PT  - JOURNAL ARTICLE
AU  - John B. Finlay
AU  - David H. Brann
AU  - Ralph Abi-Hachem
AU  - David W. Jang
AU  - Allison D. Oliva
AU  - Tiffany Ko
AU  - Rupali Gupta
AU  - Sebastian A. Wellford
AU  - E. Ashley Moseman
AU  - Sophie S. Jang
AU  - Carol H. Yan
AU  - Hiroaki Matusnami
AU  - Tatsuya Tsukahara
AU  - Sandeep Robert Datta
AU  - Bradley J. Goldstein
TI  - Persistent post-COVID-19 smell loss is associated with inflammatory infiltration and altered olfactory epithelial gene expression
AID  - 10.1101/2022.04.17.488474
DP  - 2022 Jan 01
TA  - bioRxiv
PG  - 2022.04.17.488474
4099  - http://biorxiv.org/content/early/2022/04/18/2022.04.17.488474.short
4100  - http://biorxiv.org/content/early/2022/04/18/2022.04.17.488474.full
AB  - Most human subjects infected by SARS-CoV-2 report an acute alteration in their sense of smell, and more than 25% of COVID patients report lasting olfactory dysfunction. While animal studies and human autopsy tissues have suggested mechanisms underlying acute loss of smell, the pathophysiology that underlies persistent smell loss remains unclear. Here we combine objective measurements of smell loss in patients suffering from post-acute sequelae of SARS-CoV-2 infection (PASC) with single cell sequencing and histology of the olfactory epithelium (OE). This approach reveals that the OE of patients with persistent smell loss harbors a diffuse infiltrate of T cells expressing interferon-gamma; gene expression in sustentacular cells appears to reflect a response to inflammatory signaling, which is accompanied by a reduction in the number of olfactory sensory neurons relative to support cells. These data identify a persistent epithelial inflammatory process associated with PASC, and suggests mechanisms through which this T cell-mediated inflammation alters the sense of smell.Competing Interest StatementThe authors have declared no competing interest.