Virus in Utero May Trigger Childhood Diabetes
Type 1 childhood diabetes has been increasing rapidly worldwide, but its exact cause has eluded scientists. Now, a new study from Tel Aviv University (TAU) suggests a possible trigger before birth.
If blood sugar levels aren't well-controlled, juvenile diabetes can affect nearly every organ of a child's body. And while long-term complications of the disease develop gradually, they can be disabling and even life-threatening.
A recent paper published in Diabetic Medicine presents evidence that Type 1 Diabetes is initiated in utero.
According to the research, women who contract a viral infection during pregnancy transmit viruses to their genetically susceptible fetuses, sparking the development of type 1 diabetes.
Professor Zvi Laron, professor emeritus of Pediatric Endocrinology at TAU's Sackler Faculty of Medicine, and director of the Endocrinology and Diabetes Research Unit at Schneider Children's Medical Center of Israel, as well as head of the World Health Organization (WHO) Collaborating Center for the Study of Diabetes in Youth, led the research in collaboration with an international team of researchers,
Prof. Laron is internationally known for the discovery of the Laron Syndrome, also known as Laron-type Dwarfism, an autosomal recessive disorder characterized by an insensitivity to growth hormone.
"We knew that type 1 diabetes is associated with other autoimmune diseases like Hashimoto Thyroiditis, celiac disease, and multiple sclerosis, so we investigated the season of birth for these diseases in Israel and other countries. We found that the season of the birth of children who went on to develop these diseases did indeed differ from that of the general public.
"In further studies, we found evidence that viral infections of the mother during pregnancy induced damage to the pancreas of the mother and/or her fetus, evidenced by specific antibodies including those affecting the pancreatic cells producing insulin," added Laron.
For the study, Prof. Laron and his team of researchers from Israel, the University of Washington, and Lund University, Sweden, conducted blood tests of 107 healthy pregnant women, testing for islet cell autoantibodies — evidence of diabetes years before initial symptoms.
Researchers found a striking link to winter epidemics between women tested throughout different seasons.
The presence of GAD65 antibodies in cord blood and mothers' blood indicated autoimmune damage to islet cells during gestation, possibly caused by placental transmission of viral infections or antivirus antibodies.
In other words, during viral epidemics in winter months, ten percent of healthy pregnant women who had no family background of autoimmune diseases still tested positive for autoimmune antibodies.
In addition, cord blood antibody concentrations which exceeded those of the corresponding maternal sample (and antibody-positive cord blood samples with antibody-negative maternal samples) implied a fetal immune response.
"If our hypothesis can be verified, then preventive vaccine before conception would be useful in stopping the increasing incidence of type 1 diabetes and other autoimmune diseases. There is no cure for this diabetes, so true intervention would be important not only medically but also psychologically and financially, as the costs for lifelong treatment of this chronic disease and other autoimmune diseases are great."
Zvi Laron, Professor Emeritus, Pediatric Endocrinology, TAU Sackler Faculty of Medicine, Director, Endocrinology and Diabetes Research, Schneider Children's Medical Center, Israel, head of World Health Organization Collaborating Center for the Study of Diabetes in Youth
Prof. Laron and his international collaborators are currently raising funds to expand their research to include nearly 1,000 women and their newborns.
To determine whether antivirus and/or islet cell antibodies can be detected in healthy pregnant mothers without diabetes and/or their offspring at birth in two winter viral seasons.
Maternal and cord blood sera from 107 healthy pregnant women were tested for islet cell autoantibodies using radioligand binding assays and for anti-rotavirus and anti-CoxB3 antibody using an enzyme-linked immunosorbent assay.
Glutamic acid decarboxylase (GAD)65 autoantibodies and rotavirus antibodies, present in both maternal and cord blood sera, correlated with an odds ratio of 6.89 (95% CI: 1.01–46.78). For five, 22 and 17 pregnancies, antibodies to GAD65, rotavirus and CoxB3, respectively, were detected in cord blood only and not in the corresponding maternal serum. In 10 pregnancies, rotavirus antibody titres in the cord blood exceeded those in the corresponding maternal serum by 2.5–5-fold. Increased antibody titres after the 20th week of gestation suggested CoxB3 infection in one of the 20 pregnancies and rotavirus in another.
The concurrent presence of GAD65 antibodies in cord blood and their mothers may indicate autoimmune damage to islet cells during gestation, possibly caused by cross-placental transmission of viral infections and/or antivirus antibodies. Cord blood antibody titres that exceed those of the corresponding maternal sample by >2.5-fold, or antibody-positive cord blood samples with antibody-negative maternal samples, may imply an active in utero immune response by the fetus.
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