SnRNAseq analysis of mouse placenta during ZIKV infection
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1122696 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29365146_1.fastq.gz | Fastqsanger.gz | |||
| SRR29365146_2.fastq.gz | Fastqsanger.gz | |||
| SRR29365147_1.fastq.gz | Fastqsanger.gz | |||
| SRR29365147_2.fastq.gz | Fastqsanger.gz | |||
| SRR29365148_1.fastq.gz | Fastqsanger.gz |
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Project description:The aim of this study was to study placental immune responses to ZIKV infection at the cell level. WT or MAVS-deficient placentas from mock- or ZIKV- infected pregnant WT or mutant mice were collected, and placentas from male fetuses selected to facilitate the identification of maternal and fetal clusters, and doublets. Two placentas from the same genotype and condition were pooled and processed for isolation of nuclei. Approximately 10,000 nuclei per sample were subjected to gel bead-in-emulsion (GEM) generation, reverse transcription, and construction of libraries for sequencing according to the protocol provided in the 3' gene expression v3.1 kit manual (10X Genomics). We obtained 98,661 nuclei with a median of 3,077 genes detected per nucleus after data processing and quality control. Seurat integrated analysis and graph-based clustering identified cell types in maternal and fetal compartments based on analysis of canonical cellular markers. We performed differential expression test using Wilcoxon test from Seurat to identify the changes in expression across conditions. The DSGs were then used to align to the Hallmark mouse pathway database Msigdbr (Version 7.5.1) with package fgsea (Version 1.26.0) and pathways that with P-adjusted value < 0.05 were chosen as the significantly enriched pathways. We found cell-type specific antiviral pathways driven by MAVS, and MAVS-independent induction of interferon-stimulated and antiviral genes in other cell types.
2024-06-11 | GSE269612 | GEO
Project description:snRNAseq analysis of mouse placenta during ZIKV infection
| PRJEB74704 | ENA
Project description:Zika virus (ZIKV) compromises the placental integrity infecting the fetus. However, the mechanisms associated with ZIKV penetration into the placenta leading to fetal infection, are unknown. Cystatin B (CSTB), the receptor for advanced glycation end products (RAGE), and tyrosine-protein kinase receptor UFO (AXL) have been implicated in inflammation. The purpose of this work iis work aims to investigate CSTB, RAGE, and AXL receptor expression in ZIKV infected placental tissues at term. The hypothesis is that in ZIKV-infected placenta, there is overexpression of CSTB and increased inflammation affecting the RAGE and AXL receptor expression. Pathological analyses of 22 placentas were performed to determine changes caused by ZIKV infection. Quantitative proteomics, immunofluorescence, and Western Blot analysis were performed to analyze proteins and pathways affected by ZIKV infection in frozen placenta. Pathological The pathological analysis confirmed decreased size of capillaries, hyperplasia of Hofbauer cells, disruption in the trophoblasts layer, and cell agglutination associated to with ZIKV infection of placental tissue. ZIKV infection was mostly localized to the trophoblast layer. There was a significant decrease in the expression of CSTB, RAGE and AXLCSTB, RAGE and AXL expression in ZIKV positive placenta. This downregulation can impair immune responses and facilitate virus penetration into the placenta. Results are consistent with our previous studies and literature of on ZIKV infection by activation ofng Inflammasome and Pyroptosis through caspase 1 upregulation and affecting the cellular structure, tissue remodeling, and cell differentiation by upregulation of tubulin beta and heat shock protein 27.
