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

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

Funding
Grants and gifts supporting this work came from: plus "grassroots support from over 2000 individuals who have each provided gifts in the past year to support Naviaux laboratory and Prusty laboratory research".
 * 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.)

Results

 * 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"

Investigators

 * Philipp Schreiner
 * Thomas Harrer
 * Carmen Scheibenbogen
 * Stephanie Lamer
 * Andreas Schlosser
 * Robert Naviaux
 * Bhupesh Prusty

News coverage

 * Researchers describe an underlying biological basis for mylagic encephalomyelitis/chronic fatigue syndrome

Learn more

 * Press release: For ME/CFS Patients, Viral Immunities Come at a Devastating, Lifelong Cost
 * Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, and the Coordination of Antiviral and Metabolic Phenotypes in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (Full text)