Project description:Eukaryotic cells recognize intracellular pathogens through pattern recognition receptors, including sensors of aberrant nucleic acid structures. Sensors of double-stranded RNA (dsRNA) are known to detect replication intermediates of RNA viruses. It has been suggested that annealing of mRNA from symmetrical transcription of both top and bottom strands of DNA virus genomes can produce dsRNA during infection. Supporting this hypothesis, nearly all DNA viruses encode inhibitors of dsRNA-recognition pathways. However, direct evidence that DNA viruses produce dsRNA is lacking. Contrary to dogma, we show that the nuclear-replicating DNA virus adenovirus (AdV) does not produce detectable levels of dsRNA during infection. In contrast, abundant dsRNA is detected within the nucleus of cells infected with AdV mutants that lack the virus-directed ubiquitin ligase required for efficient processing of viral RNA. In the presence of nuclear dsRNA, the cytoplasmic dsRNA sensor PKR is relocalized and activated within the nucleus. Accumulation of viral dsRNA occurs in the late phase of infection, when unspliced viral transcripts form intron/exon base pairs between top and bottom strand transcripts. We propose that DNA viruses actively promote efficient splicing and mRNA processing to limit dsRNA formation, thus avoiding detection and restriction by host nucleic acid sensors.

2021-07-15 | GSE179388 | GEO

Umbelopsis ramanniana AG strain:AG

Project description:Umbelopsis ramanniana AG transcriptome

| PRJNA373021 | ENA

Next Generation Sequencing Facilitates Quantitative Analysis of yeast cells lacking either M-2 dsRNA or both L-A-lus and M-2 dsRNA viruses

Project description:Here we determine the impact upon the loss of M-2 dsRNA alone and both L-A-lus along with M-2 on the host S. cerevisiae transcriptional changes. By performing profiling of the whole transcriptomes, we determined 486 genes differentially expressed after curing of yeast cells from M-2 dsRNA and 715 genes affected by the elimination of both M-2 and L-A-lus dsRNAs.

2017-07-26 | GSE100290 | GEO

Umbelopsis ramanniana AG strain:AG

Project description:Umbelopsis ramanniana AG strain:AG Genome sequencing

| PRJNA196032 | ENA

RNA-seq of fibroblasts from two bat species stimulated by dsRNA to trigger antiviral response

Project description:Dermal fibroblasts from megabat and microbat, stimulated with dsRNA (poly(I:C)) and controls. Bats can harbor some of the most deadliest viruses to humans while rarely displaying pathogenicity themselves. To study their innate immune response - the expression program that is initiated once a pathogen is senseds, we stimulated dermal fibroblast cells from two species (Rousettus aegyptiacus and Pipistrellus kuhlii) for four hours with dsRNA - a viral RNA mimic that triggers a rapid innate immune response. Subsequently, we profiled the response using bulk RNA-seq.

2022-10-01 | E-MTAB-10870 | biostudies-arrayexpress

Single-Cell RNA-seq of bat and human fibroblasts stimulated by dsRNA to trigger antiviral response

Project description:Dermal fibroblasts from bat and human, stimulated with dsRNA (poly(I:C)) and controls. Bats can harbor some of the most deadliest viruses to humans while rarely displaying pathogenicity themselves. To study the transcriptional divergence and cell-to-cell variability of their innate immune response - the expression program that is initiated once a pathogen is sensed, we stimulated dermal fibroblast cells from Rousettus aegyptiacus and from human for four hours with dsRNA - a viral RNA mimic that triggers a rapid innate immune response. Subsequently, we profiled the response using scRNA-seq.

2022-10-01 | E-MTAB-11056 | biostudies-arrayexpress

Stress granules are shock absorbers that prevent excessive innate immune responses to dsRNA

Project description:Proper defense against microbial infection depends on the controlled activation of the immune system. This is particularly important for the innate immune receptors that recognize viral double-stranded RNA (dsRNA) and initiate antiviral immune responses with the potential of triggering systemic inflammation and immunopathology. How the functions of the dsRNA receptors and their downstream effector molecules are coordinately regulated to avoid excessive immune response is poorly understood. We here demonstrate that stress granules (SGs), biomolecular condensates that form in response to various stresses including viral dsRNA, play key roles in regulating dsRNA-triggered immune response. Upon dsRNA stimulation, SGs recruit many innate immune molecules, including RIG-I-like receptors (RLRs), protein kinase R (PKR) and oligoadenylate synthases (OASes), target these molecules and dsRNA for autophagy and limit their functions through sequestration. In the absence of SGs, dsRNA stimulation results in hyperactivation of inflammatory signaling pathways, global translational arrest and bulk RNA degradation, altogether compromising the cellular capacity to restore homeostasis and triggering cell death. In contrast to most dsRNA-induced immune signaling pathways that are hyperactivated in the absence of SGs, a sub-branch of the RLR pathway (IRF3-dependent type I interferon signaling) shows time-dependent changes, where the initial spike in signaling is followed by a significant drop due to increased caspase-dependent negative feedback regulation. This highlights the role of SGs in regulating the delicate balance between the type I interferon pathway and cell death. Altogether, our data suggest that cells utilize SGs as shock absorbers to moderate antiviral innate immune response, thereby allowing cells to guard against its own immune system as well as viruses.

2021-05-06 | GSE173953 | GEO

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