Viral small RNAs in Sindbis virus-infected mammalian cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA211869 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR933994.fastq.gz | Fastqsanger.gz | |||
| SRR933995.fastq.gz | Fastqsanger.gz | |||
| SRR933996.fastq.gz | Fastqsanger.gz | |||
| SRR933997.fastq.gz | Fastqsanger.gz | |||
| SRR933998.fastq.gz | Fastqsanger.gz |
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Project description:Small RNAs play a critical role in host-pathogen interaction. In insects, for instance, small RNA-mediated silencing or RNA interference (RNAi) represents the main antiviral defense system. However, the antiviral role of RNAi has not been clearly proven in higher vertebrates. On the contrary, it is well established that the cell response relies on the recognition of viral RNAs by host pattern recognition receptors (PRR) to trigger the activation of the interferon pathway. Based on this evidence, we wished to contribute to this research field by identifying and characterizing small non-coding RNAs produced in mammalian cells upon RNA virus infection. We focused on Sindbis virus (SINV), the prototypical arbovirus, which by definition, is able to infect both vertebrate hosts and invertebrate vectors and triggers the interferon pathway or RNAi, respectively.
2013-11-19 | GSE48831 | GEO
Project description:Small RNAs play a critical role in host-pathogen interaction. In insects, for instance, small RNA-mediated silencing or RNA interference (RNAi) represents the main antiviral defense system. However, the antiviral role of RNAi has not been clearly proven in higher vertebrates. On the contrary, it is well established that the cell response relies on the recognition of viral RNAs by host pattern recognition receptors (PRR) to trigger the activation of the interferon pathway. Based on this evidence, we wished to contribute to this research field by identifying and characterizing small non-coding RNAs produced in mammalian cells upon RNA virus infection. We focused on Sindbis virus (SINV), the prototypical arbovirus, which by definition, is able to infect both vertebrate hosts and invertebrate vectors and triggers the interferon pathway or RNAi, respectively. Taking advantage of large scale sequencing, we cloned and sequenced small RNAs from both mock and SINV-infected mammalian cells (HEK 293 and VERO). We identified a novel population of viral small RNAs (vsRNAs) that accumulate as 20 to 30 nt species during infection. We assessed that this viral small RNA population is modified in 3'end and derived from the activation of the cellular antiviral endoribonuclease RNaseL. Altogether our results indicate a potential role for the SINV-derived small RNAs in the host defense mechanism.
2013-11-19 | E-GEOD-48831 | biostudies-arrayexpress
Project description:Viral vectors are attractive tools to express genes in neurons. Transduction of neurons with a recombinant, replication-deficient Sindbis viral vector is a method of choice for studying the effects of short-term protein overexpression on neuronal function. However, to which extent Sindbis by itself may affect neurons is not fully understood. We assessed effects of neuronal transduction with a Sindbis viral vector on the transcriptome and proteome in organotypic hippocampal slice cultures, and analyzed the electrophysiological properties of individual CA1 neurons, at 24h and 72h after viral vector injection. Whereas Sindbis caused substantial gene expression alterations, changes at the protein level were less pronounced. Alterations in transcriptome and proteome were predominantly limited to proteins involved in mediating anti-viral innate immune responses. Sindbis transduction did not affect the electrophysiological properties of individual neurons: the membrane potential, excitability and synaptic currents were similar between transduced and nontransduced CA1 neurons up to 72h after Sindbis injection. We conclude that Sindbis viral vectors are suitable for studying short-term effects of a protein of interest on electrophysiological properties of neurons, but not for studies on the regulation of gene expression.
2019-08-26 | PXD013634 | Pride
Project description:UnlabelledSmall RNAs play a critical role in host-pathogen interaction. Indeed, small RNA-mediated silencing or RNA interference (RNAi) is one of the earliest forms of antiviral immunity. Although it represents the main defense system against viruses in many organisms, the antiviral role of RNAi has not been clearly proven in higher vertebrates. However, it is well established that their response to viral infection relies on the recognition of viral RNAs by host pattern recognition receptors (PRRs) to trigger activation of the interferon pathway. In the present work, we report the existence of a novel small noncoding RNA population produced in mammalian cells upon RNA virus infection. Using Sindbis virus (SINV) as a prototypic arbovirus model, we profiled the small RNA population of infected cells in both human and African green monkey cell lines. Here, we provide evidence for the presence of discrete small RNAs of viral origin that are not associated with the RNA-induced silencing complex (RISC), that are highly expressed and detected by Northern blot analysis, and that accumulate as 21- to 28-nucleotide (nt) species during infection. We report that the cellular antiviral endoribonuclease RNase L cleaves the viral genome, producing in turn the small RNAs. Surprisingly, we uncovered the presence of a modification on the 3'-end nucleotide of SINV-derived viral small RNAs (SvsRNAs) that might be at the origin of their stability. Altogether, our findings show that stable modified small viral RNAs could represent a novel way to modulate host-virus interaction upon SINV infection.ImportanceIn a continuous arms race, viruses have to deal with host antiviral responses in order to successfully establish an infection. In mammalian cells, the host defense mechanism relies on the recognition of viral RNAs, resulting in the activation of type I interferons (IFNs). In turn, the expression of many interferon-stimulated genes (ISGs) is induced to inhibit viral replication. Here we report that the cytoplasmic, interferon-induced, cellular endoribonuclease RNase L is involved in the accumulation of a novel small RNA population of viral origin. These small RNAs are produced upon SINV infection of mammalian cells and are stabilized by a 3'-end modification. Altogether, our findings indicate that in our system RNA silencing is not active against Sindbis virus (SINV) and might open the way to a better understanding of the antiviral response mediated by a novel class of small RNAs.
