CRNA-seq of MCMV
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ABSTRACT:
PROVIDER: PRJNA874812 | ENA |
REPOSITORIES: ENA
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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: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: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:Evidence supporting the role of pathogen exposure in the development of dementia has been mounting for decades. We used murine cytomegalovirus (MCMV) as our model pathogen. We repeated infected mice every 3 months modeling the re-activation/re-infection with MCMV that occurs throughout life. We used Multiome ATAC-seq and RNA-seq to examine changes to the brain of infected animals.
2024-02-01 | GSE220848 | 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.
2012-07-01 | GSE36919 | GEO
Project description:Reactivation of latent HCMV is a significant infectious complication of organ transplantation, and current therapies target viral replication once reactivation of transcriptionally silent, latent virus has already occurred. The specific molecular pathways that activate viral gene expression are not well understood. Our studies aim to identify these factors, with the goal of developing novel therapies that prevent transcriptional reactivation in transplant recipients. MCMV is a valuable model for studying latency and reactivation of CMV induced by organ transplantation. We previously demonstrated that transplantation of MCMV-latently infected kidneys into allogeneic recipients induces transcriptional reactivation of immediate early (IE) gene expression within 48 hr. We used microarrays to profile global mouse kidney gene expression associated with transcriptional reactivation of MCMV immediate early gene expression at 48 hr after transplant of MCMV latently infected kidneys into allogeneic recipients. We identified differentially expressed genes and pathways associated with both early acute rejection and reactivation of MCMV. control vs. allograft
2015-08-27 | E-GEOD-72392 | biostudies-arrayexpress