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© Liliana Mancio, Institut Pasteur
Primary human hepatocytes co-cultured with parenchymal cells at 6 days post-seeding. The expression of human CD81 is depicted in pink
Publication : Stem cell reports

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.

Team: Plasmodium Infection and Transmission
Team: Biology of Host-parasite Interactions
Member: Liliana Mancio Silva
Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Stem cell reports - 25 Aug 2022

Scoon WA, Mancio-Silva L, Suder EL, Villacorta-Martin C, Lindstrom-Vautrin J, Bernbaum JG, Mazur S, Johnson RF, Olejnik J, Flores EY, Mithal A, Wang F, Hume AJ, Kaserman JE, March-Riera S, Wilson AA, Bhatia SN, Mühlberger E, Mostoslavsky G,

Link to Pubmed [PMID] – 36084636

Link to DOI – S2213-6711(22)00412-X10.1016/j.stemcr.2022.08.003

Stem Cell Reports 2022 Aug; ():

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.