Infectious Triggers and Mitochondrial Dysfunction in ME/CFS

Project description

Human herpesvirus 6 (HHV-6), human herpesvirus 7 (HHV-8 and Epstein-Barr virus (EBV) have all been implicated as potential infectious triggers of ME/CFS. One way in which viral infection may lead to the development of physical fatigue is through alterations to the mitochondria. The mitochondria are responsible for generating energy in the cells of the body, including in the skeletal muscles. An abnormality in energy production in muscle cells has been suggested as a possible cause of the muscle fatigue experienced by people with ME/CFS.

Viral infection will result in a protective immune response, but this immune response may also cause damage to the mitochondria. While there is evidence for this link, the exact mechanism involved is not known. And this is where Dr Prusty’s new study comes in. Dr Bhupesh Prusty is a well-established researcher at the Julius Maximilian University of Würzburg, who has been particularly interested in human herpesviruses – specifically the mechanisms underlying the reactivation of these viruses, their impact on the mitochondria, and their potential role in diseases including ME/CFS. Dr Prusty’s hypothesis is that the changes to the mitochondria seen in people with ME/CFS may be due to a number of possible factors transferred in the blood plasma, and this has been backed up by some of his previous research.

The aim of Dr Prusty’s new study is to identify and characterise some of these factors in blood samples from ME/CFS patients and healthy control subjects, and to look at the potential effects of these factors on mitochondrial function. He also plans to look at how primary viral infections might cause reactivation of latent viruses. The results will hopefully lead to a better understanding of the mechanisms leading to mitochondrial dysfunction in ME/CFS, and may help in the development of new treatments.

(Description adapted from project website: see link above)