the role of enteroviruses

The incidence of type 1 diabetes is increasing in many countries and this rise cannot be explained readily by changes in the genes that predispose to diabetes, since it is happening too quickly. Rather, it seems likely that one or more factors present in the environment is responsible for driving the increase. Among the various candidates, infection with viruses belonging to a family known as “enteroviruses” are prime suspects, since there is considerable epidemiological evidence linking exposure to these viruses with type 1 diabetes.

 

Based on such evidence, we have examined the pancreases of children who died shortly after developing type 1 diabetes and have discovered that some of the insulin-secreting beta cells appear to be infected with enterovirus. By contrast, enteroviral infection is seen only rarely in equivalent control pancreases from children who died without type 1 diabetes. These results are fully consistent with the idea that enteroviral infection may drive type 1 diabetes in, at least, some patients. We hypothesise that it may be the anti-viral response mounted by the beta-cells (rather than the infection per se) which serves to trigger islet cell autoimmunity and beta-cell loss.  Our current work is focused on developing our understanding of how the virus interacts with the host and vice versa. Through this work we expect to identify new pathways that might be targeted to minimise the development of autoimmunity in children who are at risk of developing type 1 diabetes in the future.

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