ArticleScience advances2026
Overcoming host restrictions to enable continuous passaging of GII.3 human norovirus in human intestinal enteroids.
Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Plscr1 inhibits murine norovirus entry.bioRxiv : the preprint server for biology · 2026Article
- Treatment With Ruxolitinib and TAK-779 Enhances GII.17 Human Norovirus Replication and Enables Serial Passaging in Human Intestinal Enteroids.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- Multi-Ligand Interactions Shape Human Norovirus Persistence, Transmission, and Control in Food Matrices.Viruses · 2026Review
- Comparison of human intestinal enteroid and zebrafish larva models for replication of human norovirus.Applied and environmental microbiology · 2026Article
- Tulane virus protease as a structural surrogate for inhibitor screening of human norovirus proteases.Journal of virology · 2026Article
- Antiviral strategies against human norovirus: Molecular targets, therapeutics, and vaccine development.Therapeutic advances in infectious diseaseReview
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
The establishment of human intestinal enteroids (HIEs) as a model for human norovirus (HuNoV) replication has been transformative for studying this leading cause of gastroenteritis. However, indefinite passaging of HuNoVs in HIEs remained a challenge, necessitating the use of patient stool samples as viral inocula. Using RNA-seq, we identified CXCL10, CXCL11, and CCL5 as up-regulated chemokines, suggesting their potential as host restriction factors. TAK-779, a CXCR3/CCR5/CCR2 antagonist, enhanced GII.3 HuNoV replication and viral spread in a dose- and time-dependent manner, enabling successful passaging of GII.3 HuNoV in two different HIE lines and generation of viral stocks. Sequencing passaged virus revealed one consensus change in the major capsid protein and several dynamic adaptations, suggesting emergence of variants. TAK-779 also enhanced replication of GI.1 and GII.17 strains, but not GII.4, suggesting strain-specific host interactions. This breakthrough in passaging provides insight into HuNoV-host interactions, establishes a scalable in vitro system for virus propagation, and opens avenues for structural, biochemical, and therapeutic studies.
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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 Socratic graph.