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Viruses May Cause T1D and Other Autoimmune Diseases

Viruses are the cause of many health conditions and affect the body in different ways. As scientists learn more about these viruses, they can develop targeted strategies for preventing and treating them. A major breakthrough was recently discovered involving a very common virus known as the Epstein-Barr Virus or EBV.

EBV is most commonly known for causing mononucleosis (mono) or the “kissing disease” since it is often transmitted via saliva. By age 20, more than 90 percent of the population in developed countries will be infected by the disease. This rate spikes in under-developed countries with more than 90 percent of the population being affected by age 2. There is no cure for the virus – it remains in the body for life, though may not have a noticeable impact.

However, researchers have found that the effect it can have at a cellular level may be more significant than previously realized. Scientists from the Cincinnati Children’s Hospital’s Center for Autoimmune Genomics and Etiology have published a study potentially linking EBV to seven diseases, including T1D. One of the Diabetes Research Connection’s own Scientific Review Committee members, Matthias Von Herrath, was an author on an article cited by the study in its research.

Typically, the body responds to viruses by increasing the production of antibodies by B cells. These antibodies then attack and destroy the virus. However, with EBV, the virus actually takes over the B cells and re-programs them using transcription factors. This alters the way that B cells respond and can change their basic function, which may increase the risk of developing other diseases. The scientists have narrowed it down to one factor in particular – the EBNA2 protein.

Transcription factors associated with this protein attach to and change sections of person’s genetic code. Depending on where they attach, it could contribute to different diseases including T1D, lupus, multiple sclerosis, rheumatoid arthritis, celiac disease, and more. Identifying what is happening on a cellular level could help researchers to develop more targeted treatment options and potential cures for these diseases. The study also opens doors for more in-depth research regarding how transcription factors may affect other gene variants and diseases.

These findings are very encouraging in better understanding some of the underlying factors that may contribute to T1D. More research is necessary to explore each disease in particular and the potential impact from EBV and the EBNA2 protein. The Diabetes Research Connection is excited to see where these discoveries may lead moving forward and how it could change the future of T1D treatment. The DRC provides funding to early-career scientists pursuing novel research studies on type 1 diabetes to improve prevention strategies, treatment options, and management techniques as well as potentially find a cure. Learn more about current projects and provide support by visiting http://diabetesresearchconnection.org.

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Could Viruses Play a Role in the Development of Type 1 Diabetes?

While researchers know that type 1 diabetes involves the destruction of insulin-producing beta cells or lack of production of insulin, they are still not clear on exactly what causes type 1 diabetes to develop. A great deal of time has been devoted to studying genetics and the role it may play in T1D risk. Now scientists are exploring a different avenue – the influence of viruses on diabetes risk.

A recent study led by Professor Ronald Kahn, chief academic officer at Joslin Diabetes Center, identified four viruses that can produce insulin-like hormones. These viruses were found to “produce peptides that are similar in whole or in part to 16 human hormones and regulatory proteins.” While these viruses are found in fish and amphibians, not humans, eating fish may expose the human body to the viruses and therefore have an effect.

Scientists synthesized these peptides and conducted experiments on mice and human cells to determine how they would respond. The viral insulin-like peptides (VILPs) acted like hormones, attached to human insulin receptors, and stimulated the same signaling pathways. In addition, mice were found to have lower levels of blood glucose after being exposed to the VILPs.

According to Kahn, these research findings could lead to new studies regarding type 1 diabetes and autoimmunity. The insulin-like hormones “could be an environmental trigger to start the autoimmune reaction in type 1 diabetes.” However, there is the possibility that they could work as a protective factor as well by desensitizing the immune response.

There are more than 300,000 viruses carried by mammals, but only about 7,500 have been sequenced so far, so there is the possibility that other viruses exist that may affect human cells and T1D risk as well. This study is just the start of understanding the role of microbes in human disease according to Dr. Emrah Altindis who also works at the Joslin Diabetes Center.

The depth and breadth of understanding regarding type 1 diabetes and various aspects of the disease is expanding every day. The Diabetes Research Connection is committed to supporting peer-reviewed, novel research studies that aim to improve diagnosis, treatment, and quality of life for individuals living with T1D.  Through donations from individuals, companies, and foundations, the DRC provides funding to early career scientists to pursue innovative projects. Learn more about current projects and how to support these efforts by visiting http://diabetesresearchconnection.org.

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See our approved research projects and campaigns.

Role of the integrated stress response in type 1 diabetes pathogenesis
In individuals with type 1 diabetes (T1D), the insulin-producing beta cells are spontaneously destroyed by their own immune system. The trigger that provokes the immune system to destroy the beta cells is unknown. However, accumulating evidence suggest that signals are perhaps first sent out by the stressed beta cells that eventually attracts the immune cells. Stressed cells adapt different stress mitigation systems as an adaptive response. However, when these adaptive responses go awry, it results in cell death. One of the stress response mechanisms, namely the integrated stress response (ISR) is activated under a variety of stressful stimuli to promote cell survival. However, when ISR is chronically activated, it can be damaging to the cells and can lead to cell death. The role of the ISR in the context of T1D is unknown. Therefore, in this DRC funded study, we propose to study the ISR in the beta cells to determine its role in propagating T1D.
Wearable Skin Fluorescence Imaging Patch for the Detection of Blood Glucose Level on an Engineered Skin Platform
A Potential Second Cure for T1D by Re-Educating the Patient’s Immune System
L Ferreira
Validating the Hypothesis to Cure T1D by Eliminating the Rejection of Cells From Another Person by Farming Beta Cells From a Patient’s Own Stem Cells
Han Zhu
Taming a Particularly Lethal Category of Cells May Reduce/Eliminate the Onset of T1D
JRDwyer 2022 Lab 1
Can the Inhibition of One Specific Body Gene Prevent Type 1 Diabetes?
Is Cholesterol Exacerbating T1D by Reducing the Functionality and Regeneration Ability of Residual Beta Cells?
Regeneration Ability of Residual Beta Cells
A Call to Question… Is T1D Caused by Dysfunctionality of Two Pancreatic Cells (β and α)?
Xin Tong
Novel therapy initiative with potential path to preventing T1D by targeting TWO components of T1D development (autoimmune response and beta-cell survival)
flavia pecanha