%0 Journal Article
%T Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome.
%A Walitt B
%A Singh K
%A LaMunion SR
%A Hallett M
%A Jacobson S
%A Chen K
%A Enose-Akahata Y
%A Apps R
%A Barb JJ
%A Bedard P
%A Brychta RJ
%A Buckley AW
%A Burbelo PD
%A Calco B
%A Cathay B
%A Chen L
%A Chigurupati S
%A Chen J
%A Cheung F
%A Chin LMK
%A Coleman BW
%A Courville AB
%A Deming MS
%A Drinkard B
%A Feng LR
%A Ferrucci L
%A Gabel SA
%A Gavin A
%A Goldstein DS
%A Hassanzadeh S
%A Horan SC
%A Horovitz SG
%A Johnson KR
%A Govan AJ
%A Knutson KM
%A Kreskow JD
%A Levin M
%A Lyons JJ
%A Madian N
%A Malik N
%A Mammen AL
%A McCulloch JA
%A McGurrin PM
%A Milner JD
%A Moaddel R
%A Mueller GA
%A Mukherjee A
%A Muñoz-Braceras S
%A Norato G
%A Pak K
%A Pinal-Fernandez I
%A Popa T
%A Reoma LB
%A Sack MN
%A Safavi F
%A Saligan LN
%A Sellers BA
%A Sinclair S
%A Smith B
%A Snow J
%A Solin S
%A Stussman BJ
%A Trinchieri G
%A Turner SA
%A Vetter CS
%A Vial F
%A Vizioli C
%A Williams A
%A Yang SB
%A  
%A Nath A
%J Nat Commun
%V 15
%N 1
%D 2024 Feb 21
%M 38383456
%F 17.694
%R 10.1038/s41467-024-45107-3
%X 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.