More about Type 1 Diabetes and pathogenic HERV-W 

Type 1 Diabetes (T1D) is a chronic disease resulting from the autoimmune destruction of the insulin-producing beta cells in the pancreas. As a consequence, the pancreas is no more able to produce insulin in response to increasing glucose levels in blood and T1D patients become hyperglycemic. Lifelong insulin replacement therapy is the only option for these patients to control their glycemia, as there is currently no cure for T1D. Despite improvements in insulin replacement therapy in the past decades, normoglycemia is rarely achieved by T1D patients. The absence of proper glycemia control is associated mortality and severe complications, including diabetic retinopathy, nephropathy, foot ulceration and diabetic neuropathy.

Geneuro has shown using immunodetection methods that pHERV-W-Env protein is present in the pancreas of T1D patients. Immune cells of these patients also express pHERV-W-Env mRNA. Transgenic mice expressing pHERV-W-env have been shown to display abnormalities in glucose regulation, including hyperglycemia and reduced levels of insulin. In vitro experiments on human pancreatic beta cells have demonstrated a toxic effect of pHERV-W-Env, which inhibits insulin secretion in response to glucose. This pathogenic effect can be blocked with temelimab. Overall, Geneuro has shown (1) significant expression of pHERV-W-Env in T1D patients, (2) the pathogenic effect of pHERV-W-Env in diabetic models, and (3) the positive effect of temelimab on diabetic models.