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eMediNexus 28 December 2022
According to a recent study that was published in the journal Science Translational Medicine, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been eradicated from the olfactory tissue, yet long-term anosmia following coronavirus disease 2019 (COVID-19) may still be caused by persistent T-cell mediated inflammation in the olfactory epithelium.
The olfactory epithelial samples from 24 biopsies, including samples from nine patients who had long-term smell loss that could be objectively measured following COVID-19, were analyzed in the study. Control samples included olfactory tissue biopsies from normosmic persons with and without a history of COVID-19 (three people) and from normosmic people with a COVID-19 diagnosis in the past (two people). This biopsy-based technique showed a diffuse infiltrate of T cells expressing interferon- and a change in the population makeup of myeloid cells, including enrichment of CD207+ dendritic cells and a decrease in anti-inflammatory M2 macrophages.
Despite the absence of detectable SARS-CoV-2 RNA or protein, sustentacular cells, which support the olfactory epithelium′s barrier, showed gene expression that seemed to be in response to ongoing inflammatory signaling. A decrease in the proportion of olfactory sensory neurons to sustentacular cells in the olfactory epithelium accompanied this response.
These results offer a mechanism for long-term post-COVID-19 smell loss by demonstrating that T cell-mediated inflammation endures in the olfactory epithelium even after SARS-CoV-2 has been removed from the tissue.
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