Coronavirus and influenza virus triggers antiviral RNAi immunity [AIVKO_miRNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1201125 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31796712.fastq.gz | Fastqsanger.gz | |||
| SRR31796713.fastq.gz | Fastqsanger.gz | |||
| SRR31796714.fastq.gz | Fastqsanger.gz | |||
| SRR31796715.fastq.gz | Fastqsanger.gz | |||
| SRR31796716.fastq.gz | Fastqsanger.gz |
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Project description:Coronavirus and influenza virus triggers antiviral RNAi immunity [IBV_miRNA-seq]
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Project description:RNA interference (RNAi) is a key antiviral immune mechanism in eukaryotes. However, in vertebrates such as birds and mammals, antiviral RNAi has only been observed in cells with poor interferon systems (stem cells and oocytes) or in viral suppressors of RNAi (VSR) deficiency virus infections. Our research originally discovered that infecting macrophages with wild-type coronavirus (Infectious bronchitis virus, IBV) and influenza viruses (Avian influenza virus, AIV) can trigger RNAi antiviral immunity and produce a certain amount of virus-derived siRNA (vsiRNA). These vsiRNAs have an inhibitory effect on the virus and carry out targeted silencing along the Dicer-Ago2-vsiRNA axis. Notably, these vsiRNAs are distributed throughout of the virus’s entire genome, with a predilection for A/U at the 5’ and 3’ termini of vsiRNA. In addition, Dicer cleavage produces vsiRNA based on the RWM motif, where R represents A/G, W represents A/C, and M represents A/U. Additionally, we discovered that avian LGP2 and MDA5 proteins positively impact the expression of the Dicer protein and the Dicer subtype “DicerM”, which exhibits a potent antiviral activity compared to Dicer itself. Most importantly, the psilencer4.1-plasmid constructed based on vsiRNA combined with nanomaterial polyetherimide (PEI) showed excellent anti-virus activity in specific-pathogen-free (SPF) chickens. These findings show that RNA viruses trigger the production of the vsiRNA in avian somatic cells, which is of great significance for the application of therapeutic vaccines in poultry.
2025-02-26 | GSE285056 | GEO
Project description:RNA interference (RNAi) is a key antiviral immune mechanism in eukaryotes. However, in vertebrates such as birds and mammals, antiviral RNAi has only been observed in cells with poor interferon systems (stem cells and oocytes) or in viral suppressors of RNAi (VSR) deficiency virus infections. Our research originally discovered that infecting macrophages with wild-type coronavirus (Infectious bronchitis virus, IBV) and influenza viruses (Avian influenza virus, AIV) can trigger RNAi antiviral immunity and produce a certain amount of virus-derived siRNA (vsiRNA). These vsiRNAs have an inhibitory effect on the virus and carry out targeted silencing along the Dicer-Ago2-vsiRNA axis. Notably, these vsiRNAs are distributed throughout of the virus’s entire genome, with a predilection for A/U at the 5’ and 3’ termini of vsiRNA. In addition, Dicer cleavage produces vsiRNA based on the RWM motif, where R represents A/G, W represents A/C, and M represents A/U. Additionally, we discovered that avian LGP2 and MDA5 proteins positively impact the expression of the Dicer protein and the Dicer subtype “DicerM”, which exhibits a potent antiviral activity compared to Dicer itself. Most importantly, the psilencer4.1-plasmid constructed based on vsiRNA combined with nanomaterial polyetherimide (PEI) showed excellent anti-virus activity in specific-pathogen-free (SPF) chickens. These findings show that RNA viruses trigger the production of the vsiRNA in avian somatic cells, which is of great significance for the application of therapeutic vaccines in poultry.
2025-02-26 | GSE285054 | GEO
Project description:Coronavirus and influenza virus triggers antiviral RNAi immunity [AIV-miRNA-seq]
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Project description:RNA interference (RNAi) is a key antiviral immune mechanism in eukaryotes. However, in vertebrates such as birds and mammals, antiviral RNAi has only been observed in cells with poor interferon systems (stem cells and oocytes) or in viral suppressors of RNAi (VSR) deficiency virus infections. Our research originally discovered that infecting macrophages with wild-type coronavirus (Infectious bronchitis virus, IBV) and influenza viruses (Avian influenza virus, AIV) can trigger RNAi antiviral immunity and produce a certain amount of virus-derived siRNA (vsiRNA). These vsiRNAs have an inhibitory effect on the virus and carry out targeted silencing along the Dicer-Ago2-vsiRNA axis. Notably, these vsiRNAs are distributed throughout of the virus’s entire genome, with a predilection for A/U at the 5’ and 3’ termini of vsiRNA. In addition, Dicer cleavage produces vsiRNA based on the RWM motif, where R represents A/G, W represents A/C, and M represents A/U. Additionally, we discovered that avian LGP2 and MDA5 proteins positively impact the expression of the Dicer protein and the Dicer subtype “DicerM”, which exhibits a potent antiviral activity compared to Dicer itself. Most importantly, the psilencer4.1-plasmid constructed based on vsiRNA combined with nanomaterial polyetherimide (PEI) showed excellent anti-virus activity in specific-pathogen-free (SPF) chickens. These findings show that RNA viruses trigger the production of the vsiRNA in avian somatic cells, which is of great significance for the application of therapeutic vaccines in poultry.
2025-02-26 | GSE285055 | GEO
Project description:Alphavirus infection triggers antiviral RNAi immunity in mammals
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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
Project description:While the intrinsic antiviral cell defenses of many kingdoms utilize pathogen-specific small RNAs, the antiviral response of chordates is primarily protein-based and not uniquely tailored to the incoming microbe. In an effort to explain this evolutionary bifurcation, we determined whether antiviral RNA interference (RNAi) was sufficient to replace the protein-based type I interferon (IFN-I) system of mammals. To this end, we recreated an RNAi-like response in mammals and determined its effectiveness to combat influenza A virus in vivo in the presence and absence of the canonical IFN-I system. Mammalian antiviral RNAi, elicited by either host- or virus-derived small RNAs, effectively attenuated virus and prevented disease independently of the innate immune response. These data find that chordates could have utilized RNAi as their primary antiviral cell defense and suggest that the IFN-I system emerged as a result of natural selection imposed by ancient pathogens.
2015-10-03 | GSE73698 | GEO
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.
2025-03-13 | GSE271042 | GEO
Project description:RNA interference (RNAi) functions as the major host antiviral defense in insects, while less is understood about how to utilize antiviral RNAi in controlling viral infection in insects. Enoxacin belongs to the family of synthetic antibacterial compounds based on a fluoroquinolone skeleton that has been previously found to enhance RNAi in mammalian cells. In this study, we showed that enoxacin efficiently inhibited viral replication of Drosophila C virus (DCV) and Cricket paralysis virus (CrPV) in cultured Drosophila cells. Enoxacin promoted the loading of Dicer-2-processed virus-derived siRNA into the RNA-induced silencing complex, thereby enhancing antiviral RNAi response in infected cells. Moreover, enoxacin treatment elicited an RNAi-dependent in vivo protective efficacy against DCV or CrPV challenge in adult fruit flies. In addition, enoxacin also inhibited replication of flaviviruses, including Dengue virus and Zika virus, in Aedes mosquito cells in an RNAi-dependent manner. Together, our findings demonstrated that enoxacin can enhance RNAi in insects, and enhancing RNAi by enoxacin is an effective antiviral strategy against diverse viruses in insects, which may be exploited as a broad-spectrum antiviral agent to control vector transmission of arboviruses or viral diseases in insect farming.
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