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However, the role of NK cell\u2013mediated ADCC in SARS-CoV-2 infection remains unclear, particularly whether it limits viral spread and disease severity or contributes to the immunopathogenesis of COVID-19. We hypothesized that the high-affinity CD16A\n                    <jats:sup>V176<\/jats:sup>\n                    polymorphism influences these outcomes. Using an in vitro reporter system, we demonstrated that CD16A\n                    <jats:sup>V176<\/jats:sup>\n                    is a more potent and sensitive activator than the common CD16A\n                    <jats:sup>F176<\/jats:sup>\n                    allele. To assess its clinical relevance, we analyzed 1,027 patients hospitalized with COVID-19 from the Immunophenotyping Assessment in a COVID-19 cohort (IMPACC), a comprehensive longitudinal dataset with extensive transcriptomic, proteomic, and clinical data. The high-affinity CD16A\n                    <jats:sup>V176<\/jats:sup>\n                    allele was associated with a significantly reduced risk of ICU admission, mechanical ventilation, and severe disease trajectories. Lower anti\u2013SARS-CoV-2 IgG titers were correlated to CD16A\n                    <jats:sup>V176<\/jats:sup>\n                    ; however, there was no difference in viral load across CD16A genotypes. Proteomic analysis revealed that participants homozygous for CD16A\n                    <jats:sup>V176<\/jats:sup>\n                    had lower levels of inflammatory mediators. These findings suggest that CD16A\n                    <jats:sup>V176<\/jats:sup>\n                    enhances early NK cell\u2013mediated immune responses, limiting severe respiratory complications in COVID-19. This study identifies a protective genetic factor against severe COVID-19, informing future host-directed therapeutic strategies.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.191314","type":"journal-article","created":{"date-parts":[[2025,5,22]],"date-time":"2025-05-22T12:00:32Z","timestamp":1747915232000},"source":"Crossref","is-referenced-by-count":3,"title":["High-affinity CD16A polymorphism associated with reduced risk ofsevere COVID-19"],"prefix":"10.1172","volume":"10","author":[{"given":"Anita E.","family":"Qualls","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, UCSF, San Francisco, California, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1183-8912","authenticated-orcid":true,"given":"Tasha","family":"Tsao","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, UCSF, San Francisco, California, 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