New research shows enteroviral infections may contribute to the development of T1D

A team of international researchers, supported by Breakthrough T1D, have published the results of their research study. Their study is the largest and most comprehensive to date examining human pancreas tissue for signs of viral infection in people with and without type 1 diabetes (T1D).

Connection between enteroviruses and T1D

We know that the process of developing T1D happens over time and that there are lots of things that contribute to a person developing the condition. When a person’s baseline genetic risk is combined with a ‘trigger event’ the immune system activates and begins to attack healthy beta cells. It is this process that leads to the development of a single autoantibody, an early immune warning signal that indicates a higher risk of progressing to stage 3, symptomatic T1D in the future.

Viral infections might act as one such ‘trigger event’, specifically infections caused by a family of viruses called enteroviruses. Enteroviruses don’t directly ‘cause’ type 1 diabetes, but in people with certain genetic risks, enteroviral infections may trigger the immune system to start attacking the body’s own insulin-producing cells. This research helps us understand that interplay more clearly and may lead to ways of preventing or delaying T1D.

At a glance:

• 83% of T1D-ICI donors tested positive in two or more enterovirus-related tests, compared with 0% in the group without T1D, suggesting a relationship between enterovirus infection and islet autoimmunity
• People with autoantibodies but not yet diagnosed with T1D also showed intermediate levels of infection markers, suggesting that enterovirus may be involved early in the disease process
• Results from molecular biology testing also supported the link between enterovirus presence and type 1 diabetes

Professor Sarah Richardson, a Breakthrough T1D funded researcher working on this project, said:

“Although enteroviral infections have long been associated with type 1 diabetes, it is incredibly hard to prove that they are a trigger as initial infection could happen years before symptoms appear.  This highly collaborative international study brought together teams with complementary expertise and demonstrated, using multiple different techniques, evidence of infection in the pancreas. This brings us a step closer to trials to determine if vaccination or anti-viral treatments could have a role in preventing type 1 diabetes in genetically at-risk individuals.”

Importantly, the study found evidence of long-lasting, low-level enteroviral infections, rather than acute infections in the pancreas suggesting that the persistence of the infection could trigger or maintain the autoimmune attack. This may mean that therapies to target viral triggers, like antiviral drugs and/or vaccines, may be effective in preventing or delaying the onset of type 1.

What’s next for this research?

The results of this study help to increase our understanding of the potential role that enteroviral infections play in the development of T1D. But we still need more understanding of the processes that trigger immune activation and beta cell destruction to design effective therapies to try and prevent T1D.