This is way over my head, but found this when looking for an article on vulcanism.
https://advances.sciencemag.org/content/6/31/eabc5801
Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia
Science Advances 31 Jul 2020:
Vol. 6, no. 31, eabc5801
DOI: 10.1126/sciadv.abc5801
Abstract:
Altered olfactory function is a common symptom of COVID-19, but its etiology is unknown. A key question is whether SARS-CoV-2 (CoV-2) – the causal agent in COVID-19 – affects olfaction directly, by infecting olfactory sensory neurons or their targets in the olfactory bulb, or indirectly, through perturbation of supporting cells. Here we identify cell types in the olfactory epithelium and olfactory bulb that express SARS-CoV-2 cell entry molecules. Bulk sequencing demonstrated that mouse, non-human primate and human olfactory mucosa expresses two key genes involved in CoV-2 entry, ACE2 and TMPRSS2. However, single cell sequencing revealed that ACE2 is expressed in support cells, stem cells, and perivascular cells, rather than in neurons. Immunostaining confirmed these results and revealed pervasive expression of ACE2 protein in dorsally-located olfactory epithelial sustentacular cells and olfactory bulb pericytes in the mouse. These findings suggest that CoV-2 infection of non-neuronal cell types leads to anosmia and related disturbances in odor perception in COVID-19 patients.
Introduction
SARS-CoV-2 (CoV-2) is a pandemic coronavirus that causes the COVID-19 syndrome, which can include upper respiratory infection (URI) symptoms, severe respiratory distress, acute cardiac injury and death (1-4). CoV-2 is closely related to other coronaviruses, including the causal agents in pandemic SARS and MERS (SARS-CoV and MERS-CoV, respectively) and endemic viruses typically associated with mild URI syndromes (hCoV-OC43, hCoV-HKU1, hCoV-229E and hCoV-NL63) (5-7). Clinical reports suggest that infection with CoV-2 is associated with high rates of disturbances in smell and taste perception, including anosmia (8-13). While many viruses (including coronaviruses) induce transient changes in odor perception due to inflammatory responses, in at least some cases COVID-related anosmia has been reported to occur in the absence of significant nasal inflammation or coryzal symptoms (11, 14-16). Furthermore, recovery from COVID-related anosmia often occurs over weeks (11, 17, 18), while recovery from typical post-viral anosmia — which is often caused by direct damage to olfactory sensory neurons (OSNs) — frequently takes months (19-21). These observations suggest that CoV-2 might target odor processing through mechanisms distinct from those used by other viruses, although the specific means through which CoV-2 alters odor perception remains unknown.
CoV-2 — like SARS-CoV — infects cells through interactions between its spike (S) protein and the ACE2 protein on target cells. This interaction requires cleavage of the S protein, likely by the cell surface protease TMPRSS2, although other proteases (such as Cathepsin B and L, CTSB/CTSL) may also be involved (4-6, 22-25). Other coronaviruses use different cell surface receptors and proteases to facilitate cellular entry, including DPP4, FURIN and HSPA5 for MERS-CoV, ANPEP for HCoV-229E, TMPRSS11D for SARS-CoV (in addition to ACE2 and TMPRSS2), and ST6GAL1 and ST3GAL4 for HCoV-OC43 and HCoV-HKU1 (6, 26-28).
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got that? kek