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Item #9

Key Findings: Diabetes Is Caused By A Virus

There is strong evidence suggesting that diabetes is caused by a virus, and if true, a vaccine could prevent Type 1 diabetes. 

UK scientists have found a marked difference between the way the bodies of healthy individuals respond to a virus known as Coxsackie B4 and those of newly diagnosed diabetics.

The research, published in the American journal Diabetes, is an important step forward in narrowing down the likely causes of what can be a devastating illness.

Dr Mark Peakman led the three-year-study at the Department of Immunology at Guy’s, King’s and St Thomas’ School of Medicine, and says the work is a crucial foundation for further research. ‘The implications are clear: if viruses have a proven role in the disease, there is the future possibility of developing vaccines to prevent infection and therefore Type 1 diabetes’, he says.

Type 1 diabetes is an autoimmune disease in which the body lacks insulin (which controls the sugar levels in our bloodstream), and the individual has to inject it daily instead. It usually begins in childhood, affecting as many as one in 200 people, and is worryingly on the increase. As the more serious type of diabetes, Type 1 can lead to blindness, kidney failure and heart disease in later life.

It still isn’t clear why the disease occurs, but it’s most likely to be a complex interaction between a person’s genes and their environment. Various studies have suggested that a group of viruses could be a trigger, stimulating the immune system - the body’s natural defense mechanism against disease - to attack and ‘kill off’ the cells that produce insulin. But until this study the evidence has been indirect and the immune cells involved unclear.

The candidate virus that the research team focused on was the Coxsackie B4 virus (CVB4), a bug that causes typical viral symptoms and most commonly found in children. Several years ago, a strain of this bug was recovered from the pancreas of a child dying from Type 1 diabetes. Using the genetic code of the virus and the latest DNA technology, the Action Researchers were able to grow key parts of the virus and see how the body responds to these, using blood samples of some 40 Type 1 diabetics: teenagers and young adults who had been diagnosed within the last five months.

The team found that CVB4 did stimulate the immune system very readily, and found fresh evidence that the response was different between the diabetics and a healthy non-diabetic control group, in a way that suggested recent or repeated exposure to the virus.

Dr Peakman,  says: ‘A virus is like an enemy invasion that the body fights with using an ‘infantry’ of anti-viral cells called effector cells, that counteract the virus. At the same time the body also keeps in reserve ‘troops’ of memory cells that can quickly turn into effector cells the next time the virus is encountered.

‘Our research found that there were significantly more effector cells among the diabetics than the healthy patients.’

Importantly, the differences were most pronounced the more recent the diabetic had been diagnosed.

Dr Peakman explains: ‘If the virus had nothing to do with the disease we would expect to find the same distribution of effector cells in healthy individuals and those with diabetes. But there were far more of these in the diabetics, suggesting they’d had a close and recent encounter with the CVB4 virus.’

This research is another piece of the jigsaw, says Dr Peakman, and it adds weight to a link between viruses and the development of diabetes. He hopes the study will open up new paths of research: firstly the mechanisms involved in the immune response; and secondly how we can prevent it or control it.

 *Dr Peakman’s paper is entitled: ‘Characterization of the T-cell Response to Coxsackievirus B4’, and is published in Diabetes: Vol 51, June 2002. The journal is published by the American Diabetes Association.  

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