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We analyze the nasal IFN-I\/III signature, namely the expression of ISGF-3\u2013dependent IFN-stimulated genes, in mildly symptomatic COVID-19 patients and show its correlation with serum IFN-\u03b12 levels, which peak at symptom onset and return to baseline from day 10 onward. Moreover, the nasal IFN-I\/III signature correlates with the nasopharyngeal viral load and is associated with the presence of infectious viruses. By contrast, we observe low nasal IFN-I\/III scores despite high nasal viral loads in a subset of critically ill COVID-19 patients, which correlates with the presence of autoantibodies (auto-Abs) against IFN-I in both blood and nasopharyngeal mucosa. In addition, functional assays in a reconstituted human airway epithelium model of SARS-CoV-2 infection confirm the role of such auto-Abs in abrogating the antiviral effects of IFN-I, but not those of IFN-III. Thus, IFN-I auto-Abs may compromise not only systemic but also local antiviral IFN-I immunity at the early stages of SARS-CoV-2 infection.<\/jats:p>","DOI":"10.1084\/jem.20211211","type":"journal-article","created":{"date-parts":[[2021,7,21]],"date-time":"2021-07-21T02:21:38Z","timestamp":1626834098000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":90,"title":["Early nasal type I IFN immunity against SARS-CoV-2 is compromised in patients with autoantibodies against type I IFNs"],"prefix":"10.1084","volume":"218","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3768-2378","authenticated-orcid":true,"given":"Jonathan","family":"Lopez","sequence":"first","affiliation":[{"name":"Molecular biology core facility, Civils Hospices of Lyon, Lyon Sud Hospital, Pierre-B\u00e9nite, France 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