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Examining the role of murine norovirus (MNV)-infection on intraepithelial lymphocytes (IELs).

ABSTRACT: We examined how MNV-infection affects the population and function of IELs in vivo.

ORGANISM(S): Mus musculus

PROVIDER: GSE204822 | GEO | 2022/07/01

REPOSITORIES: GEO

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Examining the role of murine norovirus (MNV)-infection on intraepithelial lymphocytes (IELs).

Project description:Examining the role of murine norovirus (MNV)-infection on intraepithelial lymphocytes (IELs).

| PRJNA842399 | ENA

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RNA-sequencing of longitudinal murine norovirus (MNV) infection in RAW264.7 mouse macrophages

Project description:The transcriptome has an abundance of information about the function of individual cells, tissues and an organism in general. Characterising the transcriptome of virus infected cells can illuminate features of the viral-host relationship that are important for pathogenesis. This study broadly aimed to quantify the host gene expression changes that occur following MNV infection. Furthermore, we aimed to identify alterations in specific biological pathways by identifying alterations in transcript abundance that increase or decrease in intensity with MNV infection over time.

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Murine Norovirus Effect on Cells

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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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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Gene expression signatures for CD8αβ+ intraepithelial lymphocytes and CD8αβ+ splenocytes.

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