ArticleStem cell reports2022
Ebola virus infection induces a delayed type I IFN response in bystander cells and the shutdown of key liver genes in human iPSC-derived hepatocytes.
Article in Stem cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Temporal transcriptomics identifies early-response and infection-condition-specific modules guiding host-directed anti-EBOV therapeutics.Microbiology spectrum · 2026Article
- How new approach methods are reshaping virology research.Journal of virology · 2026Review
- Potential Mechanisms Underlying Bleeding During Infection With Hemorrhagic Fever Viruses.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Filovirus infection disrupts epithelial barrier function and ion transport in human iPSC-derived gut organoids.PLoS pathogens · 2025Article
- Gene expression analysis identifies hub genes and pathways distinguishing fatal from survivor outcomes of Ebola virus disease.FASEB bioAdvances · 2024Article
- Mapping of susceptibility loci for Ebola virus pathogenesis in mice.Cell reports · 2024Article
- Induced pluripotent stem cells (iPSCs): molecular mechanisms of induction and applications.Signal transduction and targeted therapy · 2024Review
- Cheminformatics-Based Study Identifies Potential Ebola VP40 Inhibitors.International journal of molecular sciences · 2023Article
- Review
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19 authors.
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Abstract
Liver damage and an exacerbated inflammatory response are hallmarks of Ebola virus (EBOV) infection. Little is known about the intrinsic response to infection in human hepatocytes and their contribution to inflammation. Here, we present an induced pluripotent stem cell (iPSC)-derived hepatocyte-like cell (HLC) platform to define the hepato-intrinsic response to EBOV infection. We used this platform to show robust EBOV infection, with characteristic ultrastructural changes and evidence for viral replication. Transcriptomics analysis revealed a delayed response with minimal early transcriptomic changes, followed by a general downregulation of hepatic function and upregulation of interferon signaling, providing a potential mechanism by which hepatocytes participate in disease severity and liver damage. Using RNA-fluorescence in situ hybridization (FISH), we showed that IFNB1 and CXCL10 were mainly expressed in non-infected bystander cells. We did not observe an inflammatory signature during infection. In conclusion, iPSC-HLCs are an immune competent platform to study responses to EBOV infection.
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