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Evasion of antiviral innate immunity by SARS-CoV-2 NSP1 is exerted through H3K9 di-methylation

ABSTRACT: Evasion of antiviral innate immunity by SARS-CoV-2 NSP1 is exerted through H3K9 di-methylation

PROVIDER: PRJNA858420 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20142133_1.fastq.gz	Fastqsanger.gz
	SRR20142133_2.fastq.gz	Fastqsanger.gz
	SRR20142134_1.fastq.gz	Fastqsanger.gz
	SRR20142134_2.fastq.gz	Fastqsanger.gz
	SRR20142135_1.fastq.gz	Fastqsanger.gz

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Evasion of antiviral innate immunity by SARS-CoV-2 NSP1 is exerted through H3K9 di-methylation

Project description:The pathogen causing the current COVID-19 pandemic, the severe acute respiratory syndrome coronavirus (SARS-CoV-2), evades the innate immune machinery through the independent action of several viral proteins, including the nonstructural protein 1 (NSP1). NSP1 has multiple functions, but the relative contribution of NSP1-mediated translational repression, ribosome-proximate degradation of host mRNA, or other molecular mechanisms to viral immune evasion remains unclear. Here we combined several genome wide approaches, including RNA-seq, ribosome footprinting, and ChIP-seq to find that NSP1 predominantly affects transcription of immune-related genes. NSP1 expression in A549 cells induced Histone 3 Lysine 9 (H3K9) methylation of antiviral gene loci, leading to specific suppression of type I and type III interferon pathways. Treatment with the G9a/GLP H3K9 methyltransferase inhibitor UNC0638 reverses this suppression of antiviral genes and blocks viral replication after SARS-CoV2 infection of A549 cells. Our results call attention to epigenetic reprogramming induced by SARS-CoV2 and highlight the importance to identify innate factors regulating histone modification of gene loci targeted by SARS-CoV-2, with possible relevance to the understanding and therapy of other immunomodulatory diseases.

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