ArticleJournal of the Endocrine Society2017
Coxsackievirus-Induced Proteomic Alterations in Primary Human Islets Provide Insights for the Etiology of Diabetes.
Article in Journal of the Endocrine Society, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 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
18 citing papers in PubMed, 23 citations in OpenAlex.
- ProtectiveiScience · 2026Article
- Protocol to stress human primary pancreatic islets with diabetogenic factors for subsequent single-cell RNA sequencing.STAR protocols · 2026Article
- The Hippo terminal effector YAP boosts enterovirus replication in type 1 diabetes.Nature communications · 2025Article
- Coxsackievirus B infection invokes unique cell-type-specific responses in primary human pancreatic islets.Cell reports · 2025Article
- Article
- Review
- Immunological and virological triggers of type 1 diabetes: insights and implications.Frontiers in immunology · 2023Review
- Persistent coxsackievirus B infection and pathogenesis of type 1 diabetes mellitus.Nature reviews. Endocrinology · 2022Review
- Single-cell RNA-sequencing of peripheral blood mononuclear cells reveals widespread, context-specific gene expression regulation upon pathogenic exposure.Nature communications · 2022Article
- Persistent coxsackievirus B1 infection triggers extensive changes in the transcriptome of human pancreatic ductal cells.iScience · 2022Article
- Coxsackievirus B Type 4 Infection in β Cells Downregulates the Chaperone Prefoldin URI to Induce a MODY4-like Diabetes viaCell reports. Medicine · 2020Article
- Proteomic and Transcriptional Profiles of Human Stem Cell-Derived β Cells Following Enteroviral Challenge.Microorganisms · 2020Article
- The Role of β Cell Stress and Neo-Epitopes in the Immunopathology of Type 1 Diabetes.Frontiers in endocrinology · 2020Review
- Coxsackievirus B Persistence Modifies the Proteome and the Secretome of Pancreatic Ductal Cells.iScience · 2019Article
- The role of proteomics in assessing beta-cell dysfunction and death in type 1 diabetes.Expert review of proteomics · 2019Article
- Enterovirus infection and type 1 diabetes: unraveling the crime scene.Clinical and experimental immunology · 2019Review
- Enteroviral infections in the pathogenesis of type 1 diabetes: new insights for therapeutic intervention.Current opinion in pharmacology · 2018Review
- Virus-like infection induces human β cell dedifferentiation.JCI insight · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Enteroviral infections have been associated with the development of type 1 diabetes (T1D), a chronic inflammatory disease characterized by autoimmune destruction of insulin-producing pancreatic beta cells. Cultured human islets, including the insulin-producing beta cells, can be infected with coxsackievirus B4 (CVB4) and thus are useful for understanding cellular responses to infection. We performed quantitative mass spectrometry analysis on cultured primary human islets infected with CVB4 to identify molecules and pathways altered upon infection. Corresponding uninfected controls were included in the study for comparative protein expression analyses. Proteins were significantly and differentially regulated in human islets challenged with virus compared with their uninfected counterparts. Complementary analyses of gene transcripts in CVB4-infected primary islets over a time course validated the induction of RNA transcripts for many of the proteins that were increased in the proteomics studies. Notably, infection with CVB4 results in a considerable decrease in insulin. Genes/proteins modulated during CVB4 infection also include those involved in activation of immune responses, including type I interferon pathways linked to T1D pathogenesis and with antiviral, cell repair, and inflammatory properties. Our study applies proteomics analyses to cultured human islets challenged with virus and identifies target proteins that could be useful in T1D interventions.
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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.