Viral infections have long been linked to the development of type 1 diabetes, but how the body’s immune responses to viruses leads to damage of the insulin-producing beta cells in the human pancreas remains a mystery.

UMass Medical School infectious disease and immunology expert Jennifer Wang, MD, and postdoc Natasha Qaisar, PhD, hope to move closer to better understanding type 1 diabetes with a new 5-year, $2.96 million grant from the National Institutes of Health. They will use a new type 1 diabetes animal model with rich potential to identify autoimmune and inflammatory pathways which could be stopped in their tracks to prevent the disease from developing.

“With this new grant we will look at how viruses can trigger type 1 diabetes—a similar theme but different approach to my existing grant, which studies the effects of coxsackie virus in human diabetes models. Our ultimate goal is to use information from these studies to design preventive therapies for human type 1 diabetes,” said Dr. Wang, associate professor of medicine in the Division of Infectious Diseases and Immunology. “We hope that we can define pathways, which could be translated over to human studies to prevent it, blocking specific pathways to prevent damage.”

The grant stems from research conducted under Wang’s direction by Qaisar, who graduated from the Graduate School of Biomedical Sciences this year. With research published in Diabetes, Dr. Qaisar used the sophisticated gene-editing technique CRISPR to generate a knockout animal model lacking a key interferon receptor. With this model she identified how an innate immune process contributes to diabetes.

While these preliminary studies have shown that interferon contributes to diabetes, it is not the only factor. With the new grant, Wang and Qaisar will look at inflammatory pathways because viruses can trigger inflammation that damages the pancreas and therapeutics that could target inflammation are available. They are also hoping to identify potential early markers for impending type 1 diabetes.

“We will use this model to better understand mechanisms on the pathogenesis of type 1 diabetes,” said Qaisar. “We are focusing on early events leading to autoimmune responses to viruses, which could be clinically significant for possible preventive therapies.”