Single Cell Gene Expression and ATAC-seq of Mouse Brain Following Multiple Infections with Murine Cytomegalovirus (MCMV)
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE220848 | GEO | 2024/02/01
REPOSITORIES: GEO
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Project description:Swiss murine embryonic fibroblasts (NIH-3T3) were infected with wild-type Smith strain mouse cytomegalovirus (MCMV) at a multiplicity of infection (MOI) of 10. Sequencing libraries were prepared using the cRNA-seq protocol from the indicated time points of infection as described by Whisnant A.W. et al, Nat. Commun (2020)
2023-04-26 | GSE212285 | GEO
Project description:Swiss murine embryonic fibroblasts (NIH-3T3) were infected with wild-type Smith strain mouse cytomegalovirus (MCMV) at a multiplicity of infection (MOI) of 10. Sequencing libraries were prepared using the 4sU-seq protocol (Dölken et al., RNA 2008 and Rutkowski et al.) from the indicated time points of infection as described in Rutkowski, A.J. et al, Nat. Commun (2015)
2023-04-26 | GSE212287 | GEO
Project description:Ly49G2+ NK cells mediate essential control of murine cytomegalovirus (MCMV) infection in mice which express the H-2Dk class I molecule. As a cognate ligand for specific Ly49G2 inhibitory receptor allotypes, H-2Dk also licenses Ly49G2+ NK cells in naïve and MCMV-infected mice. These findings suggest Ly49G2 may promote antiviral NK cell activities during MCMV infection. Indeed, in mice lacking the Ly49G2 receptor, MCMV resistance is fully abrogated. Additionally, NK cells expressing Ly49R, an NK cell associated activation receptor that also recognizes H-2Dk, have their function augmented by Ly49G2 and are required for MCMV resistance.
2019-12-11 | GSE132394 | GEO
Project description:Innate and adaptive immune cells can acquire “memory” of encounters with a diverse range of activating signals to tune their response to secondary stimuli. Group 1 innate lymphoid cells (ILC1) are recently discovered tissue-resident sentinels that are essential for early host protection from intracellular pathogens at initial sites of infection. However, whether ILC1 function as short-lived effectors or persist and refine their responsiveness following pathogen challenge is not well understood. Furthermore, whether pathogen-derived antigens directly modulate tissue-resident ILC responses remains unclear. Here, we found that liver-resident ILC1 expand locally and persist following the resolution of mouse cytomegalovirus (MCMV) infection. MCMVexperienced ILC1 acquired stable transcriptional, epigenetic, and phenotypic changes, with an enhanced protective effector response to secondary MCMV challenge. Protective memory ILC1 responses were dependent on the MCMV-encoded glycoprotein m12, but not formed during bystander cytokine activation following heterologous infection. Thus, liver ILC1 acquire adaptive features in a MCMV-specific manner.
2019-05-02 | GSE128906 | GEO
Project description:Prenatal Human Cytomegalovirus (HCMV) infection often causes CNS maldevelopment. In a murine model, we detect Murine Cytomegalovirus (MCMV) in brain following intra-peritoneal inoculation at birth. Infected mice show impaired cerebellar development and impaired neurologic function on a beam balance test as adults. Among developmental genes differentially regulated, hindbrain expression of the homeodomain transcription factor HOXa5 was reduced with infection, and fewer HOXa5 expressing neurons were found in vestibular nuclei. Based on the hypothesis that immune activation connects focal viral infection and global CNS maldevelopment, we defined the components of CNS immune response. Flow cytometry showed a large increase in both number and activation of CNS monocytes. Monocytes were found in close association with infected cells by immunohistochemistry (IHC). Oligonucleotide microarrays contained herein identified many differentially expressed genes related to innate immune response. Chemokines, cytokines, cell surface receptors, and proteases are some of the many immunological genes shown to be differentially regulated by MCMV infection. These results together show that MCMV infection induces a complex immune response associated with changes in developmental gene expression and lasting neurologic defecit. Keywords: disease state comparison (virus infection) and competetive hybridization for expression analysis
2008-06-01 | GSE9945 | GEO
Project description:Swiss murine embryonic fibroblasts (NIH-3T3) were infected with wild-type Smith strain mouse cytomegalovirus (MCMV) at a multiplicity of infection (MOI) of 10. Ribosome profiling was performed at various times during infection with minor modification to the protocol described in Stern-Ginossar N et al., Science 2012. The detailed protocol is described in Rutkowski et al, Nature commun 2015, and Whisnant et al., Nature commun. 2020. Translation start site profiling was performed by culturing cells in presence of Harringtonin or Lactimidomycin for 30 min prior to cell harvest.
