Evidence map›Paper›PMID 36742327›Full record

ArticleFrontiers in immunology2023

Virus induced dysbiosis promotes type 1 diabetes onset.

Zachary J Morse, Rachel L Simister, Sean A Crowe, Marc S Horwitz, Lisa C Osborne

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 18 citations in OpenAlex.

  1. AAVrh32.33 capsid demonstrates unexpected dermal tropism regardless of immunodominant epitope.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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  14. The immunology of type 1 diabetes.Nature reviews. Immunology · 2024
    Review
  15. Article
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  17. Review
  18. International journal of molecular sciences · 2023
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Zachary J MorseDepartment of Microbiology & Immunology, Life Sciences Institute, University of British Columbia, Vancouver, BC, Canada.
Rachel L SimisterDepartment of Microbiology & Immunology, Life Sciences Institute, University of British Columbia, Vancouver, BC, Canada.
Sean A CroweDepartment of Microbiology & Immunology, Life Sciences Institute, University of British Columbia, Vancouver, BC, Canada.
Marc S HorwitzDepartment of Microbiology & Immunology, Life Sciences Institute, University of British Columbia, Vancouver, BC, Canada.
Lisa C OsborneDepartment of Microbiology & Immunology, Life Sciences Institute, University of British Columbia, Vancouver, BC, Canada.
University of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune disorders are complex diseases of unclear etiology, although evidence suggests that the convergence of genetic susceptibility and environmental factors are critical. In type 1 diabetes (T1D), enterovirus infection and disruption of the intestinal microbiota are two environmental factors that have been independently associated with T1D onset in both humans and animal models. However, the possible interaction between viral infection and the intestinal microbiota remains unknown. Here, we demonstrate that Coxsackievirus B4 (CVB4), an enterovirus that accelerates T1D onset in non-obese diabetic (NOD) mice, induced restructuring of the intestinal microbiome prior to T1D onset. Microbiome restructuring was associated with an eroded mucosal barrier, bacterial translocation to the pancreatic lymph node, and increased circulating and intestinal commensal-reactive antibodies. The CVB4-induced change in community composition was strikingly similar to that of uninfected NOD mice that spontaneously developed diabetes, implying a mutual "diabetogenic" microbiome. Notably, members of the Bifidobacteria and Akkermansia genera emerged as conspicuous members of this diabetogenic microbiome, implicating these taxa, among others, in diabetes onset. Further, fecal microbiome transfer (FMT) of the diabetogenic microbiota from CVB4-infected mice enhanced T1D susceptibility and led to diminished expression of the short chain fatty acid receptor GPR43 and fewer IL-10-expressing regulatory CD4

Indexed as

Diabetes Mellitus, Type 1Enterovirus InfectionsAnimalsDysbiosisGenetic Predisposition to DiseaseHumansIntestinesMiceMice, Inbred NODcoxsackievirusfecal microbiota transplant (FMT)microbiometype 1 diabetesviral-induced autoimmunity

Identifiers

PMID36742327
PMCPMC9892191
OpenAlexW4317388214

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.