Insights From the COVID-19 Pandemic: Change in Infection History and Islet Autoimmunity Incidence
Islet autoimmunity, which underlies the development of type 1 diabetes (T1D), is influenced by various environmental factors, including early childhood viral infections. Scientists from the GPPAD consortium, coordinated at Helmholtz Munich, recently published a study in the journal Infection. They propose that during the COVID-19 pandemic, the introduction of SARS-CoV-2 may have replaced other respiratory and gastrointestinal viruses as factors increasing the risk for islet autoimmunity. Historically, Coxsackie viruses have been considered significant modifiers of islet autoantibody risk. However, despite a marked decrease in Coxsackie virus-associated infections during the first pandemic lockdown in 2020, the incidence of islet autoantibodies did not decline, suggesting that SARS-CoV-2 may have taken its place as a risk factor.
Research indicates that viral infections in early childhood may play a critical role in increasing the risk of T1D. The COVID-19 pandemic has altered infection patterns, providing new insights into the relationship between viruses and T1D.
Data from children at increased genetic risk for T1D, enrolled in the POInT study before and during the pandemic, were analyzed. The POInT study, conducted by the Global Platform for the Prevention of Autoimmune Diabetes (GPPAD) and coordinated at the Institute of Diabetes Research at Helmholtz Munich, examines whether administering insulin powder in the first three years of life can reduce the risk of islet autoimmunity. Children were monitored for islet autoantibody development and infections were tracked until age 3 years as part of adverse event monitoring.
SARS-CoV-2: A New Potential Risk Factor for Islet Autoimmunity
Preventative measures during the COVID-19 pandemic significantly altered infection patterns in children. A decline in respiratory and gastrointestinal infections, including Coxsackie virus infections, was observed in the first year of the pandemic. Despite this, the occurrence of islet autoantibodies, biomarkers for early-stage T1D, remained unchanged in the cohort. As infection rates returned to pre-pandemic levels in the second year, the incidence of islet autoantibodies more than doubled.
The scientists hypothesize that SARS-CoV-2 replaced other viral infections, such as those associated with Coxsackie viruses, as a risk factor for islet autoantibodies at the pandemic's outset. This hypothesis aligns with the observed increase in viral infections, including SARS-CoV-2, in the second year of the pandemic, which coincided with a significant rise in islet autoantibody incidences among children. The emergence of SARS-CoV-2 may have resulted in an overall increase in viral exposures, heightening the susceptibility to T1D.
Previous research by the GPPAD group demonstrated a temporal association between COVID-19 infections and the development of islet autoantibodies in the same cohort. Their analysis revealed that early SARS-CoV-2 infections, particularly those occurring before 18 months of age, increase the risk for T1D
Original publication
Zeller, Weiss, Arnolds et al. (2024): Infection episodes and islet autoantibodies in children at increased risk for type 1 diabetes before and during the COVID‑19 pandemic. Infection. DOI: https://doi.org/10.1007/s15010-024-02312-y
