Children with a genetic predisposition to type 1 diabetes who catch Covid before the age of 18 months have a five–ten times higher risk of developing the life-long autoimmune disease.
This is the conclusion of an international team of researchers from the Global Platform for the Prevention of Autoimmune Diabetes (GPPAD), who monitored more than 850 at-risk infants between the years 2018 and 2021.
Type 1 diabetes is a life-long disorder in which the body does not produce enough insulin, the hormone that is vital for regulating blood sugar levels and maintaining the body’s energy.
The first sign of the disease is the development of autoantibodies that tag the “islet beta” cells in the pancreas — those that produce insulin — for destruction by the immune system.
The new findings build on those of previous studies that reported a correlation between viral infections — including those with SARS-CoV-2 — and type 1 diabetes. However, this is the first work to link Covid to islet autoimmunity.
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In their study, Professor Ezio Bonifacio of the Dresden University of Technology and his colleagues regularly tested for the presence of both islet autoantibodies and SARS-CoV-2 antibodies in 855 children as they aged from four to 24 months old.
Each subject was enrolled in GPPAD’s “Primary Oral Insulin Trial” (POInT) study after being determined, based on their genetics, to have a 10 percent risk of developing type 1 diabetes.
(POInT is exploring how we might be able to prevent type 1 diabetes in children by training their immune systems via the oral administration of insulin.)
The team found that nearly 20 percent of the kids studied developed antibodies against coronavirus during the pandemic, indicating that they had been infected with the virus.
On average, the children were found to be more than twice as likely to develop islet autoantibodies if they also showed signs of having contracted a SARS-CoV-2 infection.
And the prevalence of the type 1 diabetes precursor was found to be even higher when Covid infection struck particularly early.
Bonifacio said: “The timing of the islet autoantibody appearance in relation to the SARS-CoV-2 infection in these children was striking.
“The most remarkable finding, however, was that the risk of developing islet autoantibodies was highest in the children who were infected before they were 18 months old — and in particular at around one year of age.
“These children had around five-to-10–fold higher risk for developing islet autoantibodies that lead to type 1 diabetes later in life.
“It is such a critical age for children who are genetically at risk for the disease and key to why we were able to see the association.”
The team cautions that — although there was a clear temporal association between SARS-CoV-2 infection and the development of islet autoantibodies — many children still develop these diabetes precursors without the involvement of COVID-19.
Bonifacio said: “Type 1 diabetes is not a one-factor disease. However, this study again shows the link between a virus infection and type 1 diabetes right at the very start of the process and at the critical age of susceptibility.”
At present, the researchers are not sure of the exact mechanism behind the increased risk of islet autoimmunity in young children.
Nevertheless, the findings have the potential to help discover ways to stop the chronic autoimmune disease from developing in the first place.
Paper co-author Professor Anette-Gabriele Ziegler of the Helmholtz Munich Institute of Diabetes Research is the head of GPPAD.
She explained: “It begs the question as to whether vaccination against viruses associated with islet autoimmunity could be an avenue for prevention of at least some cases of type 1 diabetes.
“Type 1 diabetes is a lifelong disease affecting millions of children and adults worldwide. We are convinced that investing into early prevention strategies, such as those tested in GPPAD, is important to curtail the rising incidence of this disease in children.”
The full findings of the study were published in the journal JAMA.
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