BioAcyl Corp
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Ziegler, C. G. K., Miao, V. N., & Owings, A. H. (2021). Impaired local intrinsic immunity to SARS-CoV-2 infection in severe COVID-19. Cell, 184(18), 4713–4733.e22. Added by: Dr. Enrique Feoli (14/04/2023, 16:38) Last edited by: Dr. Enrique Feoli (14/04/2023, 16:44) |
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| Resource type: Journal Article Published DOI: 10.1016/j.cell.2021.07.023 ID no. (ISBN etc.): 0092-8674, 1097-4172 BibTeX citation key: Ziegler2021 View all bibliographic details  |
Categories: BioAcyl Corp, BioAcyl Corp Subcategories: Constitutive innate immunity, COVID-19 Creators: Miao, Owings, Ziegler Collection: Cell |
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| Abstract |
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{textless}h2{textgreater}Summary{textless}/h2{textgreater}{textless}p{textgreater}SARS-CoV-2 infection can cause severe respiratory COVID-19. However, many individuals present with isolated upper respiratory symptoms, suggesting potential to constrain viral pathology to the nasopharynx. Which cells SARS-CoV-2 primarily targets and how infection influences the respiratory epithelium remains incompletely understood. We performed scRNA-seq on nasopharyngeal swabs from 58 healthy and COVID-19 participants. During COVID-19, we observe expansion of secretory, loss of ciliated, and epithelial cell repopulation via deuterosomal cell expansion. In mild and moderate COVID-19, epithelial cells express anti-viral/interferon-responsive genes, while cells in severe COVID-19 have muted anti-viral responses despite equivalent viral loads. SARS-CoV-2 RNA$+$ host-target cells are highly heterogenous, including developing ciliated, interferon-responsive ciliated, AZGP1$high$ goblet, and KRT13$+$ "hillock"-like cells, and we identify genes associated with susceptibility, resistance, or infection response. Our study defines protective and detrimental responses to SARS-CoV-2, the direct viral targets of infection, and suggests that failed nasal epithelial anti-viral immunity may underlie and precede severe COVID-19.{textless}/p{textgreater}
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| Notes |
Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |