Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1306354 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To further understand the molecular pathogenesis of Enterovirus 71 infection, we profiled cellular microRNAs of brain tissue from suckling Kunming mice infected with EV71 and uninfected mice as comparison.
2016-10-23 | GSE89070 | GEO
Project description:Background: Zika virus (ZIKV) is a neurotropic flavivirus. The outbreak of ZIKV in 2016 created a global health emergency. However, the underlying pathogenic mechanisms remain elusive. Methods: We investigated the host response features of in vivo replication in a mouse model of ZIKV infection, by performing a series of transcriptomic and bioinformatic analyses of ZIKV and mock-infected brain tissue. Results: Tissue damage, inflammatory cells infiltration and high viral replication were observed in the brain tissue of ZIKV infected mice. RNA-Seq of the brain indicated the activation of ferroptosis pathways. Enrichment analysis of ferroptosis regulators revealed their involvement in pathways such as mineral absorption, fatty acid biosynthesis, fatty acid degradation, PPAR signaling pathway, peroxidase and adipokinesine signalling pathway. We then identified 12 interacted hub ferroptosis regulators (CYBB, HMOX1, CP, SAT1, TF, SLC39A14, FTL, LPCAT3, FTH1, SLC3A2, TP53 and SLC40A1) that were related to the differential expression of CD8+ T cells, microglia and monocytes. CYBB, HMOX1, SALT and SLAC40A1 were selected as potential biomarkers of ZIKV infection. Finally, we validated our results using RT-qPCR and outside available datasets. Conclusions: For the first time, we proposed a possible mechanism of ferroptosis in brain tissue infected by ZIKV in mice and identified the four key ferroptosis regulators.
2022-12-06 | GSE213898 | GEO
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
Project description:Administration of recombinant interferons to 3D brain organoid cultures infected with ZIKV identifies IFN-beta as compound that alleviates organoid damage and inhibits ZIKV
2021-04-09 | GSE123816 | GEO
Project description:In this work, we demonstrate that neonatal mice infected with ZIKV via intracranial injection suffers from transient olfactory dysfunction when they grow up to puberty. Moreover, ZIKV exhibits broad cellular tropism and mainly targets the olfactory ensheathing cells (OECs) in the olfactory mucosa (OM) of mice. To decipher the underlying mechanism of the observed olfactory dysfunction in ZIKV infected mice at the molecular level, RNA-Seq analyses of the OM and OB samples from ZIKV infected mice were performed in comparison with that from the control animals.
2022-10-03 | GSE214567 | GEO
Project description:Zika virus (ZIKV) is a member of the Flaviviridae family, transmitted by Aedes mosquitoes. ZIKV can be transmitted from pregnant woman to fetus and causes microcephaly and neuronal defects. Patients infected with ZIKV showed increased levels of proinflammatory cytokines compared to healthy individuals and neurological changes even after recovery. However, the detailed mechanism of how neuronal defects occurs after recovery from ZIKV infection has never been investigated in vivo. Here, we found that viral RNA loads were highest in mouse brain tissue 7 days after ZIKV infection and were equivalent to uninfected controls after 21 days, suggesting that mice recovered after 21 days of ZIKV infection. To explore the pathological mechanisms of neuronal defects after recovery from ZIKV infection, we performed RNA-sequencing in mouse cerebral cortex obtained 7 days and 21 days after ZIKV infection.
2024-05-20 | GSE265861 | GEO
Project description:Zika virus (ZIKV) infects fetal and adult human brains, and is associated with serious neurological complications including microcephaly and Guillain-Barré Syndrome (GBS). To date, no prophylactic or therapeutic treatment is available to prevent or treat ZIKV infection. Here, we performed a high content chemical screen using a library containing FDA-approved drugs or drug candidates. Two compounds, hippeastrine hydrobromide (HH) and amodiaquine dihydrochloride dihydrate (AQ), were discovered to inhibit ZIKV infection in human cortical neuron progenitor cells (hNPCs). HH was further validated to inhibit ZIKV infection and to rescue ZIKV-induced growth and differentiation defects in hNPCs and human fetal-like forebrain organoids. Finally, HH and AQ suppressed ZIKV infection in adult mouse brain in vivo. Strikingly, HH and AQ fully rescued the severe limb paralysis syndrome developed in ZIKV infected adult mice. This study identifies drug candidates for treatment of ZIKV infection and ZIKV-related neurological complications in fetal and adult patients.
2017-07-06 | GSE89334 | GEO
Project description:ZIKV-infection during pregnancy can cause microcephaly in newborns, yet the underlying mechanisms remain largely unexplored. Here, we reveal extensive and large-scale metabolic reprogramming events in ZIKV-infected mouse brains. We perform a multi-omics study comprising transcriptomics, proteomics, phosphoproteomics, and metabolomics approaches on the brains from ZIKV-infected mice. Our proteomics and metabolomics analyses uncover dramatic alteration of nicotinamide adenine dinucleotide (NAD+)-related metabolic pathways, including oxidative phosphorylation, TCA cycle, and tryptophan metabolism. Phosphoproteomics analysis indicates that MAPK and cGMP-PKG signalling may be associated with ZIKV-induced microcephaly. Importantly, we demonstrate the utility of our rich multi-omics datasets with follow-up in vivo experiments which confirm that boosting NAD+ by NAD+ or NR supplementation alleviates cell death and increases cortex thickness in ZIKV-infected mouse brains. NR supplementation increases the brain and body weight as well as improves the survival in ZIKV-infected mice. Our study provides a comprehensive resource of biological data to support future investigations of ZIKV-induced microcephaly, and demonstrates that metabolic alterations can be potentially exploited for developing therapeutic strategies.
2021-06-18 | PXD026814 |