Evidence map›Paper›PMID 35650334›Full record

ReviewNature reviews. Endocrinology2022

Persistent coxsackievirus B infection and pathogenesis of type 1 diabetes mellitus.

Magloire Pandoua Nekoua, Enagnon Kazali Alidjinou, Didier Hober

Open access · bronzeAbstract readReview
In one paragraph

Review in Nature reviews. Endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
23.9field-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.

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

88 citing papers in PubMed, 134 citations in OpenAlex.

  1. ProtectiveiScience · 2026
    Article
  2. Endocrine-Metabolic Crosstalk Between Diabetes Mellitus and Hypothyroidism: From Network Mechanisms to Translational Stratification.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  3. Article
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  5. Review
  6. Type 1 Diabetes Mellitus Pathogenesis: Mechanisms, Early Diagnostic Strategies, and Emerging Therapeutic Approaches.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
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28 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

3 authors at 1 institution in 1 country.

Magloire Pandoua NekouaLaboratoire de Virologie ULR3610, Université de Lille, CHU Lille, Lille, France.ORCID http://orcid.org/0000-0002-2981-0803
Enagnon Kazali AlidjinouLaboratoire de Virologie ULR3610, Université de Lille, CHU Lille, Lille, France.ORCID http://orcid.org/0000-0002-1106-9826
Didier HoberLaboratoire de Virologie ULR3610, Université de Lille, CHU Lille, Lille, France. didier.hober@chru-lille.fr.ORCID http://orcid.org/0000-0002-4301-2074
Université de Lille · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enteroviruses are believed to trigger or accelerate islet autoimmunity in genetically susceptible individuals, thereby resulting in loss of functional insulin-producing β-cells and type 1 diabetes mellitus (T1DM). Although enteroviruses are primarily involved in acute and lytic infections in vitro and in vivo, they can also establish a persistent infection. Prospective epidemiological studies have strongly associated the persistence of enteroviruses, especially coxsackievirus B (CVB), with the appearance of islet autoantibodies and an increased risk of T1DM. CVB can persist in pancreatic ductal and β-cells, which leads to structural or functional alterations of these cells, and to a chronic inflammatory response that promotes recruitment and activation of pre-existing autoreactive T cells and β-cell autoimmune destruction. CVB persistence in other sites, such as the intestine, blood cells and thymus, has been described; these sites could serve as a reservoir for infection or reinfection of the pancreas, and this persistence could have a role in the disturbance of tolerance to β-cells. This Review addresses the involvement of persistent enterovirus infection in triggering islet autoimmunity and T1DM, as well as current strategies to control enterovirus infections for preventing or reducing the risk of T1DM onset.

Indexed as

Diabetes Mellitus, Type 1EnterovirusInsulin-Secreting CellsEnterovirus B, HumanHumansProspective Studies

Identifiers

PMID35650334
PMCPMC9157043
OpenAlexW4281761207

What OpenQuestion holds

Textmetadata
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.