Reovirus infection induces stabilization and up-regulation of cellular transcripts that encode regulators of TGF-beta signaling
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE119061 | GEO | 2018/08/28
REPOSITORIES: GEO
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Project description:Reovirus infection induces dramatic changes in host mRNA expression. We utilized oligonucleotide microarrays to measure cellular mRNA decay rates in mock- or reovirus-infected murine L929 cells to determine if changes in host mRNA expression are a consequence of reovirus-induced alterations in cellular mRNA stability. Our analysis detected a subset of cellular transcripts that were coordinately induced and stabilized following infection with the reovirus isolates c87 and c8, strains that led to an inhibition of cellular translation, but not following infection with Dearing, a reovirus isolate that did not negatively impact cellular translation. The induced and stabilized transcripts encode multiple regulators of TGF- β signaling, including components of the Smad signaling network and apoptosis/survival pathways. The coordinate induction, through mRNA stabilization, of multiple genes that encode components of TGF-β signaling pathways represents a novel mechanism by which the host cell responds to reovirus infection.
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Project description:Reovirus infection induces stabilization and up-regulation of cellular transcripts that encode regulators of TGF-beta signaling
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Project description:A significant fraction of sudden death in young adults is due to myocarditis, an inflammatory disease of the heart, most often caused by viral infection. Here we used single-cell and spatially resolved RNA sequencing (RNA-seq) to study the cellular and spatial heterogeneity of myocarditic processes in the hearts of reovirus-infected neonatal mice at multiple predetermined time points after initial infection at the primary site of infection. We further applied these technologies to study the innate response to reovirus infection in the intestine. In addition, we performed time-dependent single-cell RNA-seq (scRNA-seq) of cardiac tissues of mice infected with a reovirus point mutant that does not cause myocarditis. To establish viral tropism, we implemented molecular enrichment of non-polyadenylated viral transcripts that were otherwise poorly represented in the transcriptomes. Our measurements give insight into the cardiac cell-type specificity of innate immune responses, into the tropism of the virus in the intestine and the heart, into the transcriptional states of cell types involved in the production of inflammatory cytokines and the recruitment of circulating immune cells, and into the cell type specific gene expression in a spatial context. Overall, our data identify cellular interactions and cell-type specific host responses during reovirus-induced myocarditis.
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Project description:Infection of the chestnut blight fungus, Cryphonectria parasitica, by hypovirus CHV1-EP713 or by reoviruses MYRV1-Cp9B21 or MYRV2-CpC18 results in reduced fungal virulence (hypovirulence). However, additional phenotypic changes caused by the two groups of mycoviruses are quite different. CHV1-EP713 infection results in depressed pigmentation and conidiation while reovirus infection has little effect on these processes. We now report that loss of female fertility and resulting absence of virus transmission through sexual spores observed after hypovirus infection was not observed for reovirus infected C. parasitica. Reovirus-infected strains were male and female fertile and able to transmit virus to ascospore progeny at a high rate when serving as a female parent. Consistent with this result, real-time RT-PCR revealed that expression of two genes involved in sexual reproduction, the pheromone precursor gene, mf2-1 and yeast Ste12-like transcriptional factor gene, Cpst12, were less reduced in reovirus-infected strains than in hypovirus-infected strains. Analysis with a custom microarray cDNA chip containing EST clones representing ca 2,200 unique C. parasitica genes identified 140 and 128 host genes that were responsive to MYRV1-Cp9B21 and MYRV2-CpC18 infection, respectively. Comparison of these virus-responsive genes revealed an overlap of 85 genes even though the overall degree of nucleotide sequence identity of the two reoviruses is less than 50%. Significantly, 84 of the 85 genes were altered in the same direction. Further comparison revealed that 51 % and 48% of the genes that were responsive to reoviruses MYRV1-Cp9B21 and MYRV2-CpC18 infection were also responsive to CHV1-EP713 infection. Finally, similar to results reported for hypovirus infection, a high percentage (59% and 66%) of the mycoreovirus responsive genes were also differentially expressed following disruption of the cellular G-protein signal transduction pathway. These data support the hypothesis that hypovirus and reovirus infections perturb common and specific C. parasitica regulatory pathways to cause hypovirulence and distinct sets of phenotypic changes. Keywords: Mycoreovirus, hypovirus, gene expression, microarray.
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