Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA347344 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4381390.fastq.gz | Fastqsanger.gz | |||
| SRR4381391.fastq.gz | Fastqsanger.gz | |||
| SRR4381392.fastq.gz | Fastqsanger.gz | |||
| SRR4381393.fastq.gz | Fastqsanger.gz | |||
| SRR4381394.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 13 |
Similar Datasets
Project description:Zika virus (ZIKV), a flavivirus transmitted primarily by Aedes mosquitoes, has spread to 59 countries and territories throughout the world. ZIKV-infected patients can have several symptoms and there is scientific consensus that ZIKV is a cause of microcephaly. Most studies are focusing on the central nervous system (CNS), and it is largely unknown whether ZIKV also affects the developing peripheral nervous system. Here, using a human pluripotent stem cell-based model, we demonstrated that Puerto Rican ZIKV strain, PRVABC59, efficiently infects human neural crest cells (hNCCs). In contrast to little infection of CNS neurons, ZIKV readily infects human peripheral neurons (hPNs), leading to cell death. Global gene expression analyses of infected hNCCs and hPNs reveal transcriptional dysregulation, notably of cell-death- and cell-cycle-related pathways. Our results identify hNCCs and hPNs as a direct ZIKV target and provide a framework to investigate the ZIKV pathology on the peripheral neurons.
2017-07-07 | GSE87750 | GEO
Project description:Growing evidences have associated Zika virus infection with congenital malformations, including microcephaly. Nonetheless, signaling mechanisms that promote the disease outcome are far from being understood, affecting the development of suitable therapeutics. In this study, we applied shotgun mass spectrometry-based proteomics combined with cell biology approaches to characterize altered molecular pathways on neurons and NPCs infected by ZIKV-BR, strain obtained from the 2015 Brazilian outbreak. Assessment of neurons differentiated from iPSC from different donors shows the importance of the host genetic background to the susceptibility of ZIKV infection, also confirmed by cytokine fingerprinting. Additionally, infected cells presented an impairment of neurogenesis and synaptogenesis processes. Moreover, ZIKV-BR infected NPCs showed unique alteration of pathways involved in neurological diseases, cell death and survival and embryonic development compared to ZIKV-AF, showing a human adaptation of the Brazilian viral strain. Taken together, these data explain CNS developmental arrest observed in Congenital Zika Virus syndrome is beyond neuronal cell death.
2019-11-12 | PXD009293 | Pride
Project description:The suspected link between infection by Zika virus (ZIKV), a re-emerging flavivirus, and microcephaly, is an urgent global health concern. The direct target cells of ZIKV in developing human fetuses are not clear. Here we show that ZIKV serially passaged in monkey and mosquito cell lines infects human induced pluripotent stem cells (hiPSCs)-derived cortical neural progenitor cells (hNPCs) with much higher efficiency compared to hiPSCs and hNPC-derived immature cortical neurons. Infected hNPCs produces infectious ZIKV particles. Importantly, ZIKV infection increases cell death and dysregulates cell cycle progression, resulted in attenuated hNPC growth. RNA-sequencing analysis of infected hNPCs further reveals transcriptional dysregulation, notably genes in cell cycle pathways. Our results identify human cortical neural precursors as a major and direct target of ZIKV infection and establish a tractable experimental model system to investigate the impact and mechanism of ZIKV on human brain development and a platform to screen therapeutic compounds.
2016-03-04 | GSE78711 | GEO
Project description:Analysis of death triggering pathways activated by experimental Zika virus infection in SH-SY5Y cells by expression profiling of 42 genes related to survival, anti-apoptotic and proapoptotic responses, and death receptors pathway, and 06 endogenous control genes. Commercially available neuroblastoma SH-SY5Y cells were grown in vitro, experimentally infected with Zika virus (MOI 0.5), and MOCK- and ZIKV-infected cells were harvested at 1 and 2 days post-infection. We used TaqMan ™ Array Human Apoptosis via Death Receptors (Thermo Fisher Scientific, MA, USA) to quantitate gene expression during ZIKV infection in SH-SY5Y cells.
