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Relative timing of type I interferon response and virus replication determines disease outcome during MERS-CoV infection

ABSTRACT: Relative timing of type I interferon response and virus replication determines disease outcome during MERS-CoV infection

PROVIDER: PRJNA545350 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9157000.fastq.gz	Fastqsanger.gz
	SRR9157001.fastq.gz	Fastqsanger.gz
	SRR9157002.fastq.gz	Fastqsanger.gz
	SRR9157003.fastq.gz	Fastqsanger.gz
	SRR9156994.fastq.gz	Fastqsanger.gz

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Relative timing of type I interferon response and virus replication determines disease outcome during MERS-CoV infection

Project description:Type 1 interferons (IFN-I) generally protect mammalian hosts from virus infections, but in some cases, IFN-I is pathogenic. Because IFN-I is protective, it is commonly used to treat virus infections for which no specific approved drug or vaccine is available. The Middle East respiratory syndrome-coronavirus (MERS-CoV) is such an infection, yet little is known about the role of IFN-I in this setting. Here we show that IFN-I signaling is protective during MERS-CoV infection. Blocking IFN-I signaling resulted in delayed virus clearance, enhanced neutrophil infiltration and impaired MERS-CoV-specific T cell responses. Notably, IFN-I administration within 1-day post infection (before virus titers peak) protected mice from lethal infection, despite a decrease in ISG (interferon stimulated gene) and inflammatory cytokine gene expression. In contrast, delayed IFN-I treatment failed to effectively inhibit virus replication, increased infiltration and activation of monocyte-macrophages and neutrophils into the lungs and enhanced pro-inflammatory cytokine expression, resulting in fatal pneumonia in an otherwise sub-lethal infection. Together, these results suggest that the relative timing of the IFN-I response and maximal virus replication is key in determining outcomes, at least in infected mice. By extension, IFN-I or combination therapy may need to be used cautiously to treat virus infections in clinical settings.

2019-05-30 | GSE131936 | GEO

IFN-I response timing relative to virus replication determines MERS coronavirus infection outcomes.

Project description:Type 1 IFNs (IFN-I) generally protect mammalian hosts from virus infections, but in some cases, IFN-I is pathogenic. Because IFN-I is protective, it is commonly used to treat virus infections for which no specific approved drug or vaccine is available. The Middle East respiratory syndrome-coronavirus (MERS-CoV) is such an infection, yet little is known about the role of IFN-I in this setting. Here, we show that IFN-I signaling is protective during MERS-CoV infection. Blocking IFN-I signaling resulted in delayed virus clearance, enhanced neutrophil infiltration, and impaired MERS-CoV-specific T cell responses. Notably, IFN-I administration within 1 day after infection (before virus titers peak) protected mice from lethal infection, despite a decrease in IFN-stimulated gene (ISG) and inflammatory cytokine gene expression. In contrast, delayed IFN-β treatment failed to effectively inhibit virus replication, increased infiltration and activation of monocytes, macrophages, and neutrophils in the lungs, and enhanced proinflammatory cytokine expression, resulting in fatal pneumonia in an otherwise sublethal infection. Together, these results suggest that the relative timing of the IFN-I response and maximal virus replication is key in determining outcomes, at least in infected mice. By extension, IFN-αβ or combination therapy may need to be used cautiously to treat viral infections in clinical settings.

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Project description:We performed RNAseq with Saccharomyces cerevisiae cells under both transient and steady-state conditions to study the regulation of genes by two pulsatile transcription factors, Msn2 and Mig1. The transient data allowed us to identify combinatorial targets while the steady-state data was used to study target expression dependence on the relative pulse timing between the two TFs.

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