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Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo

ABSTRACT: Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo

PROVIDER: PRJNA1141444 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30033600.fastq.gz	Fastqsanger.gz
	SRR30033601.fastq.gz	Fastqsanger.gz
	SRR30033602.fastq.gz	Fastqsanger.gz
	SRR30033603.fastq.gz	Fastqsanger.gz
	SRR30033604.fastq.gz	Fastqsanger.gz

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Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo. [smallRNA-Seq spleen]

Project description:In RNA interference (RNAi), long double-stranded RNA (dsRNA) is cleaved by Dicer endonuclease into small RNA interfering RNAs (siRNAs), which guide degradation of complementary RNAs. While RNAi mediates antiviral innate immunity in plants and many invertebrates, vertebrates adopted sequence-independent response and their Dicer produces siRNAs inefficiently because it is adapted to process small hairpin microRNA precursors in the gene-regulating microRNA pathway. Mammalian RNAi is thus a rudimentary pathway of unclear significance. To investigate its antiviral potential, we modified mouse Dicer locus to express a truncated variant (DicerΔHEL1) known to stimulate RNAi. Next, we analyzed how DicerΔHEL1/wt mice respond to four RNA viruses: Coxsackievirus B3 (CVB3) and encephalomyocarditis virus (ECMV) from Picornaviridae; tick-borne encephalitis virus (TBEV) from Flaviviridae; and lymphocytic choriomeningitis virus (LCMV) from Arenaviridae. Increased Dicer activity in DicerΔHEL1/wt mice had no antiviral effect. This result supports insignificant antiviral function of endogenous mammalian RNAi in vivo. However, we also report that sufficiently high expression of DicerΔHEL1 suppressed LCMV in embryonic stem cells and in a transgenic mouse model. Altogether, mice with increased Dicer activity offer a new benchmark for identifying and studying viruses susceptible to mammalian RNAi in vivo.

2024-11-08 | GSE280993 | GEO

Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo (ESCs small RNA-Seq)

2024-07-30 | GSE273331 | GEO

Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo (organs small RNA-Seq)

2024-07-30 | GSE273336 | GEO

Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo. [smallRNA-Seq spleen]

Project description:Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo. [smallRNA-Seq spleen]

| PRJNA1181804 | ENA

Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo (ESCs TrapR small RNA-Seq)

2024-07-30 | GSE273334 | GEO

Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo (ESCs small RNA-Seq)

Project description:Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo (ESCs small RNA-Seq)

| PRJNA1141448 | ENA

Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo (organs small RNA-Seq)

Project description:Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo (organs small RNA-Seq)

| PRJNA1141450 | ENA

Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo (ESCs TrapR small RNA-Seq)

Project description:Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo (ESCs TrapR small RNA-Seq)

| PRJNA1141449 | ENA

Enhanced RNAi does not provide efficient innate antiviral immunity in mice in vivo

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-07-30 | GSE273338 | GEO

Alphavirus infection triggers antiviral RNAi immunity in mammals

Project description:RNA interference (RNAi) functions as an antiviral immune response in plants and invertebrates, whereas mammalian RNAi response has been found so far only in undifferentiated cells and in differentiated cells inactive in interferon (IFN) system or in infections with viruses disabling viral suppressors of RNAi (VSRs), thereby leading to question the physiological importance of the RNAi pathway in mammals. Here, we identified that wild-type Semliki Forest virus (SFV), a prototypic alphavirus, triggered the Dicer-dependent production of abundant viral (v)siRNAs in different mammalian somatic cells in the presence of VSR. These vsiRNAs were produced from viral dsRNA replicative intermediates, almost exclusively located at the 5’ termini of the viral genome, and loaded into AGO, and they were fully active in slicing cognate viral RNAs. Besides, Sindbis virus, another alphavirus, also induced vsiRNA generation in mammalian somatic cells. AGO2 deficiency increased SFV and SINV replication, while enoxacin, a known RNAi enhancer that functions at post steps of siRNA production, efficiently reduced viral replication. The nucleotide sequence at the 5’ termini of SFV and SINV genome is conserved among the Old World alphaviruses, and mutating the conserved sequences resulted in the recombinant SFV being deficient in vsiRNA production and irresponsive to antiviral RNAi. SFV infection also enabled the production of abundant vsiRNAs and antiviral RNAi in IFN-competent adult mice, and importantly, enhanced RNAi by enoxacin protected adult mice from lethal SFV challenge and reduced the virus-induced neuropathogenesis in the central neuron system. Overall, our findings provide evidence that mammalian antiviral RNAi is active in differentiated cells and adult mice with intact IFN response even in the presence of VSR and present a therapeutic strategy against alphaviruses that include many important emerging and reemerging human pathogens.

2022-10-04 | GSE214453 | GEO

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