The effect of ZIKV and MBD-mutant ZIKVs infection on neonatal mouse brains
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ABSTRACT:
PROVIDER: PRJNA1287545 | ENA |
REPOSITORIES: ENA
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Project description:To compare the impact of WT and MBD ZIKVs on the developing brain at the molecular level, we carried out global tanscriptome analyses (RNA-seq) on one-day-old neonatal mouse brains infected with Mock, WT or MBD2 ZIKV at 3 days post-infection.
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Project description:Purpose: The goals of this study are to understand ZIKV induced immune responses in the developing brain at genome-wide level. Methods: Total RNA was isolated from E17.5 mouse brains after viral infection at E14.5. After genomic DNA and ribosomal RNA removal, fractionated RNA were subjected to strand-specific library preparation using NEBNext Ultra RNA Library Prep Kit. Sequencing was performed on Nextseq500 (Illumina). The sequencing reads that passed quality filters were analyzed with TopHat followed by Cufflinks. Results: After performed Gene Ontology analyses with RNA-seq data, our results revealed a set of genes that are associated with the immune response and apoptosis pathways. Gene Set Enrichment Analysis (GSEA) further show significant enrichments on both the immune system response and apoptosis pathways. Some of these results were also verified with qRT-PCR. Conclusions: Our results suggest that ZIKV infection triggers an aggressive immune response, which has the potential to cause exacerbation of brain damage by enhancing neuronal death and generating vascular abnormalities. Our discovery of massive neuronal death, leaky blood-brain-barrier (BBB), and astrogliosis in ZIKV infected brains is the first study to suggest that ZIKA causes extensive brain damage.
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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.
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Project description:Zika virus (ZIKV) is an emerging arbovirus of the Flaviviridae family. Although infection with ZIKV generally leads to mild disease, its recent emergence in the Americas has been associated with an increase in the development of the Guillain-Barre syndrome in adults, as well as with neurological complications, in particular congenital microcephaly, in new-borns. To date, little information is available on neuroinflammation induced by ZIKV, notably in microglial cells in the context of their metabolic activity, a series of chemical transformations that are essential for their growth, reproduction, structural maintenance and environmental responses. Therefore, in the present study we investigated the metabolomic profile of ZIKV-infected microglia. Microglial cells were exposed to ZIKV at different time points and were analyzed by a Liquid Chromatography-High Resolution mass spectrometry-based metabolomic approach.
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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.
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