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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomesof Wild Type , RIG-I-/-, MAVS -/- mice during influenza infection

ABSTRACT: Purpose: The goals of this study are to compare Next-generation sequencing (NGS)-derived transcriptome profiling (RNA-seq) in the lung of three tyeps of mice during influenza infection. Methods: Total RNA from lung was extracted using a modified TRIzol protocol and spectrophometrically quantitated. Library preparation and sequencing were conducted using 3’ inTAG next-generation sequencing . Differential gene expression for day 6 post influenza infection was determined relative to mock inoculated mice. Results: Differentially expressed genes were defined using p-value <0.01 and FDR-corrected p-value <0.1 cutoffs. We identified the transcripts in the lung of RIG-I-/-, MAVS -/- mice during influenza infection Our study represents the first detailed analysis of lung transcriptomes of Wild Type , RIG-I-/-, MAVS -/- mice during influenza infection , with biologic replicates, generated by RNA-seq technology.

ORGANISM(S): Mus musculus

PROVIDER: GSE114232 | GEO | 2018/11/28

REPOSITORIES: GEO

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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomesof Wild Type , RIG-I-/-, MAVS -/- mice during influenza infection

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomesof Wild Type , RIG-I-/-, MAVS -/- mice during influenza infection

| PRJNA470625 | ENA

Targeting APT2 improves MAVS palmitoylation and antiviral innate immunity

Project description:Innate immunity serves as the primary defense against viral and microbial infections in humans. Among its components, retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are well-characterized intracellular pattern-recognition proteins that trigger innate immune responses upon viral infection. However, the precise influence of cellular metabolites, especially fatty acids, on the regulation of RLR-mediated antiviral innate immunity remains largely elusive. Here, through screening a metabolite library, palmitic acid (PA) has been identified as a crucial metabolite responsible for modulating antiviral infections. Mechanistically, PA induces the palmitoylation of MAVS, leading to MAVS aggregation and subsequent activation, thereby enhancing the innate immune response against viral infections. Functionally, the enzyme palmitoyl-transferase ZDHHC24 plays a key role in catalyzing the palmitoylation of MAVS at both C46 and C79 residues, thereby facilitating the transduction of RLR-mediated TBK1-IRF3-IFN signaling pathway, particularly under conditions of PA stimulation or high-fat diet feeding. Conversely, the absence of ZDHHC24 significantly attenuates virus-induced innate immune responses in both cells and mice. Moreover, APT2 counteracts with ZDHHC24 to de-palmitoylate MAVS, thus inhibiting the antiviral response. Consequently, inhibition of APT2 using compounds like ML349 effectively reverses MAVS palmitoylation and activation in response to antiviral infections. These findings underscore the critical role of PA and ZDHHC24 in regulating antiviral innate immunity through MAVS palmitoylation, and suggest potential therapeutic strategies for combating viral infections, such as enhancing PA intake or specifically targeting APT2.

2024-09-10 | PXD054077 | Pride

RNA-sequencing of lung RNA from mice with compound mutations in ADAR1 and MAVS, ZBP1 or RIPK3.

Project description:The purpose of this study was to examine the role of MAVS, ZBP1 and RIPK3 in the phenotype that develops when ADAR1 activity is impaired, in particular when the Za domain of ADAR1 is mutated. Mice homozygous for a Za domain-mutant allele of Adar1 (Adar1mZa/mZa mice) and mice carrying one mZa and one null Adar1 allele (Adar1-/mZa mice) were compared with control mice that were either wild type or heterozygous for the Adar1 mZa allele (Adar1wt/mZa mice). The effects of MAVS deficiency, RIPK3 deficiency, ZBP1 deficiency or ZBP1 Za domain mutations were assessed by analysing compound mutant mice. Given the early postnatal lethal phenotype that develops in Adar1-/mZa mice, comparisons were made in RNA isolated from lung tissue from newborn mice of each genotype (5 mice per genotype). As Adar1-/mZa mice additionally lacking Mavs or Zbp1 are viable, adult mice (15-20 weeks of age) were also used for several compound mutations as donors of lung tissue.

2022-06-09 | E-MTAB-11540 | biostudies-arrayexpress

Noncanonical MAVS signaling restrains dendritic cell-driven antitumor immunity by inhibiting IL-12

Project description:MAVS-mediated cytosolic RNA sensing plays a central role in tumor immunogenicity. However, the effects of host MAVS signaling on antitumor immunity remains uncertain. Here, we demonstrate that host MAVS pathway drives accelerated tumor growth and impairs antitumor immunity, while MAVS knockout in dendritic cells (DCs) promotes tumor-reactive CD8+ T cell responses. Specifically, the CD8+ T cell priming capacity is enhanced by lack of functional MAVS in a type I interferon-independent, but IL-12-dependent, manner. Mechanistically, loss of RIG-I/MAVS cascade activates non-canonical NF-κB pathway and in turn induces IL-12 production by DCs, resulting in CD8+ T cell: DC crosstalk licensed by IFN-γ and IL-12. Moreover, ablation of host MAVS sensitizes tumors to immunotherapy and attenuates radiation resistance, thereby facilitating the maintenance of effector CD8+ T cells. These findings identify that host MAVS pathway acts as an immune checkpoint of DC-driven antitumor immunity, indicating the development of DC-based immunotherapies through MAVS signaling antagonism.

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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

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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

A systems approach reveals MAVS signaling in myeloid cells as critical in resistance to Ebola virus in murine models of infection

Project description:The unprecedented 2013-16 outbreak of Ebola virus (EBOV) in West Africa resulted in over 11,300 human deaths. Host resistance to EBOV is thought to involve RIG-I-like receptor (RLR) signaling through the adaptor protein, mitochondrial antiviral signaling (MAVS), but role of RLR-MAVS in orchestrating anti-EBOV responses in vivo is not known. Here, we apply a systems approach to MAVS-deficient mice infected with either wild-type or mouse-adapted EBOV. MAVS controlled EBOV replication through expression of IFNα, IFN-stimulated genes, and regulation of inflammatory responses in the spleen, and prevented cell death in the liver, with macrophages implicated as a major cell-type influencing host resistance. A dominant role for RLR signaling in macrophages was confirmed following conditional deletion of MAVS in LysM+ myeloid cells. These findings reveal tissue-specific transcriptional pathways controlled by RLR signaling in resistance to EBOV, and suggest that EBOV adaptation to cause disease in mice is linked in part to increased antagonism of RLR-dependent signaling.

2016-12-31 | GSE83309 | GEO

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

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Project description:Transcriptional profiling of chicken embryonic fibroblasts (DF-1 cells) comparing the effects of chicken cells transfected with duck RIG-I compared to empty-vector transfected cells following with low or highly pathogenic avian influenza. Goal was to determine the effects of duck RIG-I on influenza-induced immune gene expression. Two-condition experiment. Biological replicates for low pathogenic avian influenza infection: 3 empty-vector transfected replicates, 3 RIG-I transfected replicates. Biological replicates for highly pathogenic influenza infection: 2 empty-vector transfected replicates, 2 RIG-I transfected replicates.

2012-12-12 | E-GEOD-29596 | biostudies-arrayexpress

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