Viral “cleanliness” ties to type-1 diabetes in groundbreaking new research… more viral diversity LOWERS risk
09/06/2017 // Amy Goodrich // Views

Type 1 diabetes is a chronic autoimmune disease in which a patient’s own immune system attacks and destroys the cells needed to produce insulin to control blood-sugar levels. Doctors often diagnose this type of diabetes in childhood or early adulthood. Though the exact cause of Type 1 diabetes is unknown, new research has suggested viruses in the gut could play an important role.

A team of researchers from the Washington University School of Medicine in St. Louis, led by Professor Herbert Virgin and Dr. Guoyan Zhao, has found that certain viruses in the gut could make a person more susceptible to develop Type 1 diabetes.

The study, partly funded by the Type 1 diabetes charity JDRF, was published earlier this month in the online journal Proceedings of the National Academy of Sciences of the United States of America (PNAS).

Connection between intestinal viruses and Type 1 diabetes

For the study, the team used stool samples of a previous study — by Mikael Knip, M.D., Ph.D, of the University of Helsinki, and Ramnik Xavier, M.D., Ph.D, of Massachusetts General Hospital and Harvard Medical School — in which they analyzed the bacterial gut flora of 33 children who carried genes that increase the risk of developing Type 1 diabetes.

Every month the researchers collected stool samples from these children from birth to the age of three. Furthermore, the researchers monitored the children for the development of auto-antibodies that attack insulin-producing cells in the pancreas and Type 1 diabetes. In conclusion, the team reported significant alterations in the diversity of bacterial species in the gut before diagnosis. This study, however, only looked at bacteria in the gut — not viruses.

Brighteon.TV

Building on these results, Professor Herbert Virgin and Dr. Guoyan Zhao carefully selected 11 children who acquired auto-antibodies (five of them developed Type 1 diabetes) and 11 children who did not develop auto-antibodies or the disease.

Using the same samples, the team analyzed the viruses that were present in monthly stool samples of these 22 children. They found that children whose viral communities in the gut were less diverse were more likely to generate self-destructive antibodies that can lead to Type 1 diabetes.

One virus may offer protection against the disease, while others may increase the diabetes risk

Furthermore, the team discovered a specific virus belonging to the Circoviridae family, which is harmless in humans, that seems to have protective effects. Children who carried the virus were less likely to develop the disease later in life.

The researchers also identified another group of viruses, called bacteriophages. These viruses can infect certain bacteria in the gut. When children were carrying bacteriophages that targeted one of the major groups of intestinal bacteria (Bacteroides), the researchers reported an increased risk of developing antibodies and Type 1 diabetes.

"We identified one virus that was significantly associated with reduced risk and another group of viruses that was associated with increased risk of developing antibodies against the children's own cells," said Professor Herbert Virgin, the study's senior author. "It looks like the balance of these two groups of viruses may control the risk of developing the antibodies that can lead to Type 1 diabetes."

He added that there are many autoimmune diseases these days which could be due to the fact that we made ourselves unhealthy by not having the right viruses in our gut.

Though the results look promising, more research is needed to confirm these early results and determine whether viruses can prevent Type 1 diabetes. Therefore, Virgin and Zhao have begun animal studies to understand what effect circoviruses have on the immune system. Additionally, they also want to see if they can replicate the findings in another group of children.

Find more diabetes-related news at DiabetesScienceNews.com.

Sources include:

ScienceDaily.com

PNAS.org

JDRF.org.uk

HealthLine.com



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