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MAVS signaling shapes microglia responses to neurotropic virus infection

ABSTRACT: MAVS signaling shapes microglia responses to neurotropic virus infection

PROVIDER: PRJNA1148457 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30252106_1.fastq.gz	Fastqsanger.gz
	SRR30252106_2.fastq.gz	Fastqsanger.gz
	SRR30252107_1.fastq.gz	Fastqsanger.gz
	SRR30252107_2.fastq.gz	Fastqsanger.gz
	SRR30252108_1.fastq.gz	Fastqsanger.gz

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MAVS signaling shapes microglia responses to neurotropic virus infection

Project description:Viral encephalitis is characterized by a series of immunological reactions that can control virus infection in the brain, but dysregulated responses may cause excessive inflammation and brain damage. Microglia are brain-resident myeloid cells that are specialized on surveillance of the local environment and in case of viral brain infection they contribute to control of the infection and restriction of viral dissemination. Here, we report that after exposure to neurotropic vesicular stomatitis virus (VSV), murine in vitro microglia cultures showed rapid upregulation of a broad range of pro-inflammatory and antiviral genes, which were stably expressed over the entire 8 hours infection period. Additionally, a set of immunomodulatory genes was upregulated between 6 and 8 hours post infection. In in vitro microglia, the induction of several immune response pathways including cytokine responses was dependent on mitochondrial antiviral-signaling protein (MAVS). Consequently, in Mavs-deficient microglia control of virus infection failed as indicated by augmented accumulation of viral transcripts. Thus, in the analyzed in vitro system, MAVS signaling is critically required to achieve full microglia activation and to mediate profound antiviral effects. In Mavs-deficient mice, intranasal VSV instillation caused higher disease severity than in WT mice and the virus disseminated beyond the olfactory bulb and entered more distal brain regions. Virus spread to inner regions of the olfactory bulb, i.e., the granular cell layer, correlated with infiltration of highly inflammatory non-microglial myeloid cells into the olfactory bulb. Furthermore, increased cytokine levels were detected in the nasal cavity, the olfactory bulb and in other brain regions. Thus, microglial MAVS signaling is critically needed for virus sensing, full microglia activation, and for orchestration of protective immunity in the virus-infected CNS.

2024-08-29 | GSE274915 | GEO

The CSF1R-Microglia Axis Has Protective Host-Specific Roles During Neurotropic Picornavirus Infection

Project description:Goal: Determine the role of microglia in the antiviral response during neurotropic picornavirus infection of C57BL/6J and SJL/J mice and whether absence of microglia would affect CD4 and CD8 T cell functions. Methods: Brains from C57BL/6J and SJL/J mice treated with PLX5622 (to deplete microlgia) or control diet were harvested at 6 days post TMEV-infection. CD4+ T cells and CD8+ T cells were obtained using Easy Sep Mouse CD4+ T cell isolation Kit and Easy Sep Mouse CD8+ T cell isolation Kit (Stemcell). RNA was obtained using RNeasy (QIAGEN) and Illumina TruSeq stranded RNA Kit with Ribo-Zero Gold was then utilized to prepare cDNA library for RNA-seq. Results: Our results demonstrate strain-specific effects of the CSF1R-microglia axis in the context of neurotropic viral infection as well as inherent differences in microglial antigen presentation and subsequent T cell crosstalk that contribute to susceptibility to neurotropic picornavirus infection.

2021-05-10 | GSE160660 | GEO

M1 microglia-derived exosomes promote A1 astrocyte activation and aggravate ischemic injury via miR-331-5p/MAVS/NF-kB pathway

Project description:Ischemic stroke (IS) is one of the most serious neurological diseases, characterized by high mortality and disability rates. Glia cells, particularly microglia and astrocytes, occupy a pivotal position in the progression of IS. In response to stroke, microglia undergo polarization, transforming into either pro-inflammatory M1 phenotype or anti-inflammatory M2 phenotype. Analogously, astrocytes would polarize to pro-inflammatory A1 phenotype or anti-inflammatory A2 phenotype. It has been documented that A1 astrocytes can be activated by M1 microglia, although precise underlying mechanism remains elusive. In our study, we emulated ischemic injury using a middle cerebral artery occlusion/reperfusion (MCAO/R) model in mice and an oxygen-glucose deprivation/reoxygenation (OGD/R) model in primary astrocytes. Our findings revealed that M1 microglia could activate A1 astrocytes by secreting exosomes. According to RNA sequencing, circSTRN3 was enriched in M1 microglia-derived exosomes. Based on the review of literature and bioinformatics analysis, it was suggested that circSTRN3 could sponge miR-331-5p, while miR-331-5p could bind to MAVS and participate in the activation of NF-kB pathway and A1 astrocytes. Western blotting and qRT-PCR experiments verified this process. Furtherly, overexpression of circSTRN3 could aggravate neurological deficits, increase infarct volume, and promote cell death in MCAO/R model, whereas miR-331-5p inhibited this process. Furthermore, we conducted tests on circSTRN3 and miR-331-5p in exosomes isolated from the peripheral blood of IS patients, thereby confirming the correlation among circSTRN3, miR-331-5p, and the stroke severity score. Taken together, our study indicated that M1 microglia-derived exosomes could promote A1 astrocyte activation and exacerbate ischemic brain injury through the circSTRN3-miR331-5P/MAVS/NF-KB pathway.

