ArticleProceedings of the National Academy of Sciences of the United States of America2017
A paradox of transcriptional and functional innate interferon responses of human intestinal enteroids to enteric virus infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.
- Pooled it
- Culture-specific transcriptional drifts limit the fidelity of organoid infection models.PLoS pathogens · 2026Article
- Progress in human intestinal organoid research: applications to acute gastroenteritis viruses.Stem cell research & therapy · 2026Review
- Porcine Rotavirus NSP4 Inhibits Type I Interferon Production via NRBF2-Mediated Autophagic Degradation of MDA-5.Transboundary and emerging diseases · 2026Article
- Hypoxia increases susceptibility of human intestinal epithelial cells to rotavirus infection through repression of interferon induction.Gut microbes · 2025Article
- Innate immune sensing of rotavirus by intestinal epithelial cells leads to diarrhea.Cell host & microbe · 2025Article
- Loss of mucin 2 and MHC II molecules causes rare resistance to murine RV infection.Journal of virology · 2025Article
- In Vitro Culture of Human Norovirus in the Last 20 Years.Biomedicines · 2024Review
- Article
- Human norovirus cultivation systems and their use in antiviral research.Journal of virology · 2024Review
- Regulation of host/pathogen interactions in the gastrointestinal tract by type I and III interferons.Current opinion in immunology · 2024Review
- The application of organoids in colorectal diseases.Frontiers in pharmacology · 2024Review
- Pathoimmunological analyses of fatal E11 infection in premature infants.Frontiers in cellular and infection microbiology · 2024Article
- Rotavirus-mediated DGAT1 degradation: A pathophysiological mechanism of viral-induced malabsorptive diarrhea.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Infection of porcine enteroids and 2D differentiated intestinal epithelial cells with rotavirus A to study cell tropism and polarized immune response.Emerging microbes & infections · 2023Article
- Standardization of an antiviral pipeline for human norovirus in human intestinal enteroids demonstrates nitazoxanide has no to weak antiviral activity.Antimicrobial agents and chemotherapy · 2023Article
- Human intestinal organoids as models to study enteric bacteria and viruses.Current opinion in microbiology · 2023Review
- A Standardized Antiviral Pipeline for Human Norovirus in Human Intestinal Enteroids Demonstrates No Antiviral Activity of Nitazoxanide.bioRxiv : the preprint server for biology · 2023Article
- Risk factors and early markers for echovirus type 11 associated haemorrhage-hepatitis syndrome in neonates, a retrospective cohort study.Frontiers in pediatrics · 2023Article
- A Novel Airway-Organoid Model Based on a Nano-Self-Assembling Peptide: Construction and Application in Adenovirus Infection Studies.International journal of nanomedicine · 2023Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
The intestinal epithelium can limit enteric pathogens by producing antiviral cytokines, such as IFNs. Type I IFN (IFN-α/β) and type III IFN (IFN-λ) function at the epithelial level, and their respective efficacies depend on the specific pathogen and site of infection. However, the roles of type I and type III IFN in restricting human enteric viruses are poorly characterized as a result of the difficulties in cultivating these viruses in vitro and directly obtaining control and infected small intestinal human tissue. We infected nontransformed human intestinal enteroid cultures from multiple individuals with human rotavirus (HRV) and assessed the host epithelial response by using RNA-sequencing and functional assays. The dominant transcriptional pathway induced by HRV infection is a type III IFN-regulated response. Early after HRV infection, low levels of type III IFN protein activate IFN-stimulated genes. However, this endogenous response does not restrict HRV replication because replication-competent HRV antagonizes the type III IFN response at pre- and posttranscriptional levels. In contrast, exogenous IFN treatment restricts HRV replication, with type I IFN being more potent than type III IFN, suggesting that extraepithelial sources of type I IFN may be the critical IFN for limiting enteric virus replication in the human intestine.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.