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{"family": "Viari", "given": "Alain", "initials": "A", "orcid": "0000-0002-1329-7777", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/14f23d7c2d674af485440e138e16c6ac.json"}}, {"family": "Sanlaville", "given": "Damien", "initials": "D"}, {"family": "Schneider", "given": "Francis", "initials": "F"}, {"family": "Sibilia", "given": "Jean", "initials": "J"}, {"family": "Tharaux", "given": "Pierre-Louis", "initials": "PL", "orcid": "0000-0002-6062-5905", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1b2bbd265db948d08fd12f4f96b0c344.json"}}, {"family": "Casanova", "given": "Jean-Laurent", "initials": "JL", "orcid": "0000-0002-7782-4169", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/264335517ad94440b23a027fe66f767d.json"}}, {"family": "Hansmann", "given": "Yves", "initials": "Y", "orcid": "0000-0001-8903-0027", "researcher": {"href": 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"0000-0002-6928-9952", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d29138174e8c45d8ab9278777ee0e2d1.json"}}], "type": "journal article", "published": "2022-01-19", "journal": {"title": "Sci Transl Med", "issn": "1946-6242", "volume": "14", "issue": "628", "pages": "eabj7521", "issn-l": "1946-6234"}, "abstract": "The drivers of critical coronavirus disease 2019 (COVID-19) remain unknown. Given major confounding factors such as age and comorbidities, true mediators of this condition have remained elusive. We used a multi-omics analysis combined with artificial intelligence in a young patient cohort where major comorbidities were excluded at the onset. The cohort included 47 \u201ccritical\u201d (in the intensive care unit under mechanical ventilation) and 25 \u201cnon-critical\u201d (in a non-critical care ward) patients with COVID-19 and 22 healthy individuals. The analyses included whole-genome sequencing, whole-blood RNA sequencing, plasma and blood mononuclear cell proteomics, cytokine profiling, and high-throughput immunophenotyping. An ensemble of machine learning, deep learning, quantum annealing, and structural causal modeling were used. Patients with critical COVID-19 were characterized by exacerbated inflammation, perturbed lymphoid and myeloid compartments, increased coagulation, and viral cell biology. Among differentially expressed genes, we observed up-regulation of the metalloprotease ADAM9. This gene signature was validated in a second independent cohort of 81 critical and 73 recovered patients with COVID-19 and was further confirmed at the transcriptional and protein level and by proteolytic activity. Ex vivo ADAM9 inhibition decreased severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uptake and replication in human lung epithelial cells. In conclusion, within a young, otherwise healthy, cohort of individuals with COVID-19, we provide the landscape of biological perturbations in vivo where a unique gene signature differentiated critical from non-critical patients. We further identified ADAM9 as a driver of disease severity and a candidate therapeutic target.", "doi": "10.1126/scitranslmed.abj7521", "pmid": "34698500", "labels": [], "xrefs": [], "notes": [], "created": "2026-10-01T08:23:30.045Z", "modified": "2026-10-01T08:23:31.615Z"}]}