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The CSF1R-Microglia Axis Has Protective Host-Specific Roles During Neurotropic Picornavirus Infection

Project description:The CSF1R-Microglia Axis Has Protective Host-Specific Roles During Neurotropic Picornavirus Infection

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An Epstein–Barr Virus Protein Interaction Map Reveals NLRP3 Inflammasome Evasion Via MAVS UFMylation

Project description:Epstein-Barr virus (EBV) causes infectious mononucleosis, triggers multiple sclerosis and is associated with 200,000 cancers/year. EBV colonizes the B-cell compartment and periodically reactivates, inducing expression of 80 viral proteins. Yet much remains unknown about how EBV remodels host cells and dismantles key antiviral responses. We therefore created a proteomic map of EBV-host and EBV-EBV interactions in B-cells undergoing EBV replication, uncovering conserved herpesvirus versus EBV-specific host cell targets. The EBV-encoded G-protein coupled receptor BILF1 associated with MAVS and the UFM1 E3 ligase UFL1. Whereas UFMylation of 14-3-3 proteins drives RIG-I/MAVS signaling, BILF1-directed MAVS UFMylation instead triggered MAVS packaging into mitochondrial-derived vesicles and lysosomal proteolysis. In the absence of BILF1, EBV replication activated the NLRP3 inflammasome, which impaired viral replication and triggered pyroptosis. Our results provide a viral protein interaction network resource, reveal a UFM1-dependent pathway for selective degradation of mitochondrial cargo and highlight BILF1 as a novel therapeutic target.

2023-07-20 | PXD041336 | Pride

Sequential MAVS- and MyD88/TRIF-signaling triggers anti-viral responses of tick-borne encephalitis virus-infected murine astrocytes

Project description:Upon tick borne encephalitis virus exposure of brain-resident cells, astrocytes are important IFN-β producers that followed a biphasic response, which initially depends on MAVS- and later on MyD88/TRIF-signaling

2021-09-28 | GSE175823 | GEO

A functional conserved fragment of long intergenic non-coding RNA linc-AhRA negatively regulates innate antiviral response in microglia

Project description:To identify functional lncRNAs in microglia-neurotropic virus interaction, high-throughput RNA sequencing was performed to obtain differential expressed lncRNAs (DELs) in microglia isolated from C57BL/6J mice, infected with or without neurotropic virus herpes simplex virus type 1 (HSV-1) (MOI 1 per group). All samples contain three mice’s microglia as a mixture given the isolated amount is low.

2021-10-03 | GSE167015 | GEO

Transcriptome analysis of ΔLMP1-MAVS transfected MARC-145 cells

Project description:We found that fuse ΔLMP1 to MAVS could strengthen MAVS mediated inhibition of PRRSV replication in MARC-145 cells. To better understand the biological function of the fusion protein ΔLMP1-MAVS, overall gene expression of MARC-145 cells transfected with ΔLMP1-MAVS or MAVS was evaluated by mRNA-seq. The result showed that ΔLMP1-MAVS upregulated a number of genes associated with innate immune responses to viral infection, including plenty of interferon-stimulated genes. This study provides reference date to research the working mechanism of ΔLMP1-MAVS.

2019-03-05 | GSE111530 | GEO

STAT1 independent control of a neurotropic measles virus challenge in primary neurons and infected mice

Project description:The objective of this study was to compare the ability of mice that lack STAT1 to resolve a neurotropic viral challenge, and to assess the ability of neurons obtained from these mice to be effectively cleared of virus by interferon gamma For the array, primary neurons were isolated from embryonic mice, grown as pure cultures, exposed to recombinant interferon gamma for 3, 6 or 24 hours and harvested for microarray analysis to identify and compare the gene profiles between wild type and STAT1 knockout neurons.

2012-03-14 | E-GEOD-33057 | biostudies-arrayexpress

Distinct Gene Profiles of Bone Marrow-Derived Macrophages and Microglia During Neurotropic Coronavirus-Induced Demyelination

Project description:Distinct Gene Profiles of Bone Marrow-Derived Macrophages and Microglia During Neurotropic Coronavirus-Induced Demyelination

| PRJNA885480 | ENA