This project aims to characterize the mitochondrial function in whole peripheral blood mononuclear cells (PBMCs) in ME/CFS.
We are testing for a modification of mitochondrial central carbon metabolism, known as the itaconate shunt. The itaconate shunt is a 4-step pathway induced by infection or injury and the immune system’s response to that insult. A central tenet of this hypothesis is that ME/CFS is initiated when the itaconate shunt, normally a temporary response of the innate immune system, becomes a chronic impairment of the tricarboxylic acid cycle (TCA) in affected cells.