Evidence map›Paper›PMID 27020257›Full record

ReviewNature reviews. Endocrinology2016

Viral infections in type 1 diabetes mellitus--why the β cells?

Anne Op de Beeck, Decio L Eizirik

Registry-linked trialOpen access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04860908 (DOES COVID-19 INFECTION AND/OR VACCINATION OF PREGNANT WOMEN AFFECT THE PANCREATIC BETA CELLS OF THE FETUS BECOMING A TRIGGER FOR FUTURE DEVELOPMENT OF CHILDHOOD TYPE 1 DIABETES), which is not on this map. Cited by 179 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed, 3 pooled it
19.2field-weighted citation impact, top 1% 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.

NCT04860908 unknown statusnot on this mapstarted 2021, after this paper: background citation

Does covid-19 infection and/or vaccination of pregnant women affect the pancreatic beta cells of the fetus becoming a trigger for future development of childhood type 1 diabetes

TypeobservationalSponsorMaaynei Hayesha Medical CenterRan2021 to 2022Enrolled100ConditionsGeneration of Anti COVID-19 Antibodies in a Fetus, Whose Mother Was Exposed to COVID or Was Vaccinated During PregnancyArmsno intervention, observation only
3 · Its place in the literature

Who cites it

179 citing papers in PubMed, 3 syntheses or guidelines pooled it, 287 citations in OpenAlex.

  1. Pooled it
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  10. How loss-of-function mutations inJournal of translational autoimmunity · 2026
    Review
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  12. From bats to humans: uncoveringbioRxiv : the preprint server for biology · 2026
    Article
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119 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Anne Op de Beeck *Center for Diabetes Research, Universite Libre de Bruxelles, 808 Route de Lennik, CP618, B-1070, Brussels, Belgium.
Decio L Eizirik *Center for Diabetes Research, Universite Libre de Bruxelles, 808 Route de Lennik, CP618, B-1070, Brussels, Belgium.
Université Libre de Bruxelles · BE

Funding

Biomarkers Of Beta Cell Stress In Type 1 Diabetes (BetaMarker)UC4DK104166 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EIZIRIK, DECIO LAKS, EVANS-MOLINA, CARMELLA · 2014 to 2014
$2.4M
NIDDK NIH HHS UC4 DK104166
6 · The paper itself

Abstract

Type 1 diabetes mellitus (T1DM) is caused by progressive autoimmune-mediated loss of pancreatic β-cell mass via apoptosis. The onset of T1DM depends on environmental factors that interact with predisposing genes to induce an autoimmune assault against β cells. Epidemiological, clinical and pathology studies in humans support viral infection--particularly by enteroviruses (for example, coxsackievirus)--as an environmental trigger for the development of T1DM. Many candidate genes for T1DM, such as MDA5, PTPN2 and TYK2, regulate antiviral responses in both β cells and the immune system. Cellular permissiveness to viral infection is modulated by innate antiviral responses that vary among different tissues or cell types. Some data indicate that pancreatic islet α cells trigger a more efficient antiviral response to infection with diabetogenic viruses than do β cells, and so are able to eradicate viral infections without undergoing apoptosis. This difference could account for the varying ability of islet-cell subtypes to clear viral infections and explain why chronically infected pancreatic β cells, but not α cells, are targeted by an autoimmune response and killed during the development of T1DM. These issues and attempts to target viral infection as a preventive therapy for T1DM are discussed in the present Review.

Indexed as

AnimalsDiabetes Mellitus, Type 1HumansInsulin-Secreting CellsVirus Diseases

Identifiers

PMID27020257
PMCPMC5348720
OpenAlexW2324838759

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.