Acute murine cytomegalovirus infection boosts cell-type specific response and lipid metabolism changes in infant mice liver
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ABSTRACT:
PROVIDER: PRJNA934934 | ENA |
REPOSITORIES: ENA
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| Action | DRS | |||
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| SRR23458760.fastq.gz | Fastqsanger.gz | |||
| SRR23458761.fastq.gz | Fastqsanger.gz |
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Project description:Human cytomegalovirus (HCMV) infection in infants cause severe diseases, such as neonatal hepatitis. However, the single-cell dimensional description of the immune cell alteration during the first virus exposure process in infants, remains poorly understood. The hepatocytes play an essential role in metabolic homeostasis and detoxification. The Concomitant Effects of CMV infection on liver lipid metabolism in infants are still unclear. Here, using single-cell RNA-sequencing, we found MCMV can infect most cell types of infant mice liver, changing the number of immune cells. MCMV infection increases proliferating CD8 effector T cells and a subset of Nos2+ monocytes, which may play important roles in the early anti-viral process. Furthermore, MCMV infection subvert the protein expression profile of lipid metabolism in hepatocytes. Overall, our data provide insights as to how the immune system response to MCMV infection during the early stage of infection, and the impact of infection on lipid metabolism in infant mice hepatocytes.
2023-08-02 | GSE225309 | GEO
Project description:Human cytomegalovirus (HCMV) infection in infants cause severe diseasessuch as neonata hepatitis, However, the single-cell dimensiona description otthe immune cel alteration during the first virus exposure process in infantsremains poorly understood. The hepatocytes play an essential role in metabolichomeostasis and detoxification, The Concomitant Effects of CMV infection oriver lipid metabolism in infants are still unclear. Here, using single-cell RNAsequencing, we found MCMV can infect most cell types of infant mice liverchanging the number of immune cells, MCMV infection increases proliferatincsubset of Nos2+CD8 effectorcells and amonocytes，which may plalimportant roles in the early anti-viral process. Furthermore, MCMV infectiorsubvert the protein expression profile of lipid metabolism in hepatocytesOverall, our data provide insights as to how the immune system response toMCMY infection during the early stage of infection, and the impact of infectionon lipid metabolism in infant mice hepatocvtes.
2023-03-13 | PXD040842 |
Project description:IntroductionHuman cytomegalovirus (HCMV) infection in infants can lead to severe diseases, including neonatal hepatitis. The single-cell dimensional changes in immune cells after the initial CMV infection remain elusive, as do the effects of CMV infection on hepatic lipid metabolism.MethodsWe employed single-cell RNA-sequencing to investigate the changes in liver cell types and immune responses in infant mice following murine CMV (MCMV) infection. Additionally, we examined alterations in protein expression profiles related to lipid metabolism in hepatocytes and the role of the key transcription factor PPAR-γ in hepatocytes during CMV infection.ResultsOur study revealed that MCMV infects most liver cell types in infant mice, leading to an increase in the proportion of proliferating CD8 effector T cells and a subset of Nos2+ monocytes, potentially playing an essential role in early anti-viral responses. Furthermore, MCMV infection resulted in altered protein expression of lipid metabolism in hepatocytes. Knocking down the transcription factor PPAR-γ in hepatocytes effectively inhibited CMV infection.DiscussionOur findings underscore the immune system's response to early-stage MCMV infection and the subsequent impact on hepatic lipid metabolism in infant mice. This research provides new insights into the mechanisms of CMV infection and could pave the way for novel therapeutic strategies.
