A new study in the journal PLOS Pathogens examines how rotavirus infection contributes to autoimmune (type 1) diabetes.
The researchers, from the University of Melbourne in Australia, observed the mechanisms by which rotavirus speeds up onset of type 1 diabetes in mice.
To do this, they induced "bystander activation" in non-obese diabetic mice. This is when a virus provokes such a strong reaction from the immune system that immune cells begin attacking not only the virus, but also the body's own cells - such as the insulin-producing islet cells in the pancreas.
When the rotavirus was introduced to the mice's spleen cells, two types of immune cells were activated - antibody-producing B cells and "dendritic cells," which are an important component of a coordinated immune response.
The researchers found that this activation includes a process of "unpacking" the virus - which exposes its viral immune activators.
A chain of activation sparked by the rotavirus from a specific form of dendritic cell and on to T cells would then cause the T cells to recognize and destroy the insulin-producing islet cells. This destruction of the islet cells is what causes type 1 diabetes.
Type 1 interferon role 'deserves further analysis'
The dendritic cells were also shown to produce very high levels of the immune modulator type 1 interferon, which seems to mediate the bystander effect - in a sense, connecting the rotavirus infection to the cell destruction that causes accelerated diabetes.
"The role of type 1 interferon signaling in diabetes acceleration following rotavirus infection deserves further analysis," say the researchers, who believe that their findings on immune cells and interferon should be investigated in humans.
- Type 1 diabetes can happen at any age, but occurs most often in children and young adults
- People confirmed as having type 1 diabetes will have to take insulin for the rest of their life
- There is no screening test that can detect type 1 diabetes in people who do not have any symptoms.
"Understanding how viruses contribute to type 1 diabetes development is vital for disease prevention," they write in a summary of their research.
"Infection of children at-risk of diabetes with the gastrointestinal pathogen rotavirus is associated with increased immune responses to pancreatic islets, leading to the proposal that rotavirus infection may accelerate progression to diabetes."
Having displayed how this mechanism operates in a mouse model, they conclude that "a similar mechanism may be involved in the enhanced islet autoantibody responses of children following rotavirus infection."
Last year, a team from Stanford University School of Medicine in California also reported some success in a small trial of a "reverse" vaccine for type 1 diabetes.
What makes this "reverse" vaccine different from conventional vaccines is that, rather than being designed to boost the immune response to a protein delivered by the vaccine, the new kind of vaccine instructs the host's body to shut down the immune system when it encounters a specific gene.