2023-03-11 | PXD037388 | Pride
Project description:To identify the various host factors involved in ZIKV infection, we compared the transcriptional profile for ZIKV-infected human first-trimester placenta trophoblast cell (HTR8) and glioblastoma astrocytoma (U251-MG). Our results demonstrated that the common IFN, inflammatory cytokine, and chemokine production were activated upon ZIKV infection of these two cell types while serval DEGs were enriched in distinct biological processes related to the characteristics of cell types. Our findings identified multiple host factors associated with ZIKV pathogenesis and potential treatment of congenital zika syndrome (CZS)
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Project description:Here we use a proteomic approach to study the role of the placenta in ZIKV-induced microcephaly and the mechanisms of ZIKV to cross the placental barrier. Samples were separated into three groups: an uninfected control group (ZIKV-CZS-), a group of placentas infected by ZIKV with normal neonates (ZIKV+CZS-), and a group of placentas infected by ZIKV that developed microcephaly in newborns (ZIKV+CZS+). Zika virus causes DNA damage and impairs gene expression and mRNA translation during infection of the placenta. Processes related to viral transcytosis, like endocytosis, autophagy and disruption of actin filament were also observed in CZS-infected placentas, which could lead to a higher virus infiltration. Unncontrolled maternal immune response as well as greater expression of cellular adhesion proteins in the decidua could lead to a disruption of tolerance during pregnancy and induction of neurological malformation of the neonates
2024-07-02 | PXD023777 | Pride
Project description:Zika virus (ZIKV), a re-emerging flavivirus is associated with devastating developmental and neurological disease outcomes particularly in infants infected in utero. Towards understanding the molecular underpinning of the unique ZIKV disease pathologies, numerous transcriptome-wide studies have been undertaken. Notably, these studies have overlooked the assimilation of RNA-seq analysis from ZIKV-infected patients with cell culture and cell model systems. We determined that ZIKV-infection in human lung adenocarcinoma A549 cells, mirrored both transcriptional and alternative splicing profiles from previously published RNA-seq data of peripheral blood mononuclear cells collected from pediatric patients during early, late acute, and convalescent phases of ZIKV infection. Our analyses show that ZIKV infection in cultured cells correlates with transcriptional changes in patients, while the overlap in alternative splicing profiles was not as extensive. Overall, our data indicate that cell culture model systems support dissection of select molecular changes detected in patients and established the foundation for future studies elucidating the biological implications of alternative splicing during ZIKV infection.
2024-08-02 | GSE265922 | GEO
Project description:Zika virus (ZIKV) has been associated with microcephaly and other brain abnormalities; however, the molecular consequences of ZIKV to human brain development are still not fully understood. Here we describe alterations in human neurospheres derived from induced pluripotent stem (iPS) cells infected with the strain of Zika virus that is circulating in Brazil. Combining proteomics and mRNA transcriptional profiling, over 500 proteins and genes associated with the Brazilian ZIKV infection were found to be differentially expressed. These genes and proteins provide an interactome map, which indicates that ZIKV controls the expression of RNA processing bodies, miRNA biogenesis and splicing factors required for self-replication. It also suggests that impairments in the molecular pathways underpinning cell cycle and neuronal differentiation are caused by ZIKV. These results point to biological mechanisms implicated in brain malformations, which are important to further the understanding of ZIKV infection and can be exploited as therapeutic potential targets to mitigate it.
2018-08-29 | PXD010866 | Pride
Project description:Zika virus (ZIKV) has been associated with microcephaly and other brain abnormalities; however, the molecular consequences of ZIKV to human brain development are still not fully understood. Here we describe alterations in human neurospheres derived from induced pluripotent stem (iPS) cells infected with the strain of Zika virus that is circulating in Brazil. Combining proteomics and mRNA transcriptional profiling, over 500 proteins and genes associated with the Brazilian ZIKV infection were found to be differentially expressed. These genes and proteins provide an interactome map, which indicates that ZIKV controls the expression of RNA processing bodies, miRNA biogenesis and splicing factors required for self-replication. It also suggests that impairments in the molecular pathways underpinning cell cycle and neuronal differentiation are caused by ZIKV. These results point to biological mechanisms implicated in brain malformations, which are important to further the understanding of ZIKV infection and can be exploited as therapeutic potential targets to mitigate it.
2018-10-27 | PXD004588 | Pride
Project description:Purpose: While type I interferons (IFN) are important for control of viral replication, we see that, upon infection of Ifnar-/- females were crossed to Ifnar+/- males with ZIKV, only Ifnar+/- fetuses are resorbed or develop severe growth restriction. To identify how IFN may be altering placenta development, we performed RNAsequencing on infected and uninfected Ifnar-/- and Ifnar+/- placentas. Methods: Ifnar-/- females were crossed to Ifnar+/- males and infected intravaginally with Cambodian ZIKV at E5.5. Placentas were harvested from infected and uninfected pregnant dams at E10.5. Results/ Conclusions: Comparison of ZIKV-infected Ifnar-/- and Ifnar+/- shows an elevated interferon stimulated gene (ISG) signature in Ifnar+/- placentas but does not reveal any underlying developmental defects that may be causing defects in placenta development.
2017-12-31 | GSE98423 | GEO
Project description:multiomic snRNAseq/snATACseq of human implantation sites, placenta and decidua
| PRJEB59732 | ENA