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Human cytomegalovirus dysregulates neurodevelopmental pathways in cerebral organoids

ABSTRACT: This study investigated the viral mechanisms of fetal neural malformation using in vitro human cerebral organoids to model congenital CMV infection

ORGANISM(S): Homo sapiens

PROVIDER: GSE217832 | GEO | 2024/03/27

REPOSITORIES: GEO

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Human cytomegalovirus (CMV) dysregulates neurodevelopmental pathways in cerebral organoids

Project description: Not available

| S-EPMC10951402 | biostudies-literature

Human cytomegalovirus dysregulates neurodevelopmental pathways in cerebral organoids

Project description:Human cytomegalovirus dysregulates neurodevelopmental pathways in cerebral organoids

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Downregulation of Neurodevelopmental Gene Expression in iPSC-Derived Cerebral Organoids Upon Infection by Human Cytomegalovirus

Project description:We report the application of bulk RNA sequencing on cerebral organoids infected with HCMV TB40eGFP virus or uninfected, within the infected groups the organoids were sorted into 3 distinct populations prior to sequencing based on GFP expression as a proxy for level of infection. These populations have been denoted GFP (+), GFP Inter, GFP (-), for each sorted population 3 organoids of the same line and from the same differentiation were combined to ensure sufficient cell numbers for bulk sequencing analysis.

2022-03-01 | GSE193759 | GEO

Downregulation of neurodevelopmental gene expression in iPSC-derived cerebral organoids upon infection by human cytomegalovirus.

Project description:Human cytomegalovirus (HCMV) is a betaherpesvirus that can cause severe birth defects including vision and hearing loss, microcephaly, and seizures. Currently, no approved treatment options exist for in utero infections. Here, we aimed to determine the impact of HCMV infection on the transcriptome of developing neurons in an organoid model system. Cell populations isolated from organoids based on a marker for infection and transcriptomes were defined. We uncovered downregulation in key cortical, neurodevelopmental, and functional gene pathways which occurred regardless of the degree of infection. To test the contributions of specific HCMV immediate early proteins known to disrupt neural differentiation, we infected NPCs using a recombinant virus harboring a destabilization domain. Despite suppressing their expression, HCMV-mediated transcriptional downregulation still occurred. Together, our studies have revealed that HCMV infection causes a profound downregulation of neurodevelopmental genes and suggest a role for other viral factors in this process.

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Histone Modification in Cerebral Arteriovenous Malformation

Project description:Histone Modification in Cerebral Arteriovenous Malformation

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Human Otic progenitor cell models of congenital hearing loss applied to to Zika virus and cytomegalovirus infections

Project description:Congenital hearing loss is a common chronic condition affecting children in both developed and developing nations. In many cases, congenital hearing loss is ultimately attributed to viral infection, most often by cytomegalovirus (CMV), but also in Congenital Zika Syndrome (CZS). The mechanisms by which CMV and ZIKV virus cause these cranial developmental defects have not been elucidated. Inner ear development has been particularly difficult to study, given the inaccessibility and scarcity of the tissue in animal models or on human autopsy; however, it is now possible to culture stem-cell derived otic progenitor cells (OPCs). Here we describe successful in-vitro infection of OPCs with either CMV or ZIKV. We find that ZIKV infection rapidly and strongly induces the expression of type I IFN and inflammatory genes, while simultaneously decreasing otic cell viability in culture that is at least in part attributable to apoptosis. In contrast, CMV infection did not appear to elicit either of these effects and instead demonstrated a clear dysregulation of the expression of many key genes and pathways associated with inner ear development and function, including Cochlin, NGFR, SOX11 and TGF-β signaling. These findings suggest that ZIKV and CMV infections cause congenital hearing loss through very different pathways; that is, by killing progenitor cells in the case of ZIKV infection, and via disruption of critical developmental pathways in the case of CMV infection. In addition to demonstrating differential hCMV and ZIKV pathogenesis mechanisms in OPCs, this study highlights the advantages of otic progenitor cell models for the study of congenital hearing loss induced by viral infection.

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Project description:Pluripotent stem cells (PSC) can differentiate inot any cell type of an organism. Their remarkable capability of self-organization enables the formation of three-dimensional structures that resembles miniature organs, including cerebral organoids. These organoids can recreate early steps of the human cerebral cortex development, and show great potential for modeling human diseases, particularly for those with a developmental component. This data evidences stem cell-derived cerebral organoids as a key model to study brain development and neurodevelopmental, neurodegenerative and neuropsychiatric diseases.

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Project description:Single cell ATAC-seq (scATAC-seq) was performed on bonobo induced pluripotent stem cells (iPSC) derived cerebral organoids. scATAC-seq was performed on day 60 (2 months old cerebral organoid) and day 120 (4 months old cerebral organoid).

2019-10-16 | E-MTAB-8083 | biostudies-arrayexpress

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Project description:Single cell ATAC-seq (scATAC-seq) was performed at various stages of differentiation of human pluripotent stem cells to 4 month old cerebral organoids. scATAC-seq was performed on the following days of differentiation: day 0 (pluripotent stem cell), day 4 (embryoid body), day 10 (neuroectoderm), day 15 (neuroepithelium), day 30 (1 month old cerebral organoid), day 60 (2 months old cerebral organoid), and day 120 (4 months old cerebral organoid).

2019-10-16 | E-MTAB-8089 | biostudies-arrayexpress

Bulk ATAC-seq of primate cerebral organoids

Project description:Bulk ATAC-seq was performed on human, chimpanzee, bonobo, and macaque stem cell-derived cerebral organoids. ATAC-seq was performed on day 60 (2 months old) and day 120 (4 months old) cerebral organoids.

2019-10-16 | E-MTAB-8228 | biostudies-arrayexpress

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