Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, and the Coordination of Antiviral and Metabolic Phenotypes in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

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Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, and the Coordination of Antiviral and Metabolic Phenotypes in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Funding[edit | edit source]

Grants and gifts supporting this work came from:

  • Solve ME/CFS Initiative (Ramsay Research Award)
  • HHV-6 Foundation (to B.K.P.)
  • the University of California San Diego Christini Fund
  • Lennox Foundation
  • JMS Fund
  • Khosla Foundation
  • Westreich Foundation,
  • Malone Foundation (to R.K.N.)

plus "grassroots support from over 2000 individuals who have each provided gifts in the past year to support Naviaux laboratory and Prusty laboratory research".[1]

Results[edit | edit source]

  • HHV-6 reactivation was shown to cause mitochondria dysfunction in patients with ME/CFS
  • antiviral activity was found in the blood serum of patients with ME/CFS
  • the antiviral activity was "tightly associated with an activity that fragments the mitochondrial network and decreases cellular energy (ATP) production"

Criticism[edit | edit source]

Investigators[edit | edit source]

Commentary[edit | edit source]

This paper will be a paradigm shift in our understanding of potential infectious causes behind ME/CFS. Human herpesvirus 6 and HHV-7 have long been thought to play a role in this disease, but there was hardly any causative mechanism known before — Bhupesh Prusty

News coverage[edit | edit source]

See also[edit | edit source]

Learn more[edit | edit source]

References[edit | edit source]