A recent study published in the prestigious journal JAMA has found a potential link between SARS-CoV-2 infections in infants and the development of type 1 diabetes. The study, conducted by researchers, aimed to investigate whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections were associated with the development of islet autoimmunity, which precedes the onset of type 1 diabetes during childhood.
Type 1 diabetes is known to be preceded by the production of autoantibodies against proteins in the islet β-cells in the pancreas. The highest susceptibility for autoantibody development occurs at around the age of one and is influenced by genetic factors, immune function, functioning of islet β-cells, and response to viral infections of the respiratory system in the first year of life.
With the COVID-19 pandemic leading to increased childhood exposure to respiratory viruses, studies have noticed a rise in the incidence of type 1 diabetes in children. Given that SARS-CoV-2 can cause infections in the pancreas, researchers sought to determine whether it could potentially trigger islet autoimmunity, but previous studies have not conclusively linked SARS-CoV-2 infections to the development of islet autoantibodies.
To explore this further, the researchers conducted the Primary Oral Insulin Trial (POINT) between 2018 and 2021. The trial involved infants aged four to seven months with at least a 10% genetically defined risk of developing islet autoimmunity. Blood samples were collected longitudinally to detect islet autoantibodies, with samples taken from baseline and subsequent visits up until the age of 6.5 years.
The study used specific assays to measure antibodies against SARS-CoV-2 and the hemagglutinin 5 neuraminidase 1 (H5N1) influenza A virus. Samples were also tested for islet autoantibodies against insulinoma-associated antigen 2 (IA-2), glutamate acid decarboxylase 65 (GAD65), zinc transporter 8 (ZnT8), and insulin.
The findings indicated a temporal association between SARS-CoV-2 infections and the development of islet β-cell autoantibodies in infants with a genetic predisposition to type 1 diabetes. Out of the 884 infants included in the study, 170 developed antibodies against SARS-CoV-2, and of these, 60 developed islet autoantibodies. Some infants developed islet autoantibodies concurrently with SARS-CoV-2 antibodies, while others developed autoantibodies after testing positive for SARS-CoV-2 antibodies.
After adjusting for age, sex, and country, the researchers found a hazard ratio of 3.5 for the production of islet autoantibodies in children who tested positive for antibodies against SARS-CoV-2. The incidence rate per 100 person-years for developing islet autoantibodies was higher in infants with SARS-CoV-2 antibodies compared to those without.
The study provides valuable insights into the association between SARS-CoV-2 infections in children and the development of type 1 diabetes. It suggests that COVID-19 may act as a risk factor for the development of islet autoimmunity in infants with a higher genetic risk of type 1 diabetes.
Further research is needed to fully understand the mechanisms underlying this association and to confirm these findings. Nevertheless, the study highlights the importance of monitoring infants who have had SARS-CoV-2 infections for the development of islet autoantibodies and potential future risk of type 1 diabetes.
