NPJ genomic medicine · 2021
TBK1 and TNFRSF13B mutations and an autoinflammatory disease in a child with lethal COVID-19.
СтатьяНазвание и аннотация: Перевод в очереди
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Schmidt Axel, Peters Sophia, Knaus Alexej, Sabir Hemmen, Hamsen Frauke, Maj Carlo, Fazaal Julia, Sivalingam Sugirthan, Savchenko Oleksandr, Mantri Aakash, Holzinger Dirk, Neudorf Ulrich, Müller Andreas, Ludwig Kerstin U, Krawitz Peter M, Engels Hartmut, Nöthen Markus M, Bagci Soyhan
Аннотация
Among children, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections are typically mild. Here, we describe the case of a 3.5-year-old girl with an unusually severe presentation of coronavirus disease (COVID-19). The child had an autoinflammatory disorder of unknown etiology, which had been treated using prednisolone and methotrexate, and her parents were half cousins of Turkish descent. After 5 days of nonspecific viral infection symptoms, tonic-clonic seizures occurred followed by acute cardiac insufficiency, multi-organ insufficiency, and ultimate death. Trio exome sequencing identified a homozygous splice-variant in the gene TBK1, and a homozygous missense variant in the gene TNFRSF13B. Heterozygous deleterious variants in the TBK1 gene have been associated with severe COVID-19, and the variant in the TNFRSF13B gene has been associated with common variable immunodeficiency (CVID). We suggest that the identified variants, the autoinflammatory disorder and its treatment, or a combination of these factors probably predisposed to lethal COVID-19 in the present case.