Expresssion data from reovirus treated breast cancer cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE69813 | GEO | 2015/06/13
SECONDARY ACCESSION(S): PRJNA286858
REPOSITORIES: GEO
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Project description:Packaging of segmented, double-stranded RNA viral genomes requires coordination of multiple viral proteins and RNA segments. For mammalian orthoreovirus (reovirus), evidence suggests either all ten or zero viral RNA segments are simultaneously packaged in a highly coordinated process hypothesized to exclude host RNA. Accordingly, reovirus generates genome-containing virions and “genomeless” top component particles. However, despite ostensibly lacking the genome, top component particles maintain a low level of infectivity. Whether reovirus particles can package host RNA is unknown. To gain insight into reovirus packaging potential and mechanisms, we employed next-generation RNA-sequencing to define the viral and host RNA content of purified reovirus virions and top component particles. Reovirus top component particles contained double-stranded viral RNA segments in similar proportions but at reduced levels compared to virions. Top component particles also were enriched for numerous host RNAs, especially short, non-polyadenylated transcripts, that differed by reovirus strain, independent of the viral polymerase. In contrast, virions were enriched for very few host RNAs. Collectively, these findings indicate that genome packaging into reovirus virions is exquisitely selective, while incorporation of host RNAs into top component particles is more promiscuous or differentially selective and may contribute to or result from inefficient viral RNA packaging.
2021-06-08 | GSE164270 | GEO
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:Reovirus propagates with high efficiency in KRAS mutated colorectal cancer (CRC). About 45-50% of CRC patients possess KRAS mutation. Oncolytic reovirus treatment in combination with chemotherapy was tested in patient samples possessing KRAS mutated metastatic CRC. This is the raw data from the peripheral mononuclear cell (PBMC) samples at 4 timepoints (pre treatment, 48 hours, day 8, and day 15).
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Project description:Ischemia reperfusion (I/R) injury is an unavoidable event occurring during heart transplantation, leading to graft failures and lower long-term survival rate of the recipient. IR causes apoptosis / death of cardiomyocytes, resulting from up-regulation of apoptotic genes and down-regulation of anti-apoptotic genes. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process.
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Project description:Analysis of reovirus-induced host responses at the level of gene expression. Results provide insights into how reovirus infection breaks tolerance to dietary antigens and promotes the development of celiac disease.
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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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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.
2007-04-20 | GSE7546 | GEO
Project description: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.
2018-08-28 | GSE119061 | GEO