In type 1 diabetes, the immune system attacks the insulin-producing beta cells in the pancreas. Scientists believe that a mix of genetic and environmental factors are behind such attacks. And there’s growing evidence that viruses could be one potential environmental trigger.
Several viral suspects have been studied for their possible role in triggering or accelerating type 1 diabetes.
Enteroviruses
This common group of viruses, particularly coxsackievirus B, has some of the strongest evidence connecting them to type 1 diabetes.
The TEDDY study follows children who have a high genetic risk of type 1 diabetes from birth. It showed that children who had long-lasting enterovirus infections had a higher risk of developing type 1 diabetes. Other research has found traces of these viruses in pancreas samples from people before type 1 symptoms appear, at diagnosis, and even years later.
Rotavirus
Rotavirus is a common gut virus in children. Some studies suggest that rotavirus infections might influence the risk of developing type 1 diabetes.
For instance, a US study involving over 1.4 million children found a 33% reduction in the risk of type 1 diabetes among children who’d been vaccinated against rotavirus, compared to those who weren’t. But studies in other countries haven’t seen the same effect.
Covid-19
During the covid-19 pandemic, studies observed an increase in new cases of type 1 diabetes in children. And early lab studies suggested the virus may directly harm the pancreas.
But the evidence is still evolving and mixed. For example, a recent Australian study of 1,300 children found that Covid-19 infections were not linked to the early stages of type 1 diabetes development.
Epstein-Barr Virus (EBV)
EBV is a very common virus that can cause glandular fever. Studies have found that it may trigger certain immune cells to become overactive, potentially leading to the type 1 immune attack.
But overall, there is no firm evidence that any viruses directly cause type 1 diabetes and it's important to remember that most children who catch these viruses never develop the condition.
Why might viruses contribute to type 1?
Researchers have several possible theories:
- The immune system’s response to a virus could cause it to go into overdrive and mistakenly attack nearby beta cells.
- Parts of some viruses look like parts of beta cells, confusing the immune system into attacking them.
- Certain viruses may infect and harm beta cells directly.
- Some people have particular genes that could make the immune system more prone to overreact to viruses, and accidently attack beta cells in the process.
Breaking the viral links
Given the potential link between viruses and type 1 diabetes, scientists are exploring if preventing or treating viral infections could be a new way to delay or prevent type 1 diabetes.
For example, an international study is looking at whether getting the Covid-19 vaccine in the first year of life can reduce the chance of developing type 1 diabetes in children at high genetic risk of the condition.
Small trials with children newly diagnosed with type 1 diabetes have also shown that antiviral drugs may help preserve some of their insulin production for up to a year, compared to those who didn’t get the antivirals. However, larger trials are needed to confirm these findings.
Our research
A deeper understanding of how and why viruses might trigger type 1 diabetes will be key to finding better ways to stop the condition.
Thanks to the generous donation of £300,000 from the Bukhman Foundation, we’re supporting Dr Kasra Bahador's research at the University of Cambridge to investigate why only a small number of children go on to develop type 1 diabetes after catching enteroviruses.
The goal is to build a detailed map of different immune responses, which could help uncover immune changes that tip the balance from a normal immune reaction to a virus, to an autoimmune attack and the beginning of type 1 diabetes.
This could help identify children at higher risk of type 1, and point to new ways of reducing that risk by targeting the immune responses related to viruses.
