There is no single cause of type 1 diabetes (T1D). Though scientists know that T1D involves the body destroying insulin-producing islet cells in the pancreas, there is not one specific trigger. In fact, researchers believe that genetics, environment, and immunologic capability all play a role and put individuals at different risks for developing the disease.
A recent study from investigators at Columbia University’s Mailman School of Public Health has found that the presence of certain non-polio enteroviruses may impact islet autoimmunity and lead to type 1 diabetes. They looked at the abundance of these viruses in blood and stool samples from 93 Australian children. Forty-three of the children had type 1 diabetes precursor islet autoimmunity while 48 children were matched as controls.
Using an incredibly powerful viral sequencing tool, they found 129 viruses—including five enteroviruses—that were present in higher levels in children with islet autoimmunity than those in the control group. Individuals with strong immune systems tend to eliminate enteroviruses rather quickly, usually within three to four weeks. With a slower immune response, it could take up to three months.
Risk increases when these viruses spread to children’s pancreases. Scientists are exploring how they affect pancreatic islet cells and interfere with function potentially causing beta-cell destruction and type 1 diabetes. While more research is necessary to further understand the impact enteroviruses may have, these new findings help scientists to refine their studies of the disease and its development.
While not involved with this study, the Diabetes Research Connection supports novel, peer-reviewed research studies focused on the development and treatment of type 1 diabetes as well as improving quality of life for individuals living with the disease. Up to $75,000 in funding is available for early career scientists through support from individuals, corporations, and foundations.