The most common cause of severe diarrhea in children, the rotavirus infection, has been shown to accelerate the development of type 1 diabetes in mice, according to new University of Melbourne research.
The study, published today in PLOS Pathogens, explored the ways the rotavirus infection contributes to autoimmune disease in mice, and researchers believe the breakthrough could be relevant to human infection with rotavirus.
The research found that it may be the "bystander effect" that causes the rotavirus infection to accelerate the onset of type 1 diabetes. The "bystander effect" suggests that the virus provokes a strong activation of the immune system, which then spills over, allowing the immune system to attack not only the viral intruder but some of the body's own cells, in this case the insulin-producing cells in the pancreas.
Lead researcher Associate Professor Barbara Coulson from the Peter Doherty Institute for Infection and Immunity said the research was the first to find that rotavirus activates this type of immune response in mice.
"This bystander mechanism provides a potential explanation for the acceleration of type 1 diabetes development by rotavirus infection in mice."
"It is possible that the same process could operate following human rotavirus infection, and lead to a more rapid progression of children towards type 1 diabetes. Further studies are needed to determine the relevance of our findings to humans," she said.
"Ultimately, this should help us understand the link between virus infection and the development of type 1 diabetes."
"Understanding how rotavirus affects human type 1 diabetes development is expected to facilitate the implementation of preventative treatment for children at risk this disease. For example, treatments that dampen down the particular type of immune response caused by rotavirus may be beneficial," she concluded.
- Jessica A. Pane, Nicole L. Webster, Barbara S. Coulson. Rotavirus Activates Lymphocytes from Non-Obese Diabetic Mice by Triggering Toll-Like Receptor 7 Signaling and Interferon Production in Plasmacytoid Dendritic Cells. PLoS Pathogens, 2014; 10 (3): e1003998 DOI: 10.1371/journal.ppat.1003998
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