The new findings suggest a lack of association between SARS-CoV-2 infection and autoimmunity related to the development of type 1 diabetes (T1D).
No relationship between infection and development was observed after screening more than 50,000 young patients from various populations in Colorado and Bavaria, Germany.
“Long-term follow-up of people with preexisting autoimmunity is needed to determine whether SARS-CoV-2 accelerates the progression to clinical diabetes,” wrote study author Marian Rewers, MD, PhD, Barbara Davis Center for Diabetes, University of Colorado School of Medicine.
An increased incidence of clinical diabetes has been reported in children with prior infection with COVID-19. Thus, Rewers and colleagues noted that it may be plausible that the virus could trigger an autoimmune response in islets or accelerate metabolic decompensation in individuals with established islet autoimmunity.
The hypothesis tested was that previous SARS-CoV-2 infection was associated with autoimmunity predicting future T1D. In 2020 and 2021, a cross-sectional screening for islet autoantibodies was offered to people aged 1–18 years participating in the Autoimmunity Screening for Kids (ASK) in Colorado and children 1–10.9 years enrolled in the Fr1da study in Germany.
Autoantibody-negative children were further followed up after SARS-CoV-2 antibody detection with blood sample collection every 3 months in Bavaria.
The study defined previous SARS-CoV-2 infection by the presence of antibodies to both the SARS-CoV-2 receptor binding domain and nucleocapsid proteins. In addition, autoantibodies to insulin, glutamic acid decarboxylase, islet antigen 2, and zinc transporter 8 autoantibodies were measured using comparable methods.
Study outcomes included the presence of multiple or single high-affinity islet autoantibodies having a 50% and 30% risk of progression to clinical diabetes within 5 years, respectively. The researchers used multivariable logistic regression to assess independent associations between prior infection and islet autoimmunity and to test for interactions by study site.
Results identified prior SARS-CoV-2 infection in 1524 (32.3%) of 4717 Colorado youth (mean age, 8.6 years; 50.3% female) and in 2862 (6.1%) of 47,253 Bavarian children (mean age, 3.9 years; 48.9). % female).
The data show that multiple islet autoantibodies were detected in 21 Colorado youth (0.45%) and in 141 Bavarian children (0.30%). In addition, 26 (0.55%) and 54 (0.11%) of the Colorado and Bavarian youth were positive for a single high-affinity islet autoantibody, respectively.
The researchers noted that the prevalence of multiple or single high-affinity islet autoantibodies did not differ significantly among youth with prior SARS-CoV-2 infection compared to those without prior infection in Colorado (1.18% vs 0.91%, P = 0.43) or Bavaria ( 0.42% vs 0.41%; P = 0.88).
The results further suggest that prior infection was not significantly associated with the presence of multiple islet autoantibodies (odds ratio, 1.06). [95% CI, 0.59 – 1.80]; P = 0.83) or a single high-affinity islet autoantibody (odds ratio, 1.34 [95% CI, 0.70 – 2.44]; P = 0.36) after controlling for confounders.
No significant interaction was reported between study site and association with SARS-CoV-2 infection, sex, age, or family history of T1D.
Rewers noted that limitations of the study included the low prevalence of autoantibodies, weakening the ability to detect an increased risk associated with SARS-CoV-2 infection. Furthermore, the cross-sectional design did not allow us to determine the timing of autoantibody development before or after infection.
The study, “SARS-CoV-2 infections and presymptomatic type 1 diabetes autoimmunity in children and adolescents from Colorado, USA and Bavaria, Germany,” was published in JAMA.