Mitochondrial Dysfunction and Herpesviruses in ME/CFS

The lecture by Dr. Prusty addressed the relationship between mitochondrial dysfunction, herpesviruses and autoimmunity in ME/CFS and PCS. According to studies, autoantibodies against various herpes viruses were found in both patient groups, which indicates virus reactivation during SARS-CoV-2 infection. Dr. Prusty showed how certain viral proteins can trigger mitochondrial dysfunction. A current approach analysed 120 autoantibodies simultaneously and measured the immune response using immunoglobulins G and M (IgG/IgM). A higher IgM response was associated with increased ME/CFS symptom burden and greater sensitivity to non-self antigens (e.g., house dust mites, cat dander). In addition, there is evidence that the concentration of fibronectin in the blood and cells is increased in ME/CFS patients. This glycoprotein plays a role in blood clotting and tissue regeneration and acts as cell glue. Dr. Prusty suggested that the interplay of fibronectin and autoantibodies could explain a vicious cycle within cells involving mitochondrial fragmentation, endothelial dysfunction and microclotting in ME/CFS.