ArticleCell reports2025
Coxsackievirus B infection invokes unique cell-type-specific responses in primary human pancreatic islets.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- ProtectiveiScience · 2026Article
- SARS-CoV-2 seeds IAPP aggregation and β-cell failure.Signal transduction and targeted therapy · 2026Article
- Article
- Protocol to stress human primary pancreatic islets with diabetogenic factors for subsequent single-cell RNA sequencing.STAR protocols · 2026Article
- Whole-genome CRISPR screening identifies genetic modifiers of stem cell-derived islet transplantation.Stem cells translational medicine · 2026Article
- The perfect storm: unraveling the interplay of genetic predisposition and viral triggers in type 1 diabetes pathogenesis.Frontiers in endocrinology · 2025Review
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8 authors.
Funding
Abstract
Coxsackievirus B (CVB) is implicated as an environmental trigger for type 1 diabetes (T1D). While CVB impairs islet function and viability, its impact on individual primary human islet cell types remains unclear. Here, we use single-cell RNA sequencing and functional studies to show that CVB3 induces distinct cell-type-specific transcriptional and mitochondrial responses in human cadaveric islets. Contrary to prior claims, our analysis reveals no evidence of preferential viral tropism for β and ductal cells, instead demonstrating comparable infection rates across both endocrine and exocrine compartments. β, α, and ductal cells show the most robust transcriptional responses to infection, with ductal cells, not β cells, exhibiting the strongest interferon- and HLA-associated responses. Notably, the long non-coding MIR7-3HG modulates viral RNA expression, titer, apoptosis, and autophagy upon knockdown in stem-cell-derived islets. These findings challenge long-standing assumptions about islet-specific viral targeting and demonstrate cell-specific responses to CVB3 infection relevant to T1D.
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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.