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Filovirus Infection Disrupts Epithelial Barrier Function and Ion Transport in Human iPSC-Derived Gut Organoids

GSE298600 Homo sapiens Expression profiling by high throughput sequencing 9 samples Submitted 2025/11/10 Platform GPL30173
Summary
Gastrointestinal (GI) dysfunction, characterized by severe diarrhea and dehydration, is a central contributor to morbidity and mortality in filovirus disease in patients, yet the role of the epithelium in this clinical outcome remains poorly defined. Here, we employ induced pluripotent stem cell (iPSC)-derived human intestinal (HIOs) and colonic organoids (HCOs) to model Ebola virus (EBOV) and Marburg virus (MARV) infection. These organoids are permissive to filovirus infection and support viral replication. Bulk RNA sequencing revealed distinct intestinal and colonic epithelial responses, including apical and junctional disruption and a delayed virus-specific induction of interferon-stimulated genes. Moreover, infection impaired adenylate cyclase signaling and CFTR-mediated ion transport, providing mechanistic insight into virus- induced secretory diarrhea. This platform recapitulates key features of human GI pathology in filoviral disease and serves as a powerful system to dissect host-pathogen interactions and identify therapeutic targets.
Published in
Filovirus infection disrupts epithelial barrier function and ion transport in human iPSC-derived gut organoids
Flores EY, Hume AJ, Olejnik J et al. · PLoS pathogens 2025 · PMID 41284734 · doi:10.1371/journal.ppat.1013698
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Also filed as BioProject PRJNA1270006 and SRA study SRP588878. Searching any of these in the dataset finder brings you back here.

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