Virus exposure could ‘trigger’ risk of type-1 diabetes

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trigger new diabetes
trigger new diabetes

A new study published in Cell Reports has investigated how exposure to certain triggers can increase the risk of type-1 diabetes.

Researchers from The Westmead Institute for Medical Research in western Sydney are looking at an array of potential triggers that could increase the risk of type-1 diabetes. Results of a recent study have shown how exposure to coxsackievirus can increase this risk.

What is coxsackievirus?

Coxsackievirus is a common virus that causes diseases including myocarditis, hand, foot and mouth disease, and gastroenteritis.

The study discovered that a key transcription factor (proteins that help turn specific genes on or off) called hypoxia inducible factor 1-alpha (HIF-1A) is behind this increase in risk. Researchers found that mice missing HIF-1A in beta cells (β-cells) had a much higher risk of type-1 diabetes after infection with viruses, including coxsackievirus.

Lack of β-cell HIF-1A increased β-cell death and, in turn, increased the incidence of type-1 diabetes.

‘Recover or die’

Lead researcher Professor Jenny Gunton says the findings highlight the key role β-cells play in the risk of diabetes.

“If they are healthy, then β-cells recover normally after stresses like viral infections, and diabetes does not develop,” she said. “But, if β-cells don’t cope well with these stresses, it can trigger the immune process that leads to type-1 diabetes.

“Our study also showed that the increase in diabetes risk can result from exposure to other stresses, including toxins. So β-cells play a crucial part in preventing their own death when faced with environmental triggers for type-1 diabetes.

“We have now identified that HIF-1A as an important factor in this ‘decision’ about whether the cells recover or die. This is the first β-cell specific model to show increased risk of type-1 diabetes with a range of triggers.”

Pathway to prevention?

The findings highlight HIF-1A as a potential pathway for the development of new preventative measures and suggest the possibility that a vaccine for coxsackievirus could help prevent type-1 diabetes in at-risk people.

“While there is a strong genetic component to type-1 diabetes, genes alone cannot explain the rising global rates of type-1 diabetes,” Professor Gunton said.

“Currently, the only cures for type-1 diabetes are whole-pancreas or islet transplantation, and people have to take insulin for the rest of their lives. So potential preventative strategies are exciting.”