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Bhupesh Prusty

“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:

✓ Bringing new researchers into the field. The Ramsay awards enabled an expert virologist to apply his skill to the ME/CFS field.

✓ Added to the cumulative, scientific knowledge. The first study produced by this project titled “HHV-6 encoded small non-coding RNAs define an intermediate and early stage in viral reactivation” was published in Genomic Medicine. Read it here. Dr. Prusty, senior co-author Robert Naviaux, MD, PhD, and collaborators published a second paper in ImmunoHorizons showing a connection between HHV-6 reactivation, antiviral activity, and consequences to energy metabolism in ME/CFS. Co-authors include Philipp Schreiner, Stephanie Lamer and Andreas Schlosser, Julius-Maximilians University, Germany; Thomas Harrer, University of Erlangen-Nuremberg; and Carmen Scheibenbogen, Charite-Universitatsmedizin Berlin. Read the full paper here and a breakdown below.

 Publication in ImmunoHorizons
    >>> What you need to know

  • There is evidence that mitochondria play a key role in the cell’s antiviral response, in addition to producing energy for cells.
  • Dr. Prusty and colleagues previously found that a small bit of HHV-6A RNA (also found in other types of herpesvirus) is able to stop mitochondria from joining together to participate in antiviral defense. Increased fragmentation of mitochondria also reduces the respiratory capacity of the cell and produces lower levels of ATP.
  • The research team observed culture medium associated with HHV-6 reactivation caused mitochondria to fragment when it was applied to healthy cultured cells.
  • The research team also found that serum from ME/CFS patients (who fulfilled the Canadian Consensus Criteria) caused mitochondria to fragment when applied to healthy cell culture. Removal of the ME/CFS patients’ serum from the cells resulted in the mitochondria transforming back into an elongated form.
  • Dr. Prusty believes this model of HHV-6 reactivation causing mitochondrial dysfunction could apply to other pathogens associated with ME/CFS as well.
  • The findings are consistent with the cell danger response (CDR) theory, proposed by the study’s senior co-author Robert Naviaux, MD, PhD, which explains chronic disease as a consequence of disruptions to a natural process by which our mitochondria protect and defend themselves and our bodies from threats

Read the research team’s study abstract here
Read an interview with Dr. Prusty here

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. echoua 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.