Browsing by Author "Burbelo, Peter"

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    Autoantibodies Against Proteins Previously Associated With Autoimmunity in Adult and Pediatric Patients With COVID-19 and Children With MIS-C
    (2022) Burbelo, Peter; Castagnoli, Riccardo; Shimizu, Chisato; Delmonte, Ottavia; Dobbs, Kerry; Discepolo, Valentina; Lo Vecchio, Andrea; Guarino, Alfredo; Licciardi, Francesco; Ramenghi, Ugo; Rey, Emma; Vial, Cecilia; Marseglia, Gian; Licari, Amelia; Montagna, Daniela; Rossi, Camillo; Montealegre, Gina; Barron, Karyl; Warner, Blake; Chiorini, John; Espinosa, Yazmin; Noguera, Loreani; Dropulic, Lesia; Truong, Meng; Gerstbacher, Dana; Mató, Sayonara; Kanegaye, John; Tremoulet, Adriana; Pediatric Emergency Medicine Kawasaki Group; Eisenstein, Eli; Su, Helen; Imberti, Luisa; Poli, Cecilia; Burns, Jane; Notarangelo, Luigi; Cohen, Jeffrey
    The antibody profile against autoantigens previously associated with autoimmune diseases and other human proteins in patients with COVID-19 or multisystem inflammatory syndrome in children (MIS-C) remains poorly defined. Here we show that 30% of adults with COVID-19 had autoantibodies against the lung antigen KCNRG, and 34% had antibodies to the SLE-associated Smith-D3 protein. Children with COVID-19 rarely had autoantibodies; one of 59 children had GAD65 autoantibodies associated with acute onset of insulin-dependent diabetes. While autoantibodies associated with SLE/Sjögren's syndrome (Ro52, Ro60, and La) and/or autoimmune gastritis (gastric ATPase) were detected in 74% (40/54) of MIS-C patients, further analysis of these patients and of children with Kawasaki disease (KD), showed that the administration of intravenous immunoglobulin (IVIG) was largely responsible for detection of these autoantibodies in both groups of patients. Monitoring in vivo decay of the autoantibodies in MIS-C children showed that the IVIG-derived Ro52, Ro60, and La autoantibodies declined to undetectable levels by 45-60 days, but gastric ATPase autoantibodies declined more slowly requiring >100 days until undetectable. Further testing of IgG and/or IgA antibodies against a subset of potential targets identified by published autoantigen array studies of MIS-C failed to detect autoantibodies against most (16/18) of these proteins in patients with MIS-C who had not received IVIG. However, Troponin C2 and KLHL12 autoantibodies were detected in 2 of 20 and 1 of 20 patients with MIS-C, respectively. Overall, these results suggest that IVIG therapy may be a confounding factor in autoantibody measurements in MIS-C and that antibodies against antigens associated with autoimmune diseases or other human proteins are uncommon in MIS-C.
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    Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome
    (2024) Walitt, Brian; Singh, Komudi; LaMunion, Samuel; Hallett , Mark; Jacobson, Steve; Chen, Kong; Enose-Akahata, Yoshimi; Apps, Richard; Barb, Jennifer; Bedard, Patrick; Brychta, Robert; Buckley, Ashura; Burbelo, Peter; Calco, Brice; Cathay, Brianna; Chen, Li; Chigurupati, Snigdha; Chen, Jinguo; Cheung, Foo; Chin, Lisa; Coleman, Benjamin; Courville, Amber; Deming, Madeleine; Drinkard, Bart; Feng, Li; Ferrucci, Luigi; Gabel, Scott; Gavin, Angelique; Goldstein, David; Hassanzadeh, Shahin; Horan, Sean; Horovitz, Silvina; Johnson, Kory; Govan, Anita; Knutson, Kristine; Kreskow, Joy; Levin, Mark; Lyons, Jonathan; Madian, Nicholas; Vial Undurraga, Felipe
    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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