Guisad-Hernandez, PalomaBlanco-Lobo, PilarVillaoslada, Isabelde-Felipe, BeatrizLucena, Jose MMartin-Gutierrez, GuillermoCastro, María JoseGutierrez-Valencia, AliciaSanchez-Codez, Maria IsabelGaboli, MirellaNeth, OlafOlbrich, Peter2023-02-092023-02-092021-06-09Guisado Hernández P, Blanco Lobo P, Villaoslada I, de Felipe B, Lucena JM, Martín Gutierrez G, et al. SARS-CoV-2 infection in a pediatrics STAT1 GOF patient under Ruxolitinib therapy-a matter of balance? J Clin Immunol. 2021 Oct;41(7):1502-1506.http://hdl.handle.net/10668/17982Recently, 94 inborn errors of immunity (IEI) patients suffering from COVID-19 have been described, overall demonstrating a mild phenotype [1] although more severe disease manifestations have been suggested for patients with alterations in the interferon (IFN) signaling pathway, including auto-antibodies against type I IFN [2]. Patients with STAT1 GOF mutations show a complex and often severe phenotype, combining an increased susceptibility of fungal, (myco-) bacterial and viral infections as well as autoimmune and autoinflammatory manifestations [3]. Characteristically, in response to type I and type II IFN stimulation, these patients show STAT1 hyperphosphorylation [3, 4]. Whether in the context of SARS-CoV-2 infection, the hyperactivation of the IFN-JAK1/2-STAT1 pathway would be protective (antiviral effect) or deleterious (hyperinflammation) is unclear. Ruxolitinib (a selective JAK1/2 inhibitor) has been successfully used in STAT1 GOF patients controlling many disease manifestations [5] and also resulted in improved pulmonary function and faster recovery from lymphopenia in previously healthy individuals suffering from severe COVID-19enCOVID-19Interferon-Stimulated Gene Factor 3PyrazolesCOVID-19 Drug TreatmentChildFemaleHumansJanus KinasesMutationNitrilesPyrimidinesSARS-CoV-2Severity of Illness IndexSARS-CoV-2 infection in a pediatrics STAT1 GOF patient under Ruxolitinib therapy-a matter of balance?letter to the editor34109505Restricted AccessCOVID-19MutaciónSARS-CoV-2LinfopeniaVirosisInterferonesInsuficiencia multiorgánicaAntineoplásicos inmunológicosDiabetes mellitus tipo 210.1007/s10875-021-01081-91573-2592PMC8189704https://link.springer.com/content/pdf/10.1007/s10875-021-01081-9.pdfhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8189704/pdf