Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional Profile of ZIKV Infection in HTR8 cells and U251 cells

ABSTRACT: 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)

ORGANISM(S): Homo sapiens

PROVIDER: GSE234128 | GEO | 2023/06/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Proteomic profiles of ZIKV-positive placentas of fetuses with microcephaly

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

Molecular Alterations of Extracellular Matrix in the Brain of Newborns with Congenital Zika Syndrome

Project description:Zika virus (ZIKV) infection during pregnancy could cause a set of severe abnormalities in the fetus known as congenital Zika syndrome (CZS). Experiments using animal models and in vitro systems significantly contributed to our understanding of the physiopathology of ZIKV infection. However, the molecular basis of CZS is not yet studied in humans. Here, we used a systems biology approach to integrate transcriptomic, proteomic and genomic data from post-mortem brains of neonates with CZS. We observed that collagen genes were greatly reduced in CZS brains at both the RNA and protein levels and that neonates with CZS have several polymorphisms in collagen genes associated with osteogenesis imperfect and arthrogryposis. These findings were validated using immunohistochemistry and collagen staining of ZIKV infected and non-infected samples. Additionally, it was found that cell adhesion genes that are essential for neurite outgrowth and axon guidance were up-regulated and thereby confirmed the neuronal migration defects observed. This work provided new insights into the underlying mechanisms of CZS and revealed host genes associated with CZS susceptibility.

2020-05-18 | GSE125554 | GEO

RNA-seq of hiPSCs-derived NPCs from 3 pairs of dizygotic discordant twins for Congenital Zika syndrome

Project description:Congenital Zika syndrome (CZS), caused by Zika virus (ZIKV) infection, has been associated to impairment of early brain development, particularly related to neural progenitor cells (NPCs) survival and growth. In this work we report in a high-throughput manner (RNA-Seq) the differences in the transcriptomes of hiPSCs(human induced pluripotent stem cells)-derived NPCs from 3 pairs of discordant twins for Congenital Zika syndrome (CZS). We found significant differences in the expression levels of genes relevant to the regulation of neural development between the NPCs from CZS-affected and non-affected twins, suggesting that epigenetic differences may contribute to the different susceptibilities of NPCs to ZIKV infection.

2018-02-27 | GSE102128 | GEO

ZIKV infection differentially affects the transcriptional profiles in HTR8 and U251 cells.

Project description:The mechanism by which Zika virus (ZIKV) causes severe birth defects in pregnant women remains unclear. Cell tropisms in placenta and brain play a crucial role in ZIKV pathogenesis, leading to congenital Zika syndrome (CZS). To identify the host factors involved in ZIKV infection, we compared the transcriptional profiles of ZIKV-infected human first-trimester placental trophoblast cells HTR8/SVneo and a human glioblastoma astrocytoma cell line U251. Our results demonstrated that ZIKV exhibited lower rates of mRNA replication and protein expression in HTR8 than in U251 cells, while showing a higher release of infectious viral particles. However, a greater number of differentially expressed genes (DEGs) were found in ZIKV-infected U251 cells than in ZIKV-infected HTR8 cells. Several of these DEGs were enriched in distinct biological processes related to the characteristics of each cell type that may contribute to foetal damage. Both cell types exhibited activation of common interferons, inflammatory cytokines, and chemokine production upon ZIKV infection. Moreover, the neutralization of tumour necrosis factor-alpha (TNF-α) promoted ZIKV infection in both trophoblasts and glioblastoma astrocytoma cells. Overall, we identified multiple DEGs associated with ZIKV pathogenesis.

| S-EPMC10410584 | biostudies-literature

Molecular Signatures Associated with ZIKV Exposure in Human Cortical Neural Progenitors and Astrocytes

Project description:Zika virus (ZIKV) infection causes microcephaly and has been linked to other brain abnormalities. How ZIKV impairs brain development and function remains elusive. Here we systematically profiled transcriptomes of human neural progenitor cells (hNPCs) and astrocytes exposed to Asian ZIKVC, African ZIKVM, and Dengue virus (DENV). DENV causes distinct gene expression changes; and ZIKV has a broader impact on the expression of gene involved in DNA replication and repair. While overall expression profiles are similar, ZIKVC, but not ZIKVM, induces upregulation of viral response genes. Upon ZIKV infection, astrocytes exhibit more prominent transcriptome changes than hNPCs, particularly enriching genes related to inflammatory response and cytokine production pathways. Our analyses reveal cell-type- and strain-specific molecular signatures associated with ZIKV infection, and identify astrocytes as a major direct target of ZIKV. Further investigation of ZIKV-host interactions based our transcriptomic datasets may help to illuminate neural virulence determinants of ZIKV in patients. Gene Expression Analyses of the cells infected with different flaviviruses

