Āé¶¹“«Ć½

Viral infection may prime some people for diabetes

Viruses that cause diarrhoea and vomiting may also trigger type-1 diabetes in children with a particular genetic make-up, a study finds

Viruses that cause diarrhoea and vomiting may also trigger diabetes in children with a particular genetic make-up. The finding could one day lead to ā€œdiabetesā€ vaccines that might be targeted at children with certain genes.

Some children are genetically predisposed to develop type-1 diabetes, but studies of identical twins show that if one twin gets the disease, the other has only a 40% chance of developing it too, suggesting that an environmental trigger is also at work.

One suspect is a family of viruses called Coxsackie B enteroviruses (CVBs). In type-1 diabetes, the body attacks and destroys insulin-producing pancreatic cells called beta cells. It is thought that when CVBs infect beta cells, they may trigger this ā€œautoimmunityā€, but only in children with a particular genetic make-up.

This would make sense as the genes that are linked to type-1 diabetes code for proteins involved in the immune response. However, evidence supporting the theory has relied on a small number of samples. For example, in 2007, evidence of CVB infection was reported in two of five patients with type-1 diabetes, but not in 26 non-diabetic controls.

Tell-tale protein

To test the CVB theory in a much larger group, a team led by Noel Morgan at the in Plymouth, UK, analysed tissue taken from the pancreases of 72 children who had died of type-1 diabetes shortly after becoming ill.

In more than 60% of the pancreases, they found a protein that makes up CBV’s viral coating, in the beta cells. There was almost no evidence of infection in control tissue samples taken from children who had not had diabetes.

ā€œThis is the first time that scientists have been able to provide such extensive evidence for the relationship between enteroviral infection of the beta cells and the development of type 1 diabetes,ā€ says Morgan.

ā€˜Conservative estimate’

Although 40% of the samples did not show evidence of CBV, Adrian Bone of the University of Brighton, UK, says the people that provided these samples may still have been infected with CBV – evidence of it just didn’t show up in the protein test. ā€œThe protein isn’t completely stable, so 60% is a conservative estimate,ā€ he says.

The next step will be working out which strains of CBV trigger type-1 diabetes, and testing whether these can be used in a vaccine that prevents the disease, says Bone.

ā€œThe study is hugely significant because for the first time we have a large enough study of pancreas post mortem samples from patients who died near to diagnosis – this has been lacking and therefore we have had to rely on the odd case report,ā€ says Mark Peakman at King’s College London School of Medicine.

Journal reference:

Topics: Genetics