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. 2023 Dec 25;21(2):134–143. doi: 10.1038/s41423-023-01119-5

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — The stages of the immune response to SARS-CoV-2 in the olfactory mucosa. A SARS-CoV-2 uses ACE2 to enter sustentacular cells and antagonize the induction of interferons. B Infiltrating neutrophils and macrophages produce inflammatory cytokines. Sustentacular cells are lost, epithelial structure deteriorates, and olfactory sensory neurons undergo disruption of nuclear architecture and cell death. C After SARS-CoV-2 has been cleared by the immune response, T cells and plasma cells populate the tissue. Plasma cells produce locally protective mucosal antibody. T cells may contribute to sustained inflammation, preventing proper epithelial regeneration in some cases and preventing restoration of the sense of smell