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Abers, Michael S; Rosen, Lindsey B; Delmonte, Ottavia M; Shaw, Elana; Bastard, Paul; Imberti, Luisa; Quaresima, Virginia; Biondi, Andrea; Bonfanti, Paolo; Castagnoli, Riccardo; Casanova, Jean-Laurent; Su, Helen C; Notarangelo, Luigi D; Holland, Steven M; Lionakis, Michail S
Immunology and cell biology, October 2021, Volume: 99, Issue: 9Journal Article
Type-I interferons (IFNs) mediate antiviral activity and have emerged as important immune mediators during coronavirus disease 19 (COVID-19). Several lines of evidence suggest that impaired type-I IFN signaling may predispose to severe COVID-19. However, the pathophysiologic mechanisms that contribute to illness severity remain unclear. In this study, our goal was to gain insight into how type-I IFNs influence outcomes in patients with COVID-19. To achieve this goal, we compared clinical outcomes between 26 patients with neutralizing type-I IFN autoantibodies (AAbs) and 192 patients without AAbs who were hospitalized for COVID-19 at three Italian hospitals. The presence of circulating AAbs to type-I IFNs was associated with an increased risk of admission to the intensive care unit and a delayed time to viral clearance. However, survival was not adversely affected by the presence of type-I IFN AAbs. Our findings provide further support for the role of type-I IFN AAbs in impairing host antiviral defense and promoting the development of critical COVID-19 pneumonia in severe acute respiratory syndrome coronavirus 2-infected individuals.
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