cisgenderedAggie said:
I'm more of a molecular person and all my neuro days was developmental, so forgive if I misunderstand. I think the key suggested by this paper is that they aren't showing evidence of neuroinvasive infection. The nasal epithelium is supposed to be highly regenerative though, right? So the delay in return has more to do with epithelial shedding and regeneration. This isn't unlike smoke burning out your sense of smell for a few days.
No idea if taste works the same way.
Correct. As the olfactory sensory neurons do not have ACE-2 and tmprss 2 receptors, the authors hypothesize that the mechanism of anosmia and hyposmia or dysosmia is not via direct viral infection of these neurons. Rather, they propose that the virus directly infects other nearby nasal epithelial cells and then this probably initiates a local cytokine-mediated neuropathy which causes disruption of the sensory neuron's neural architecture.
Obviously, this cytokine mediated inflammatory pathway is quite localized - hence the lack of mechanical obstruction seen in many of these patients who contract COVID. This is not consistent with how most viral-induced URIs are causing anosmia/hyposmia/dysosmia. This is why we normally treat sudden loss of sense of smell with steroids, without a whole lot of great evidence as to efficacy.
As far as recovery goes, I'm not sure I would categorize the nasal OLFACTORY epithelium as highly regenerative. The rest of the epithelium is definitely more easily regenerated than the olfactory epithelium. This is probably why it has been seen that recovery can take a year or more after a viral induced anosmia.
HTH. Don't ask me for more - that article was painful, and it's Friday.
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