A Short Corticosteroid Course Reduces Symptoms and Immunological Alterations Underlying Long-COVID

Despite the growing number of patients with persistent symptoms after acute SARS-CoV-2 infection, the pathophysiology underlying long-COVID is not yet well characterized, and there is no established therapy. We performed a deep immune profiling in nine patients with persistent symptoms (PSP), before...

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Detalles Bibliográficos
Autores: Utrero Rico, Alberto, Ruiz Ruigómez, María, Laguna Goya, Rocío, Arrieta Ortubay, Estíbaliz, Chivite Lacaba, Marta, González Cuadrado, Cecilia, Lalueza Blanco, Antonio, Almendro Vázquez, Patricia, Serrano, Antonio, Aguado García, José María, Lumbreras Bermejo, Carlos Juan, Paz Artal, Estela Natividad
Tipo de recurso: artículo
Fecha de publicación:2021
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/4651
Acceso en línea:https://hdl.handle.net/20.500.14352/4651
Access Level:acceso abierto
Palabra clave:Long-COVID
Immunological alterations
Corticosteroids
Inmunología
2412 Inmunología
Descripción
Sumario:Despite the growing number of patients with persistent symptoms after acute SARS-CoV-2 infection, the pathophysiology underlying long-COVID is not yet well characterized, and there is no established therapy. We performed a deep immune profiling in nine patients with persistent symptoms (PSP), before and after a 4-day prednisone course, and five post-COVID-19 patients without persistent symptoms (NSP). PSP showed a perturbed distribution of circulating mononuclear cell populations. Symptoms in PSP were accompanied by a pro-inflammatory phenotype characterized by increased conventional dendritic cells and augmented expression of antigen presentation, co-stimulation, migration, and activation markers in monocytes. The adaptive immunity compartment in PSP showed a Th1-predominance, decreased naïve and regulatory T cells, and augmentation of the PD-1 exhaustion marker. These immune alterations reverted after the corticosteroid treatment and were maintained during the 4-month follow-up, and their normalization correlated with clinical amelioration. The current work highlights an immunopathogenic basis together with a possible role for steroids in the treatment for long-COVID.

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