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Updated: May 11, 2026

A High-Throughput Multiplexed Screening for Type 1 Diabetes, Celiac Diseases, and COVID-19
Published on: July 5, 2022
Next-generation sequencing for viruses in children with rapid-onset type 1 diabetes
H-S Lee1, T Briese2, C Winkler3,4
1Pediatric Epidemiology Center, Department of Pediatrics, University of South Florida, Tampa, FL, USA.
Insights
This study investigated if viruses trigger rapid-onset type 1 diabetes in children. Researchers found no increased viral presence or infection history in children with rapid-onset diabetes, suggesting viruses may not be the primary cause.
Area of Science:
- Virology
- Immunology
- Pediatrics
Background:
- Viruses are suspected triggers for autoimmune (type 1) diabetes.
- Investigating rapid-onset type 1 diabetes may reveal specific causative viruses.
Purpose of the Study:
- To determine if viral infections precede rapid-onset type 1 diabetes in children.
- To identify potential viral agents involved in the pathogenesis of autoimmune diabetes.
Main Methods:
- Next-generation sequencing used to detect viruses in plasma samples.
- Examined infection and fever history in children from The Environmental Determinants of Diabetes in the Young (TEDDY) study.
- Compared rapid-onset type 1 diabetes cases with matched islet-autoantibody-negative controls.
Main Results:
- No significant difference in viral detection rates between rapid-onset type 1 diabetes patients and controls.
- Similar infection histories reported in both groups.
- Fewer fever episodes noted in children with rapid-onset type 1 diabetes.
Conclusions:
- The study findings do not support the hypothesis of viral infections (viraemia) around seroconversion in young children with rapid-onset type 1 diabetes.
- Current evidence does not link viral exposure to the rapid development of type 1 diabetes in the studied cohort.
Aims/Hypothesis:
Viruses are candidate causative agents in the pathogenesis of autoimmune (type 1) diabetes. We hypothesised that children with a rapid onset of type 1 diabetes may have been exposed to such agents shortly before the initiation of islet autoimmunity, possibly at high dose, and thus study of these children could help identify viruses involved in the development of autoimmune diabetes.
Methods:
We used next-generation sequencing to search for viruses in plasma samples and examined the history of infection and fever in children enrolled in The Environmental Determinants of Diabetes in the Young (TEDDY) study who progressed to type 1 diabetes within 6 months from the appearance of islet autoimmunity, and in matched islet-autoantibody-negative controls.
Results:
Viruses were not detected more frequently in plasma from rapid-onset patients than in controls during the period surrounding seroconversion. In addition, infection histories were found to be similar between children with rapid-onset diabetes and control children, although episodes of fever were reported less frequently in children with rapid-onset diabetes.
Conclusions/Interpretation:
These findings do not support the presence of viraemia around the time of seroconversion in young children with rapid-onset type 1 diabetes.
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