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Nature communications · 2024

Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome.

СтатьяПоддержка NIH: внешняя программаResearch Support, N.I.H., IntramuralНазвание и аннотация: Перевод в очереди
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Walitt Brian, Singh Komudi, LaMunion Samuel R, Hallett Mark, Jacobson Steve, Chen Kong, Enose-Akahata Yoshimi, Apps Richard, Barb Jennifer J, Bedard Patrick, Brychta Robert J, Buckley Ashura Williams, Burbelo Peter D, Calco Brice, Cathay Brianna, Chen Li, Chigurupati Snigdha, Chen Jinguo, Cheung Foo, Chin Lisa M K, Coleman Benjamin W, Courville Amber B, Deming Madeleine S, Drinkard Bart, Feng Li Rebekah, Ferrucci Luigi, Gabel Scott A, Gavin Angelique, Goldstein David S, Hassanzadeh Shahin, Horan Sean C, Horovitz Silvina G, Johnson Kory R, Govan Anita Jones, Knutson Kristine M, Kreskow Joy D, Levin Mark, Lyons Jonathan J, Madian Nicholas, Malik Nasir, Mammen Andrew L, McCulloch John A, McGurrin Patrick M, Milner Joshua D, Moaddel Ruin, Mueller Geoffrey A, Mukherjee Amrita, Muñoz-Braceras Sandra, Norato Gina, Pak Katherine, Pinal-Fernandez Iago, Popa Traian, Reoma Lauren B, Sack Michael N, Safavi Farinaz, Saligan Leorey N, Sellers Brian A, Sinclair Stephen, Smith Bryan, Snow Joseph, Solin Stacey, Stussman Barbara J, Trinchieri Giorgio, Turner Sara A, Vetter C Stephenie, Vial Felipe, Vizioli Carlotta, Williams Ashley, Yang Shanna B, Center for Human Immunology, Autoimmunity, and Inflammation (CHI) Consortium, Nath Avindra

Аннотация

Post-infectious myalgic encephalomyelitis/chronic fatigue syndrome (PI-ME/CFS) is a disabling disorder, yet the clinical phenotype is poorly defined, the pathophysiology is unknown, and no disease-modifying treatments are available. We used rigorous criteria to recruit PI-ME/CFS participants with matched controls to conduct deep phenotyping. Among the many physical and cognitive complaints, one defining feature of PI-ME/CFS was an alteration of effort preference, rather than physical or central fatigue, due to dysfunction of integrative brain regions potentially associated with central catechol pathway dysregulation, with consequences on autonomic functioning and physical conditioning. Immune profiling suggested chronic antigenic stimulation with increase in naïve and decrease in switched memory B-cells. Alterations in gene expression profiles of peripheral blood mononuclear cells and metabolic pathways were consistent with cellular phenotypic studies and demonstrated differences according to sex. Together these clinical abnormalities and biomarker differences provide unique insight into the underlying pathophysiology of PI-ME/CFS, which may guide future intervention.

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