“HHV-6 Mediated Mitochondrial Modulation and Its Association to ME/CFS”
PI: Bhupesh Prusty, PhD
University of Wuerzberg
Bhupesh Prusty (PhD), a molecular virologist at the University of Wuerberg, designed his Ramsay project to explore the hypothesis that mitochondrial dysfunction in ME/CFS has a pathogenic connection. He focused on HHV-6 (a herpesvirus that has been implicated in chronic conditions) based on his previous findings of HHV-6 activation and changes to mitochondria. Dr. Prusty and his collaborators honed an experimental system to study early stages of viral reactivation. Their work also points to a mechanism that accounts for how, even with a low number of copies of the virus in the blood, HHV-6-infected cells might still impact energy production in adjacent or distant cells through factors secreted in the blood plasma of ME/CFS patients.
Major Ramsay goals fulfilled:
✓ Added to the cumulative, scientific knowledge. The study “HHV-6 encoded small non-coding RNAs define an intermediate and early stage in viral reactivation” was published in Genomic Medicine. Read it here
✓ Bringing new researchers into the field. The Ramsay awards enabled an expert virologist to apply his skill to the field of ME/CFS.
In addition to contributing to ME/CFS research literature through his Ramsay project, Dr. Prusty also co-wrote a review on chronic viral infection in ME/CFS in the October 2018 edition of Translational Medicine, on behalf of the European Consortium (EUROMENE) on ME/CFS. The review surveyed studies on the potential role of various viruses and molecular mechanisms, including altered immune cells, changes in mitochondria, and autoimmunity in the development of ME/CFS. Advances in understanding the behavior of various pathogens caused the review authors to cast doubts over the validity of several past findings. However, the authors conclude there is evidence for a role of viral infection in at least a subgroup of ME/CFS patients. They recommend future strategies to improve studies through subtyping the patient population, standardization, the use of disease controls, and longitudinal data collection.