2023-04-26 | GSE212288 | GEO
Project description:Swiss murine embryonic fibroblasts (NIH-3T3) were infected with wild-type Smith strain mouse cytomegalovirus (MCMV) at a multiplicity of infection (MOI) of 10. Metabolic RNA labelling was performed using 400µM 4sU for one hour prior to cell lysis. Total RNA was isolated using the Trizol protocol and U-to-C conversions were induced by IAA treatment according to the SLAM-seq protocol (Herzog et al., Nature Methods 2017). Sequencing libraries were prepared using the dRNA-seq protocol from the indicated time points of infection as described by Whisnant A.W. et al, Nat. Commun (2020).
2023-04-26 | GSE212286 | GEO
Project description:One goal of viral infection is to reprogram the host cell to optimize viral replication. As part of this process, viral miRNAs may compete for components of the miRNA/siRNA pathway as well as regulate cellular targets. Mouse Cytomegalovirus has been described to generate large numbers of viral miRNAs during lytic infection and was therefore used to analyze the impact of viral miRNAs on the host cell small RNA system as well as to check for sorting of viral small RNAs into specific Ago-proteins. Deep sequencing analysis of MCMV infected cells revealed that viral miRNAs represent only app. 13% of all detected miRNAs. All previously described MCMV miRNAs with the exception of miR-m88-1* were confirmed and for the MCMV miR-m01-1 hairpin an additional miRNA, designated miR-m01-1-3p, was found. Its presence was confirmed by qPCR and Northern Blot. Deep sequencing after RISC IP with antibodies specific for either Ago1 or Ago2 showed that all MCMV miRNAs are loaded into both RISC complexes. The ratio of MCMV to mouse miRNAs was not increased after immunoprecipitation of Ago-proteins. Viral miRNAs therefore do not overwhelm the host miRNA processing system nor are they preferentially incorporated into RISC. We found that 3 mouse miRNAs showed an altered expression due to MCMV infection. Down-regulation of miR-27a, as previously described, could be confirmed. In addition, miR-26a was down-regulated and an up-regulation of miR-7a dependent on viral protein expression could be observed. Examination of small RNA expression in uninfected vs. infected cells, immunoprecipitation + sequencing of Ago1 and Ago2 loaded small RNAs in infected cells
2012-06-30 | E-GEOD-36919 | biostudies-arrayexpress
Project description:The systematic temporal gene expression analysis of primary macrophages activated under immune (interferon-gamma) and productive viral infection with murine cytomegalovirus (mCMV). The primary objective of the study is to define, in an unbiased manner, cause-and-effect relationships in the program of gene activation in this cellular system. The even spacing and time intervals (every 30 minutes) makes this study amenable to modelling of gene networks in the system. A kinetic analysis of mCMV infection on the gene expression of murine (BALB/c) bone marrow-derived macrophages (BMDMs) over the first 12 hours, sampling every 30 minutes. Agilent mouse genome arrays were used to determine the differences in gene expression between mock and mCMV infected. The 25 samples collected for the mock infected were pooled and treated as a pooled control. Pooled control was labelled with Cy3 dye and hybridised with every other sample (labelled with Cy5 dye) = 25 dual-dye array hybridisations. The reference channel of the dual-channel hybridisations was only used to normalise the expression of the test channel, rather than used to calculate ratio data. Thus, the normalised data represent log2 single-channel data.
2015-07-10 | E-GEOD-42503 | biostudies-arrayexpress
Project description:Recent work indicates that salivary glands are able to constitutively recruit CD8+ T cells and retain them as tissue resident memory T cells (TRM), independently of local infection, inflammation or antigen. To understand the mechanisms supporting T cell recruitment to the salivary gland, we compared T cell migration to the salivary gland in mice infected or not with murine cytomegalovirus (MCMV), a herpesvirus that infects the salivary gland and promotes the accumulation of salivary gland TRM. We found that acute MCMV infection increased rapid T cell recruitment to the salivary gland, but that equal numbers of activated CD8+ 44 T cells eventually accumulated in both infected and uninfected glands. T cell recruitment to uninfected salivary glands depended on chemokines and the integrin α4. Several chemokines were expressed in the salivary glands of both infected and uninfected mice and many of these could promote the migration of MCMV-specific T cells in vitro. MCMV infection increased expression of chemokines that interact with the receptors CXCR3 and CCR5, but neither receptor was needed for T cell recruitment to the salivary gland during MCMV infection. Unexpectedly however, the chemokine receptor CXCR3 was critical for T cell accumulation in uninfected salivary glands. Together, these data suggest that CXCR3 and the integrin α4 mediate T cell recruitment to uninfected salivary glands, but that redundant mechanisms mediate T cell recruitment after MCMV infection.
2018-01-15 | GSE107338 | GEO