2016-08-23 | E-GEOD-80434 | biostudies-arrayexpress

Determination of system level alterations in host transcriptome due to Zika virus (ZIKV) infection in retinal pigment epithelium

Project description:Zika Virus (ZIKV) induces ocular complications in infants born from ZIKV infected mothers during pregnancy. We previously reported that ZIKV is permeable to cells lining the blood-retinal barrier. In this study, we measure the alteration of host transcriptome by ZIKV using primary retinal pigmented epithelial (RPE) cells.

2022-03-18 | GSE169066 | GEO

RNASeq of African green monkey (Vero) cells and human malignant glioblastoma multiforme (U251) cells infected at a multiplicity of infection (MOI) of 3 with the Asian/American Zika virus (ZIKV), PE243; and the African ZIKV strain, Dak84

Project description:Vero and U251 cells were infected with the Asian/American ZIKV (PE243) and the African ZIKV (Dak84) at MOI:3 to assess the viral transcriptome in two cell lines. Samples were harvested at 24 hours post-infection (h p.i.) by flash-freezing, without cycloheximide pre-treatment. Ribosomal RNA was removed using Illumina's RiboZero kit, and RNA was hydrolysed and then gel purified to select fragments 25-35nt long. Fragments were cloned into adapters using the TruSeq small RNA adapter kit and sequenced on Illumina NextSeq.

2024-09-04 | E-MTAB-12967 | biostudies-arrayexpress

RiboSeq of African green monkey (Vero) cells and human malignant glioblastoma multiforme (U251) cells infected at a multiplicity of infection (MOI) of 3 with the Asian/American Zika virus (ZIKV), PE243; and the African ZIKV strain, Dak84

Project description:Vero and U251 cells were infected with the Asian/American ZIKV (PE243) and the African ZIKV (Dak84) at MOI:3 to assess the viral transcriptome in two cell lines. Samples were harvested at 24 hours post-infection (h p.i.) by flash-freezing, without cycloheximide pre-treatment. RNase I treatment was carried out, following which ribosomes and enclosed RNA were isolated by centrifugation through a sucrose cushion. RNA was extracted, ribosomal RNA was removed using Illumina's RiboZero kit, and remaining RNA was gel purified to select fragments 25-35nt long. Fragments were cloned into adapters using the TruSeq small RNA adapter kit and sequenced on Illumina NextSeq.

2024-09-04 | E-MTAB-12970 | biostudies-arrayexpress

ZIKV prevents host mRNA export from the nucleus by disrupting UPF1 function

Project description:Zika virus (ZIKV) is a mosquito-borne virus that can have dramatic neurodevelopmental consequences when infection occurs in utero. Previous studies demonstrated that ZIKV downregulates the master regulator of nonsense mediated decay, UPF1. To examine whether this process contributes to disruption of neural development, we investigated the effect of ZIKV infection on UPF1 interaction with host RNA in neural progenitor cells. Here, we show that ZIKV-mediated disruption of UPF1 function in neural progenitor cells causes retention of mRNA in the nucleus, resulting in decreased protein levels of specific transcripts involved in neural differentiation.

2022-12-22 | GSE160201 | GEO

Molecular Signatures Associated with ZIKV Exposure in Human Cortical Neural Progenitors

Project description:Zika virus (ZIKV) infection causes microcephaly and has been linked to other brain abnormalities. How ZIKV impairs brain development and function remains elusive. Here we systematically profiled transcriptomes of human neural progenitor cells (hNPCs) exposed to Asian ZIKVC, African ZIKVM, and Dengue virus (DENV). DENV causes distinct gene expression changes; and ZIKV has a broader impact on the expression of gene involved in DNA replication and repair. While overall expression profiles are similar, ZIKVC, but not ZIKVM, induces upregulation of viral response genes. Our analyses reveal virus- and strain-specific molecular signatures associated with ZIKV infection. Further investigation of ZIKV-host interactions based our transcriptomic datasets may help to illuminate neural virulence determinants of ZIKV in patients.

2016-08-23 | GSE80434 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data