New understanding of the role viruses play in the development of autoimmune diseases

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Researchers at the La Jolla Institute for Allergy & Immunology have added a significant milestone to scientific understanding of the role viruses play in the development of autoimmune diseases, such as diabetes.

Matthias von Herrath, M.D., and a team of scientists found that while viruses alone do not initiate autoimmune diseases, they can accelerate their development when paired with a genetic predisposition to autoimmune diseases.

This discovery, based on controlled laboratory studies of mice, represents the first demonstration in a living organism of the ability of viruses to increase the likelihood of the development of autoimmune diseases. The finding is an important advance and could help in the future development of therapies for the treatment or prevention of diabetes and other autoimmune illnesses.

The finding was published Monday in a scientific paper in the Journal of Clinical Investigation entitled "A Viral Epitope that Mimics a Self Antigen Can Accelerate But Not Initiate Autoimmune Diabetes." In autoimmune diseases, the immune system, which normally wards off invading viruses and bacteria, instead mistakenly attacks normal body tissues, leading to illness. Dr. von Herrath's study dealt with the autoimmune form or type I diabetes, but the findings can also be applied to other autoimmune diseases. Examples of other autoimmune diseases include lupus or SLE, multiple sclerosis (MS), and rheumatoid arthritis.

Dr. von Herrath's research focused on a concept known as "molecular mimicry" or cross-reactivity. This occurs when the body¡¦s immune system recognizes not only part of a virus, but also a molecule in the body that looks very similar, and begins attacking cells that have that molecule assuming it is an actual virus. "We knew from evidence that cross-reactivity is common, but what we didn't know was whether that could actually accelerate the development of autoimmune disease in some individuals," said Dr. von Herrath, adding that it has long been theorized to play a role. "We found that it is unlikely that this cross-reactivity causes disease in someone who is not genetically predisposed to an autoimmune disease," he said. "However, if you superimpose cross-reactivity to a virus onto a genetic predisposition to an autoimmune disease, then it is much more likely that you'll develop the disease, and it happens faster."

Dr. von Herrath said the finding opens the door to further research to find associations between certain viruses and certain genetic predispositions to autoimmune diseases. He said this could shape large scale clinical studies of people with existing autoimmune diseases, to identify - through their medical histories -- which viruses, when paired with which genetic predispositions, can cause certain autoimmune diseases to erupt.

Mitchell Kronenberg, Ph.D., LIAI President and Scientific Director, said the finding has major implications for future advancements in protecting people from autoimmune diseases. "By building on this research, we may one day be able to advise people genetically predisposed to multiple sclerosis, for instance, to avoid certain viruses or bacteria or to be vaccinated against them in order to prevent actual development of autoimmune disease," he said.

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