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Increased viral tolerance mediates by antiviral RNA interference in bat cells

ABSTRACT: Increased viral tolerance mediates by antiviral RNA interference in bat cells

PROVIDER: PRJNA915074 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22868507.fastq.gz	Fastqsanger.gz
	SRR22868508.fastq.gz	Fastqsanger.gz
	SRR22868509.fastq.gz	Fastqsanger.gz
	SRR22868510.fastq.gz	Fastqsanger.gz
	SRR22868511.fastq.gz	Fastqsanger.gz

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Increased viral tolerance mediates by antiviral RNA interference in bat cells

Project description:Bats harbor highly virulent viruses that can infect other mammals, including humans, posing questions about their immune tolerance mechanisms. Bat cells employ multiple strategies to limit virus replication and virus-induced immunopathology, but the coexistence of bats and fatal viruses remains poorly understood. Here, we investigated the antiviral RNA interference (RNAi) pathway in bat cells and discovered that they have an enhanced antiviral RNAi response, producing canonical viral small interfering RNAs (vsiRNAs) upon Sindbis virus (SINV) infection that were missing in human cells. Disruption of Dicer function resulted in increased viral load for three different RNA viruses in bat cells, indicating an interferon-independent antiviral pathway. Furthermore, our findings reveal the simultaneous engagement of Dicer and pattern-recognition receptors (PRRs), such as retinoic acid-inducible gene I (RIG-I), with double-stranded RNA, suggesting that Dicer attenuates the interferon response initiation in bat cells. These insights advance our comprehension of the distinctive strategies bats employ to coexist with viruses.

2024-07-12 | GSE221607 | GEO

Increased viral tolerance mediates by antiviral RNA interference in bat cells

2024-07-12 | PXD053906 | Pride

Antiviral RNA interference in mammalian cells

Project description:Plants and invertebrates protect themselves from viruses through RNA interference (RNAi), yet it remains unknown whether this defense mechanism exists in mammals. Antiviral RNAi involves the processing of viral long double-stranded (ds) RNA molecules into small interfering RNAs (siRNAs) by the ribonuclease (RNAse) III Dicer. These siRNAs are incorporated into effector complex(es) containing members of the Argonaute (Ago) protein family and guide silencing of complementary target viral RNAs. Here, we detect the accumulation of phased Dicer-dependent virus-derived siRNA (viRNAs) and demonstrate their loading into Ago2 after infection of mouse embryonic stem (ES) cells with Encephalomyocarditis virus (EMCV). We further show that the production of these viRNAs is drastically reduced, yet not completely abolished, if ES cells are first induced to differentiate before infection. Finally, we reveal that the mammalian virus Nodamura virus (NoV) encodes for a protein that counteracts such antiviral RNAi in ES cells supporting the existence of an effective RNAi-based immunity in mammals. Infection of wild-type or mutant mouse ES cells and analysis of small RNAs from total extracts or immunoprecipitated components of the RNAi pathway

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ADAR1 biology can hinder effective antiviral RNA interference

Project description:ADAR1 biology can hinder effective antiviral RNA interference

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Somatic reprogramming of pteropus bat cells provides new insights in bat antiviral response

Project description:Somatic reprogramming of pteropus bat cells provides new insights in bat antiviral response

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Antiviral RNA interference in disease vector (Asian longhorned) ticks

Project description:Antiviral RNA interference in disease vector (Asian longhorned) ticks

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Antiviral RNA interference in mammalian cells

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ADAR1 biology can hinder effective antiviral RNA interference

Project description:Viruses constantly evolve and adapt to the antiviral defenses of their hosts. The biology of viral circumvention of these selective pressures can often be attributed to the acquisition of novel antagonistic gene products or by rapid genome change that prevents host recognition. To study viral evasion of RNA interference (RNAi)-based defenses, we established a robust antiviral system in mammalian cells using recombinant Sendai virus designed to be targeted by endogenous host microRNAs (miRNAs) with perfect complementarity. Using this system, we previously demonstrated the intrinsic ability of positive-strand RNA viruses to escape this selective pressure via homologous recombination, which was not observed in negative-strand RNA viruses. Here we show that given extensive time, escape of miRNA-targeted Sendai virus was enabled by host adenosine deaminase acting on RNA 1 (ADAR1). Independent of the viral transcript targeted, ADAR1 editing resulted in disruption of the miRNA-silencing motif, suggesting an intolerance for extensive RNA:RNA interactions necessary for antiviral RNAi. This was further supported in N. benthamiana, where exogenous expression of ADAR1 interfered with endogenous RNAi. Together, these results suggest that ADAR1 diminishes the effectiveness of RNAi and may explain why it is absent in species that utilize this antiviral defense system.

2023-03-21 | GSE227592 | GEO

Zebrafish as an animal model for the antiviral RNA interference pathway

Project description:Zebrafish as an animal model for the antiviral RNA interference pathway

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Flavivirus induces and antagonizes antiviral RNA interference in both mammals and mosquitoes

Project description:Flavivirus induces and antagonizes antiviral RNA interference in both mammals and mosquitoes

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