ArticleGut2026
iPSC-induced multilineage liver organoids, small intestinal organoids and brain organoids sustain pangenotype hepatitis E virus propagation.
Article in Gut, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
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Who cites it
10 citing papers in PubMed.
- Real-time sensing-integrated organoid-on-a-chip platforms: Technological progress and emerging biomedical applications.Bioactive materials · 2026Review
- Review
- Extra-Hepatic Manifestations of Hepatitis E Virus (HEV): A Narrative Review on Meningoencephalitis.Life (Basel, Switzerland) · 2026Review
- Liver Organoids: From Disease Modelling to Regenerative Medicine.Cell proliferation · 2026Review
- The evolution of in vitro culture systems for the study of hepatitis E virus infection.Virology · 2026Review
- Organoids: generation strategies, applications, and future challenges.Stem cell research & therapy · 2026Review
- Hepatitis E virus replication is maintained in proliferative cells within the intestinal crypt.Science advances · 2026Article
- Engineering Organoid Platforms for Pathogenesis Research.Research (Washington, D.C.) · 2026Review
- Mesenchymal stem cell-derived extracellular vesicles: emerging cell-free therapeutics for kidney diseases.Frontiers in immunology · 2026Review
- Hepatitis E virus-associated neurological injury and neurotropic cellular mechanisms.Frontiers in cellular and infection microbiology · 2026Review
Corrections and comments
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatitis E virus (HEV), the leading global cause of acute viral hepatitis, lacks robust
objectiveWe evaluated induced pluripotent stem cell (iPSC)-induced human liver, intestinal and brain organoids (hLOs, hIOs and hBOs) as platforms for HEV infection and replication.
methodsMultilineage organoids were infected with clinical HEV genotypes 1, 3 and 4. Viral tropism, host responses and antiviral efficacy were assessed.
resultsAll organoids supported the complete life cycle of HEV. hLOs exhibited infection in hepatocytes, cholangiocytes, macrophages and stellate cells, accompanied by elevated interleukin-6 levels, impaired hepatic function (reduced secretion of albumin and Factor IX) and increased levels of alanine aminotransferase and aspartate aminotransferase, indicating hepatocellular injury. hIOs demonstrated broad epithelial (enterocyte, goblet, Paneth and endocrine) and mesenchymal infection, with disrupted barrier function (loss of tight junction proteins), proinflammatory cytokines upregulation and initiation of epithelial-mesenchymal transition. hBOs showed neuronal tropism, infecting glutamatergic, dopaminergic and GABAergic neurons, as well as astrocytes and oligodendrocytes. An increased number of TH
conclusionThis study established iPSC-induced multilineage organoid infection models, confirming HEV's capacity for pan-tissue infection and revealing potential pathogenic mechanisms in the liver, intestine and nervous system. This platform provides valuable tools for HEV virology research and antiviral drug development, underscoring the unique value of organoid technology in infectious disease research.
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