Early transcriptional changes in rabies virus-infected neurons and extended effects on neuronal functions
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA739691 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14871100_1.fastq.gz | Fastqsanger.gz | |||
| SRR14871100_2.fastq.gz | Fastqsanger.gz | |||
| SRR14871101_1.fastq.gz | Fastqsanger.gz | |||
| SRR14871101_2.fastq.gz | Fastqsanger.gz | |||
| SRR14871102_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 68 |
Similar Datasets
Project description:Street-strain rabies virus primarily replicates in central nervous system without inducing significant immune response or structural damages on neurons, but the manifested symptoms of rabies indicate inherent neuronal dysfunctions in CNS. To understand the underlying state of rabies virus-infected neurons and find probable mechanisms for the neuronal dysfunction, we performed RNA-Seq at multiple time-points. This dataset provides RNA-Seq results of wild-type and mutant rabies virus-infected neuron transcriptome, with clear differential expressions between conditions. Through comparative analysis of different time-points, we have found that the matrix protein of rabies virus plays an important role in early suppression of host gene expression and maintaining control over immune response and other processes. The signaling pathways previously known to interact with rabies virus were confirmed to be modulated in this dataset, and contribute to neuronal function-associated processes. We have verified the regulation of gene expressions that could impact neuronal functions collectively, and demonstrated in calcium imaging that indeed the oscillation of calcium trace in neurons are influenced by rabies virus infection.
2021-11-04 | GSE178583 | GEO
Project description:Cortical circuit tracing using modified rabies virus can identify input neurons making direct monosynaptic connections onto neurons of interest. However, challenges remain in our ability to establish the cell type identity of rabies-labeled input neurons. While transcriptomics may offer an avenue to characterize inputs, the extent of rabies-induced transcriptional changes in distinct neuronal cell types remains unclear and whether these changes preclude characterization of rabies-infected neurons according to established transcriptomic cell types is unknown. We used single-nucleus RNA sequencing to survey the gene expression profiles of rabies-infected neurons and assessed their correspondence with established transcriptomic cell types. We demonstrated that when using transcriptome-wide RNA profiles, rabies-infected cortical neurons can be transcriptomically characterized despite global and cell-type-specific rabies-induced transcriptional changes. Notably, we found differential modulation of neuronal marker gene expression, suggesting that caution should be taken when attempting to characterize rabies-infected cells with single genes or small gene sets.
2022-05-25 | GSE196771 | GEO
Project description:This experiment is part of the project that primarily aims to utilize 3D hydrogel-based hiPSC-derived neuronal model to study rabies virus infection in the central nervous system. Having established the optimal 3D neuronal model, we then investigated the growth kinetics of two strains of rabies virus (TH and CVS-11) and comparatively analyzed the 2D and 3D culture models. We performed a gene expression analysis using NanoString to determine whether changes in gene expression could explain the differences in virus growth kinetics of two strains of rabies virus observed between the 2D and 3D neuronal culture models. Gene expression analysis of the neuropathological pathway observed during rabies virus infection demonstrated a vast number of differentially expressed genes in the 3D model as compared to the 2D model.
2023-08-23 | GSE231664 | GEO
Project description:To investigate the effects of rabies infection on neuronal gene expression, we compared gene profiles of rabies infected and non-infected GABAergic neurons in the Zebrafish olfactory bulb.
2022-07-07 | E-MTAB-11083 | biostudies-arrayexpress
Project description:Rabies is a zoonotic disease caused by rabies virus (RABV). As rabies advances, patients develop a variety of severe neurological symptoms that inevitably lead to coma and death. Unlike other neurotropic viruses that can induce symptoms of a similar range, RABV-infected post-mortem brains do not show significant signs of inflammation nor the structural damages on neurons. This suggests that the observed neurological symptoms possibly originate from dysfunctions of neurons. However, many aspects of neuronal dysfunctions in the context of RABV infection are only partially understood, and therefore require further investigation. In this study, we used differentiated neurons to characterize the RABV-induced transcriptomic changes at the early time-points of infection. We found that the genes modulated in response to the infection are particularly involved in cell cycle, gene expression, immune response, and neuronal function-associated processes. Comparing a wild-type RABV to a mutant virus harboring altered matrix proteins, we found that the RABV matrix protein plays an important role in the early down-regulation of host genes, of which a significant number is involved in neuronal functions. The kinetics of differentially expressed genes (DEGs) are also different between the wild type and mutant virus datasets. The number of modulated genes remained constant upon wild-type RABV infection up to 24 h post-infection, but dramatically increased in the mutant condition. This result suggests that the intact viral matrix protein is important to control the size of host gene modulation. We then examined the signaling pathways previously studied in relation to the innate immune responses against RABV, and found that these pathways contribute to the changes in neuronal function-associated processes. We further examined a set of regulated genes that could impact neuronal functions collectively, and demonstrated in calcium imaging that indeed the spontaneous activity of neurons is influenced by RABV infection. Overall, our findings suggest that neuronal function-associated genes are modulated by RABV early on, potentially through the viral matrix protein-interacting signaling molecules and their downstream pathways.