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Project description:Decoding murine cytomegalovirus
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Project description:Extensive molecular and prognostic characterization of wild-type MLL infant ALL. Background: Approximately 20% of all infant ALL cases carry wild-type (or germline) MLL genes. To date, wild-type MLL infant ALL patients are generally regarded as young pediatric precursor B-ALL patients, but extensive characterization of this specific patient group largely remains unacknowledged. Methods: We here studied a relatively large cohort of 78 wild-type MLL infant ALL samples, using clinical parameters, array-comparative genomic hybridization analysis, gene expression profiling, multiplex ligation-dependent probe amplification, and conventional sequencing. Findings: Wild-type MLL infant ALL patients are generally characterized by a lower incidence of favourable prognostic factors than pediatric (non-infant) B-ALL patients, and patients at high risk of therapy failure typically display an immature pro-B immunophenotype or respond poorly to prednisone. Using gene expression profiling, we found MEIS1 expression to additionally be highly predictive for clinical outcome in wild-type MLL infant ALL with a favourable prognosis in the wild-type MLL infants with low MEIS1 expression (DFS 88%% versus 50%, p=0•01). Overall the incidence of DNA copy number variations and genetic abnormalities in genes involved in B-cell differentiation is lower in wild-type MLL infant ALL patients as compared with pediatric precursor B-ALL patients. Interpretation: Wild-type MLL infant ALL represents a highly heterogeneous patient group, which cannot be unified by one or a few known recurrent genomic aberrations. High-level MEIS1 expression and an immature pro-B immunophenotype in high-risk wild-type MLL infant ALL patients shows parallel with the unfavourable prognosis of MLL-rearranged infant ALL patients. In contrast, wild-type MLL infant ALL patients expressing lower levels of MEIS1 and displaying more differentiated (pre-B or common) phenotypes may well be more related to pediatric precursor B-ALL patients older than 1 year of age. We advocate that a treatment strategy in wild-type MLL infant ALL based on MEIS1 expression could be beneficial for improving survival. Gene expression profiling of wild-type MLL infant ALL. Additional wild-type MLL infant ALL patient samples (n=17) to the earlier samples published under GSE19475 (GSM485309 to GSM485322).
2014-10-01 | E-GEOD-58565 | biostudies-arrayexpress
Project description:The aggressive MLL-rearranged leukemias are well-known for their unique gene-expression profiles. The goal of this study was to characterize the MLL-specific DNA methylation profiles in infant acute lymphoblastic leukemia (ALL). Genome-wide DNA methylation profiling was performed on primary infant ALL samples. The majority of infant ALL samples demonstrated severe DNA hypermethylation compared with normal pediatric bone marrows, which implies that targeting of DNA methylation may be an interesting option for future therapeutic strategies in MLL-rearranged infant ALL. Using ALL cell lines carrying the MLL translocation t(4;11) (SEMK2 and RS4;11) as a model for the patient cells, we demonstrated that the hypermethylated genes are sensitive to demethylation.
2009-11-23 | GSE18400 | GEO
Project description:Comparison of gene expression profiles of human foreskin fibroblasts (HFF) infected with 3 clinical isolates of cytomegalovirus strains representing three glycoprotein B genotypes. Keywords: other
2003-07-16 | GSE501 | GEO
Project description:Extensive molecular and prognostic characterization of wild-type MLL infant ALL. Background: Approximately 20% of all infant ALL cases carry wild-type (or germline) MLL genes. To date, wild-type MLL infant ALL patients are generally regarded as young pediatric precursor B-ALL patients, but extensive characterization of this specific patient group largely remains unacknowledged. Methods: We here studied a relatively large cohort of 78 wild-type MLL infant ALL samples, using clinical parameters, array-comparative genomic hybridization analysis, gene expression profiling, multiplex ligation-dependent probe amplification, and conventional sequencing. Findings: Wild-type MLL infant ALL patients are generally characterized by a lower incidence of favourable prognostic factors than pediatric (non-infant) B-ALL patients, and patients at high risk of therapy failure typically display an immature pro-B immunophenotype or respond poorly to prednisone. Using gene expression profiling, we found MEIS1 expression to additionally be highly predictive for clinical outcome in wild-type MLL infant ALL with a favourable prognosis in the wild-type MLL infants with low MEIS1 expression (DFS 88%% versus 50%, p=0•01). Overall the incidence of DNA copy number variations and genetic abnormalities in genes involved in B-cell differentiation is lower in wild-type MLL infant ALL patients as compared with pediatric precursor B-ALL patients. Interpretation: Wild-type MLL infant ALL represents a highly heterogeneous patient group, which cannot be unified by one or a few known recurrent genomic aberrations. High-level MEIS1 expression and an immature pro-B immunophenotype in high-risk wild-type MLL infant ALL patients shows parallel with the unfavourable prognosis of MLL-rearranged infant ALL patients. In contrast, wild-type MLL infant ALL patients expressing lower levels of MEIS1 and displaying more differentiated (pre-B or common) phenotypes may well be more related to pediatric precursor B-ALL patients older than 1 year of age. We advocate that a treatment strategy in wild-type MLL infant ALL based on MEIS1 expression could be beneficial for improving survival.
2014-10-01 | GSE58565 | GEO