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Nuclear AGO2 Supports Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

ABSTRACT: Nuclear AGO2 Supports Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

PROVIDER: PRJNA1044764 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26941029.fastq.gz	Fastqsanger.gz
	SRR26941030.fastq.gz	Fastqsanger.gz
	SRR26941031.fastq.gz	Fastqsanger.gz
	SRR26941032.fastq.gz	Fastqsanger.gz
	SRR26941033.fastq.gz	Fastqsanger.gz

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Nuclear AGO2 Supports Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

Project description:Nuclear AGO2 Supports Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

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Nuclear AGO2 Supports Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

Project description:The role of Argonaute (AGO) proteins and the RNA interference (RNAi) machinery in mammalian antiviral response has been debated. Therefore, we set out to investigate how mammalian RNAi impacts influenza A virus (IAV) infection. We demonstrate that IAV infection triggers nuclear accumulation of AGO2, which is directly facilitated by p53 activation. Mechanistically, we show that IAV induces nuclear AGO2 targeting of TRIM71, a proposed AGO2 E3 ligase, and type-I interferon-pathway genes for silencing. Hence, the RNAi machinery is highjacked by the virus to evade the immune system and support viral replication. We demonstrate that the FDA approved drug arsenic trioxide prevents nuclear AGO2:p53 accumulation, thereby increasing interferon response and decreasing viral replication in vitro and in a mouse model in vivo. Our data indicates that targeting the AGO2:p53-mediated silencing of innate immunity may offer a promising strategy to mitigate viral infections.

2025-03-23 | GSE248546 | GEO

Nuclear AGO2 Supports Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

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Nuclear RNAi Modulates Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

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Influenza virus facilitates its infectivity by activating p53 to inhibit the expression of interferon-induced transmembrane proteins (IFITMs)

Project description:Transcriptome analysis of mock or H1N1 IAV PR8 infected p53WT A549 and p53null A549-KO3 cells by Affymetrix GeneChip Human Transcriptome 2.0 Arrays to achieve a set of genes those are regulated by p53 and responsive to IAV infection. Influenza A virus infection activates cellular p53, however it has not been clear whether this process has pro- or anti- viral effects. In this study, using human isogenic p53 wildtype A549 cells and p53null A549-KO3 cells generated from the CRISPR/Cas9 technology, we report that p53null cells exhibit significantly reduced viral propagation property when infected with influenza A virus (H1N1/A/Puerto Rico/8/34). Here, using genome-wide microarray analysis we revealed that p53 regulates the expression of a large set of interferon-inducible genes, some of which are directly associated with viral infectivity and later experimentally validated to be responsible for p53-regulated IAV infectivity.

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mRNAs associated with Ago2: Ago2, Ago2+miR-1, Ago2+miR-124, mock transfected

Project description:As a core RISC component, Ago2 associates with miRNAs and target mRNAs. To identify these mRNAs, we ran lysate from HEK293T cells over a FLAG resin from 2 conditions: +FLAG-Ago2, +mock transfection. To identify mRNAs associated with specific miRNAs, we ran lysate from HEK293T cells over a FLAG resin from 2 conditions: +FLAG-Ago2 & miR-1, and +FLAG-Ago2 & miR-124. Set of arrays that are part of repeated experiments Compound Based Treatment: mock transfected Keywords: Biological Replicate

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