Type 1 diabetes is an autoimmune condition affecting more than 18,000 young people each year. New research investigates the link between the disease and a type of enterovirus infection in children.
The Centers for Disease Control and Prevention (CDC)
According to the CDC, more than 18,000 young people were reportedly diagnosed with T1D each year in 2008 and 2009.
The condition is typically diagnosed in young children and adults, and it occurs when the body’s immune system does not recognize its own insulin-producing beta cells. Instead, it attacks and damages them.
The body needs insulin to turn the glucose in its bloodstream into energy.
T1D can be detected before it enters its clinical stage by identifying the autoantibodies that attack the beta cells.
The findings were published in Diabetologia, the journal of the European Association for the Study of Diabetes.
The team – led by Prof. Heikki Hyöty and Dr. Hanna Honkanen – analyzed a total of 1,673 stool samples from 129 children who had tested positive for islet autoantibodies, and another 3,108 stool samples from a control group of 282 children who were only screened for enterovirus.
All the stool samples were tested for the presence of the virus RNA using reverse transcription polymerase chain reaction.
Of the 282 control children, 169 turned out to have the enteroviral infection. By contrast, from the 129 case children, 108 went on to develop infections. This amounts to a mean of 0.6 infections per child in the control group versus a mean of 0.8 infections per child in the case children.
In other words, children with T1D had three times more enteroviral infections than control children.
Using a prospective birth cohort enabled the researchers to analyze the associations between enterovirus infections and the beginning of the beta cell-damaging process within a specific time frame. This helped account for time-dependent variables.
The scientists were therefore able to notice the difference in infections even before the autoantibodies appeared. Prior to the autoantibodies, the difference was between 0.4 infections per child in the control group, compared with 0.6 in the case group.
In fact, the time-dependent analysis revealed that the infection excess had occurred more than 12 months before the first detection of islet autoantibodies.
The enterovirus types most frequently encountered were coxsackievirus A4 (accounting for 28 percent of the genotyped viruses), coxsackievirus A2, (which made up 14 percent of the viruses), and coxsackievirus A16 (which represented 11 percent of the viruses).
The authors point out that this is the largest study to date that has analyzed enteroviruses in longitudinal stool samples of children who showed signs of a beta cell-damaging process at the time of the observation.
However, they also point out some of the study’s limitations. For example, being restricted to one country means that the results may not be generalizable to other populations. Furthermore, the study did not take respiratory samples, which might have helped to detect some enteroviruses with higher accuracy.
Dr. Honkanen and team conclude:
“The present study suggests that enterovirus infections in young children are associated with the appearance of islet autoantibodies with a time lag of about 1 year. This finding supports previous observations from other prospective studies suggesting that enterovirus infections may play a role in the initiation of the beta cell-damaging process.”
Finally, the authors highlight the “crucial” importance of systematic enterovirus screening for developing a vaccine against these viruses.
“It will also be important to explore the possibility of creating a vaccine against these viruses to find out whether it could prevent type 1 diabetes,” the researchers add.