An international group of researchers led by a team from Harvard have identified that anosmia occurs not through infection of olfactory sensory neurons but of their associated, supportive cells.
The olfactory epithelium contains olfactory sensory neurons (OSN), which detect and transmit odours to the brain, sustentacular cells that provide structural support to the OSNs and olfactory stem cells that create new OSNs.
In a yet to be peer-reviewed study, the team focused on two genes, ACE2 and TMPRSS2, which encode for proteins which help COVID-19 gain entry into cells. These genes expressed their respective proteins in the sustentacular and stem cells but not in the OSNs. In other words, primary infection of non-neuronal cells, rather than the OSNs cells may be the main reason why COVID-19 leads to anosmia.
The authors speculated that infection of these supportive cells might lead to inflammation which could impede effective odour transmission or damage to either the sustentacular or stem cells that ultimately affected the structure of the olfactory epithelium and thus smell perception.
While their work is preliminary, it may account for why loss of smell is only temporary in some patients (because the supportive cells recover) or permanent, which has been observed in a subset of patients, due to irreparable damage of the olfactory epithelium.
Reference
Brann DH et al. Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia. Sci Adv 2020; July 24: DOI: 10.1126/sciadv.abc5801