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Project description:A time course of infection of the alphavirus Sindbis virus (SINV) was used to investigate the presence of viral specific vsRNA and the changes in miRNAs profiles in human embryonic kidney 293 cells (HEK293) by high throughput DNA sequencing. Deep sequencing of small RNAs early in SINV infection (4 and 6 hpi) showed low abundance (0.8%) of viral specific RNAs (vsRNAs) , with a random uniform distribution not typical of Dicer products, suggesting they arise from non-specific degradation. Sequencing showed little variation of cellular microRNAs (miRNAs) at 4 and 6 hpi compared to uninfected cells. Twelve miRNAs exhibiting some minor differential expression by sequencing, showed insignificant modulation by Northern blot analysis.
2013-12-01 | GSE46254 | GEO
Project description:A time course of infection of the alphavirus Sindbis virus (SINV) was used to investigate the presence of viral specific vsRNA and the changes in miRNAs profiles in human embryonic kidney 293 cells (HEK293) by high throughput DNA sequencing. Deep sequencing of small RNAs early in SINV infection (4 and 6 hpi) showed low abundance (0.8%) of viral specific RNAs (vsRNAs) , with a random uniform distribution not typical of Dicer products, suggesting they arise from non-specific degradation. Sequencing showed little variation of cellular microRNAs (miRNAs) at 4 and 6 hpi compared to uninfected cells. Twelve miRNAs exhibiting some minor differential expression by sequencing, showed insignificant modulation by Northern blot analysis. RNA was isolated from mock infected and SINV inoculated HEK 293 cells at 4hpi and 6hpi cDNA libraries were generated for the small RNA (sRNA) content of the cells and sequenced using Illumina GA II, which yielded between 29.1M and 30.5M reads per sample
2013-12-01 | E-GEOD-46254 | biostudies-arrayexpress
Project description:Microarray analysis comparing cells that are resistant to Sindbis virus-induced cell death (clones 9, 43) versus cells that are sensitive to Sindbis virus-induced cell death (WT293) Keywords = Sindbis alphavirus functinal phenotype Keywords: repeat sample
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Project description:We focus our analyses on the description of viral small RNAs (FHVdeltaB2 or FHV) and based on genetic and molecular evidende, classify them and discuss their relevance in antiviral defense. Small RNAs from adult Drosophila flies from different genetic backgrounds and infected with FHV-deltaB2 or FHV were sequenced using the illumina platform.
2011-11-12 | E-GEOD-32011 | biostudies-arrayexpress
Project description:We focus our analyses on the description of viral small RNAs (FHVdeltaB2 or FHV) and based on genetic and molecular evidende, classify them and discuss their relevance in antiviral defense.
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Project description:RNA viruses rely on cellular RNA-binding proteins (RBPs) to infect the host cell. However, the repertoire of the cellular RBPs exploited by viruses is largely unknown. Using the ‘RNA interactome capture’ method, we profiled in a proteome-wide scale the RBP-RNA interactions occurring during sindbis virus (SINV) infection. We discover that SINV affects the activity of hundreds of RBPs, essentially rewiring the host RNA-bound proteome. Such alterations do not relate to changes in protein abundance but are rather due to subcellular redistribution of RBPs and pervasive transcriptome remodelling. Strikingly, RBPs stimulated by SINV accumulate in the cytoplasmic compartments where the virus replicates and interact with viral RNA. Perturbation of these RBPs can restrict or promote infection; for example, GEMIN5 binds to key regulatory regions of SINV RNAs and inhibits viral protein expression. Importantly, we show that drug based RBP intervention may have potential as therapeutic strategy against viruses.
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