Researchers at the University of Melbourne have identified a way that a rotavirus infection, often referred to as ‘stomach flu’, could contribute to the development of type 1 diabetes.
The discovery lends more weight to the possibility that certain viral infections could act as triggers for the condition in those already at risk.
It is already known that in mice that are genetically prone to developing type 1, infection with rotavirus can speed up the onset of the condition. In humans, a combination of a genetic predisposition and an infection from certain viruses (including enteroviruses like the Coxsackie B virus and rotavirus) is thought to increase a person’s risk for type 1 andJDRF researchers are trying to find out more about how this process could work.
The Australian team, led by Dr Barbara Coulson, aimed to expand on this knowledge by discovering the mechanism by which a rotavirus infection could affect the development of type 1 in mice.
They found that when certain immune cells encountered rotavirus, they activated B and T cells of the immune system – the cells that form the basis of our immune system’s response to infection.
The researchers found that exposure to rotavirus seemed to overstimulate the immune system, meaning that in addition to causing the body’s normal response to infection, it also triggered an ‘autoimmune’ response resulting in destruction of insulin-producing beta cells by a subset of T cells.
Coulson and colleagues at the University of Melbourne (pictured) believe that part of the reason this overstimulation occurs is due to a large increase in the amount of a protein called type I interferon. JDRF-funded researchers Ricardo Ferreira and John Todd previously found that genes activated by type I interferon could be implicated in the development of type 1 diabetes.
The researchers suggest future research into this protein could offer insights into the development of type 1 diabetes, saying that ‘the role of type 1 interferon signalling in diabetes acceleration following rotavirus infection deserves further analysis.’
Helen Albert, acting Head of Research Communication at JDRF, said: ‘This work adds weight to claims of a link between infection with certain viruses and development of type 1. Research such as this will help scientists understand more about how the condition develops and the best ways to prevent it developing in the first place.’
The research was published in the journal PLOS Pathogens.