2021-12-01 | GSE162096 | GEO
Project description:We report the Zika Virus E protein causes alterations in human fetal neural stem cells by dysregulation miRNome of fNSCs. We screened four ZV proteins (three non-structural and the E protein) and demonstrated that ZV E protein induces quiescence in human fNSCs and hampers growth of neurospheres. Further employing small RNA NGS we investigate that Zika Virus E protein causes differential expression of 25 miRNAs 24 hours post ectopic expression. Bioinformatic analysis using GO annotation for the targets of differentially expressed miRNAs revealed that upregulated miRNAs are involved in biological processes, including metabolic processes whereas downregulated miRNAs regulate cell cycle and its processes along with metabolic processes. This supports our findings that E protein alters cell cycle dynamics. Our study provides evidence and mechanisms of involvement of ZV E protein and potential miRNAs in Zika Virus induced microcephaly.
2018-12-26 | GSE108791 | GEO
Project description:To search for host factors regulating Zika virus infection, we performed a genome-wide loss-of-function CRISPR/Cas9 screen in haploid human ESCs. The regulators were identified by the quantification of enrichment of their mutant clones within a pooled loss-of-function library upon Zika virus infection.
2023-05-31 | E-MTAB-11945 | biostudies-arrayexpress
Project description:We studied the impact of ZIKA virus infection on DNA methylation in whole organoids, organoid derived astrocytes, neurons neural progeniotors and hESC or iPSC derived astrocytes, neurons, neural progenotor cells
2018-01-12 | GSE109104 | GEO
Project description:Transcriptional profiling of human astrocyte cells (SVG) infected with Zika virus. Goal was to identify temporal changes in gene expression post infected by Zika virus.
2017-10-13 | GSE89915 | GEO
Project description:Patients with recent pandemic of Coronavirus Disease-19 (COVID-19) complains of neurological symptoms unlike typical coronavirus infections. However, the absence of studies utilizing proper models of human peripheral nerve is hampering an understanding of COVID-19 pathogenesis. We, here, employed human embryonic stem cell derived peripheral neurons to validate change in transcriptome in human peripheral neurons. Transcriptome analysis of infected peripheral neurons indicates that chemosensory abnormalities in olfaction and gustation are associated with dysfunction and death of peripheral neurons.
2021-03-01 | GSE161281 | GEO
Project description:To determine the effect of Zika virus infection on pre-implantation embryonic development, we performed single blastocyst RNA-Seq on MOCK and ZIKV infected embryos. ZIKV infection results in an increased risk of spontaneous abortion and poor intrauterine growth although the mechanisms underlying fetal loss remain undetermined. Little is known about the impact of ZIKV infection during the earliest stages of pregnancy, or pre- and peri-implantation, because most current studies of ZIKV infection in pregnancy models focus on post-implantation stages. Here, we demonstrate that trophectoderm cells of pre-implantation human and mouse embryos can be efficiently infected with ZIKV, and that trophectoderm can propagate virus causing cell death of neural progenitors. These findings were corroborated by our demonstration that hESC-derived trophectoderm cells are infected by ZIKV in a dose dependent manner. RNAseq of single blastocysts revealed key transcriptional changes in cellular and physiologic functions upon ZIKV infection, including nervous system development and function, prior to commitment to the neural cell lineage. Finally, the pregnancy rate of mice infected pre-implantation was > 50% lower than females infected at E4.5. These results demonstrate that pre-implantation ZIKV infection of trophectoderm leads to miscarriage or spontaneous abortion. Moreover, pre- and peri-implantation ZIKV infects trophectoderm cells that propagate virus over time causing cell death in neural progenitors. Cumulatively, these data demonstrate that vertical pre- and peri-implantation ZIKV infection of trophectoderm impairs fetal development and causes neural progenitor cell death, elucidating a previously unappreciated association of pre- and peri-implantation ZIKV infection and microcephaly.
2019-08-16 | GSE133254 | GEO