (VZV)-infected human dermal fibroblasts (HDF)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA497243 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8069690_1.fastq.gz | Fastqsanger.gz | |||
| SRR8069690_2.fastq.gz | Fastqsanger.gz | |||
| SRR8069691_1.fastq.gz | Fastqsanger.gz | |||
| SRR8069691_2.fastq.gz | Fastqsanger.gz | |||
| SRR8069692_1.fastq.gz | Fastqsanger.gz |
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Project description:Hosts have evolved numerous mechanisms to prevent primary viral infections. Interferon signaling is an important host defense mechanism against primary infection. Interferon gamma (IFN-γ) is a potent cytokine produced following primary varicella-zoster virus (VZV) infection. Furthermore, VZV reactivation correlates with a decline in IFN-γ-producing immune cells. Our previous results showed that pretreatment with 20 ng/ml of IFN-γ completely inhibited VZV replication in lung fibroblast MRC-5 and retinal epithelial ARPE-19, suggesting that IFN-γ-stimulated protein(s) inhibit viral replication. Our microarray analysis revealed that a small subset of interferon-stimulated genes (ISGs) was upregulated by greater than 3.5-fold at 8 h post-treatment in both ARPE-19 and MRC-5 cells compared to those of melanoma MeWo cells. The depletion of IFITM1 and IRF1 by siRNA in IFN-γ-treated cells significantly increased (from 0 to ~1x103 pfu/105 cells) VZV yields. In contrast, the depletion of a nontargeting control (siNTC) did not increase virus yield. Ectopic expression of interferon-induced transmembrane protein 1 (IFITM1) reduced the level of IE62 protein as well as intracellular VZV yield in both ARPE-19 and MeWo cells, but did not reduce the expression level of IE62 mRNA, suggesting that IFITM1 expression reduces the expression level of IE62 by post-transcriptional regulation. IFITM1 also reduced the expression levels of VZV IE62, HSV-1 ICP4, and EHV-1 IEP in ARPE-19 cells
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