| S-EPMC8713068 | biostudies-literature
Project description:Rabies virus (RABV) is a highly neurotropic pathogen that typically leads to mortality of infected animals and humans. The precise etiology of rabies neuropathogenesis is unknown, though it is hypothesized to be due either to neuronal death or dysfunction. Our approach to study the survival and integrity of RABV-infected neurons was to infect Cre reporter mice with recombinant RABV expressing Cre-recombinase (RABV-Cre) to switch neurons constitutively expressing tdTomato (red) to expression of a Cre-inducible EGFP (green), permanently marking neurons that had been infected in vivo. We were able to isolate these previously infected neurons (“infected”) by flow cytometry and assayed their gene expression profiles compared to uninfected cells (“uninfected”) from the same mice.
2012-06-28 | GSE38975 | GEO
Project description:Rabies virus (RABV) is a highly neurotropic pathogen that typically leads to mortality of infected animals and humans. The precise etiology of rabies neuropathogenesis is unknown, though it is hypothesized to be due either to neuronal death or dysfunction. Our approach to study the survival and integrity of RABV-infected neurons was to infect Cre reporter mice with recombinant RABV expressing Cre-recombinase (RABV-Cre) to switch neurons constitutively expressing tdTomato (red) to expression of a Cre-inducible EGFP (green), permanently marking neurons that had been infected in vivo. We were able to isolate these previously infected neurons (“infected”) by flow cytometry and assayed their gene expression profiles compared to uninfected cells (“uninfected”) from the same mice.
2012-06-28 | GSE38970 | GEO
Project description:Rabies is an ancient infectious disease but still lacking efficient therapeutic approach despite of vaccine. In this study, we have identified a novel cytoplasmic lncRNA, namely rabies virus related lncRNA 1(RVRL1), whose expression in neuronal cells is up-regulated upon the infection of the causative agent of rabies, the neurotropic virus rabies virus (RABV). RVRL1 effectively inhibits RABV infection both in neuronal cells and in a mouse model. RVRL1 binds to EZH2 and disrupts the PRC2 complex, which is consistent with the inverse relationship between RVRL1 expression and the cellular H3K27me3 level. RVRL1 expression positively regulates the expression of PCP4L1 encoding a 10 kD peptide, which is shown to inhibit RABV replication. These findings highlight a novel mechanism for lncRNAs to upregulate the expression of antiviral genes, and define two potential anti-rabies reagents including an antiviral lncRNA and an antiviral peptide.
2020-09-08 | GSE107285 | GEO
Project description:Rabies is an ancient infectious disease but still lacking efficient therapeutic approach despite of vaccine. In this study, we have identified a novel cytoplasmic lncRNA, namely rabies virus related lncRNA 1(RVRL1), whose expression in neuronal cells is up-regulated upon the infection of the causative agent of rabies, the neurotropic virus rabies virus (RABV). RVRL1 effectively inhibits RABV infection both in neuronal cells and in a mouse model. RVRL1 binds to EZH2 and disrupts the PRC2 complex, which is consistent with the inverse relationship between RVRL1 expression and the cellular H3K27me3 level. RVRL1 expression positively regulates the expression of PCP4L1 encoding a 10 kD peptide, which is shown to inhibit RABV replication. These findings highlight a novel mechanism for lncRNAs to upregulate the expression of antiviral genes, and define two potential anti-rabies reagents including an antiviral lncRNA and an antiviral peptide.
2020-09-08 | GSE107277 | GEO
Project description:Rabies is a fatal zoonotic disease posing a threat to the public health globally. Rabies virus (RABV) is excreted in the saliva of infected animals, and is primarily transmitted through bite contact. Salivary glands play an important role for virus propagation. However, the significance of salivary glands is less studied in RABV pathogenic mechanisms. To identify functionally important genes in the salivary glands, we employed RNA sequencing (RNA-seq) to establish and analyze mRNA expression profiles in parotid tissue infected with two RABV strains, CVS-11 and PB4. We map the transcriptome changes in response to RABV infection in parotid tissue for the first time. This work provides new clues to the study of RABV-affected salivary gland function and RABV transmission mechanisms in parotid tissue. And the salivary gland-enriched transcripts could be potential targets of interest for rabies disease control.
2023-11-26 | GSE248365 | GEO