ArticleJournal of virology2022
Type III and Not Type I Interferons Efficiently Prevent the Spread of Rotavirus in Human Intestinal Epithelial Cells.
Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Intestinal Organoids as Models to Study Viruses: Current Application and Future Perspective.Journal of microbiology and biotechnology · 2026Review
- Subtype-specific functions of basal IFNλs.Journal of virology · 2026Review
- Rotavirus mucosal immunology: insights and research priorities from an international convening in Liverpool, March 2024.NPJ vaccines · 2026Article
- Basal IFNλ2/3 signaling is required for ISG expression and viral control in human intestinal epithelial cells.PLoS pathogens · 2026Article
- Interplay between flaviviruses and the interferon response: mechanisms of immune evasion and therapeutic implications.Frontiers in pharmacology · 2026Review
- Hypoxia increases susceptibility of human intestinal epithelial cells to rotavirus infection through repression of interferon induction.Gut microbes · 2025Article
- Basal IFN-λ2/3 expression mediates tight junction formation in human epithelial cells.The EMBO journal · 2025Article
- Article
- Recent insights and advances in gut microbiota's influence on host antiviral immunity.Frontiers in microbiology · 2025Review
- Integrating network pharmacology with pharmacological research to elucidate the mechanism of modified Gegen Qinlian Decoction in treating porcine epidemic diarrhea.Scientific reports · 2024Article
- Meeting the Challenge of Controlling Viral Immunopathology.International journal of molecular sciences · 2024Review
- Regulation of host/pathogen interactions in the gastrointestinal tract by type I and III interferons.Current opinion in immunology · 2024Review
- The population context is a driver of the heterogeneous response of epithelial cells to interferons.Molecular systems biology · 2024Article
- Role of type-I and type-III interferons in gastrointestinal homeostasis and pathogenesis.Current opinion in immunology · 2024Review
- 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
- Extended methods for spatial cell classification with DBSCAN-CellX.Scientific reports · 2023Article
- Differential transcriptome response following infection of porcine ileal enteroids with species A and C rotaviruses.Virology journal · 2023Article
- Blockade of interferon signaling decreases gut barrier integrity and promotes severe West Nile virus disease.Nature communications · 2023Article
- Deletion of Interferon Lambda Receptor Elucidates Susceptibility to the Murine Model of Biliary Atresia.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023Article
- Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Rotavirus infects intestinal epithelial cells and is the leading cause of gastroenteritis in infants worldwide. Upon viral infection, intestinal cells produce type I and type III interferons (IFNs) to alert the tissue and promote an antiviral state. These two types of IFN bind to different receptors but induce similar pathways that stimulate the activation of interferon-stimulated genes (ISGs) to combat viral infection. In this work, we studied the spread of a fluorescent wild-type (WT) SA11 rotavirus in human colorectal cancer cells lacking specific interferon receptors and compared it to that of an NSP1 mutant rotavirus that cannot interfere with the host intrinsic innate immune response. We could show that the WT rotavirus efficiently blocks the production of type I IFNs but that type III IFNs are still produced, whereas the NSP1 mutant rotavirus allows the production of both. Interestingly, while both exogenously added type I and type III IFNs could efficiently protect cells against rotavirus infection, endogenous type III IFNs were found to be key to limit infection of human intestinal cells by rotavirus. By using a fluorescent reporter cell line to highlight the cells mounting an antiviral program, we could show that paracrine signaling driven by type III IFNs efficiently controls the spread of both WT and NSP1 mutant rotavirus. Our results strongly suggest that NSP1 efficiently blocks the type I IFN-mediated antiviral response; however, its restriction of the type III IFN-mediated one is not sufficient to prevent type III IFNs from partially inhibiting viral spread in intestinal epithelial cells. Additionally, our findings further highlight the importance of type III IFNs in controlling rotavirus infection, which could be exploited as antiviral therapeutic measures.
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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.