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Murine Norovirus (MNV) infection results in anti-inflammatory response downstream of amino acids depletion in macrophages.

ABSTRACT: Murine Norovirus (MNV) infection results in anti-inflammatory response downstream of amino acids depletion in macrophages.

PROVIDER: PRJNA707233 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13872000_1.fastq.gz	Fastqsanger.gz
	SRR13872000_2.fastq.gz	Fastqsanger.gz
	SRR13872001_1.fastq.gz	Fastqsanger.gz
	SRR13872001_2.fastq.gz	Fastqsanger.gz
	SRR13872002_1.fastq.gz	Fastqsanger.gz

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Murine Norovirus (MNV) infection results in anti-inflammatory response downstream of amino acids depletion in macrophages.

Project description:Purpose: Characterisation of MNV induced host genetic reprogramming and translational control exerted over the host response by comparison of available cytoplasmic transcripts and their association with polysomes. Results: RNaseq data showed an inadequate response to MNV infection downstream of MDA5 activation coupled with a cellular response to a metabolic stress. In particular, all 296 significantly regulated transcripts showed a strong correlation between a transcript availability in the cytoplasm and its recrutment to the polysomal fraction as addressed using the R package 'Anota2seq'. Genome annotation analyses using Cytoscape highlighted the host response to the viral infection but showed a cluster of genes involved in response to stress and the related intrinsic apoptotic pathways suggesting a prevalence of a metabolic stress response over the innate immune response to the viral replication. Conclusions: Our study provides the first understanding analysis of the host response to MNV at the level of available cytoplasmic mRNA and their recruitment to the actively translating fractions. It described an absence of translational control over the host innate immune response but highlight and inadequate NF-kB response correlating with an ectopic anti-inflammatory response to amino acid starvation.

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Characterization of the chemokine response of RAW264.7 cells to infection by murine norovirus

Project description:RAW264.7 macrophages infected with MNV-1 and mock infected gene expression measured by microarray. To be published in Waugh, E. Chen, A. Baird, M. Fleming, S. Brown, C.M. and V K. Ward (2014) Characterization of the chemokine response of RAW264.7 cells to infection by murine norovirus. Virus Genes Four Samples, two mock and two MNV-1 infected.

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Project description:Murine norovirus (MNV) is genetically similar to human norovirus (HuNoV), and offers both an efficient in vitro cell culture system and animal model by which to investigate the molecular basis of replication. Here, we present a detailed global view of the cellular alterations that occur during the progression of a norovirus infection. The transcriptome of a synchronously infected population of MNV-infected murine macrophage-like cell line (RAW264.7) was determined at 8, 14, and 20 hours post infection. The cellular genetic response was analyzed both globally and by specific pathways. Viral replication was monitored by RNA-seq and quantitative real-time PCR in context of the cellular phenotypic response. The majority of transcriptionally up regulated genes were related to the IFN response. Additionally, there was a global increase in gene transcripts associated with immune response and inflammation. A transcriptional decrease was observed across many cellular processes, but particularly for genes involved in lipid homeostasis and cell cycle. The peak of the transcriptional immune response correlated with detected viral genome copies and changes in cellular phenotype including nuclear condensation. A more complete understanding of host response to norovirus infection will help to highlight the cellular pathways critical for a more effective immune response as well as those that may be exploited by the virus for therapeutic development.

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Project description:Changes in gene expression on MNV infection of RAW264.7 cells RAW264.7 cells were infected with MNV-1 at a multiplicity of infection of 1, or mock infected, for 12 hours

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Project description:The persistent murine norovirus strain MNVCR6 is a model for human norovirus and enteric viral persistence. MNVCR6 causes chronic infection by directly infecting tuft cells, rare chemosensory epithelial cells. Although MNVCR6 induces functional MNV-specific CD8+ T cells, these lymphocytes fail to clear infection. To clarify how tuft cells promote immune escape, we interrogated tuft cell interactions with CD8+ T cells by adoptively transferring JEDI (Just EGFP Death Inducing) CD8+ T cells into tuft cell reporter mice (Gfi1b-GFP). Surprisingly, some tuft cells partially resist JEDI CD8+ T cell-mediated killing – unlike Lgr5+ intestinal stem cells and extraintestinal tuft cells – despite seemingly normal antigen presentation. When targeting tuft cells, JEDI CD8+ T cells predominantly adopt a T resident memory phenotype with decreased effector and cytotoxic capacity, enabling tuft cell survival. Importantly, JEDI CD8+ T cells neither clear nor prevent MNVCR6 infection in the colon, the site of viral persistence, despite targeting a virus-independent antigen (e.g., GFP).

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Intestinal tuft cell immune privilege enables norovirus persistence

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