The most common neurological symptom of COVID-19 is loss of smell. Usually, the sense of smell is restored within 6 weeks. However, in 10% of patients, COVID-19 leads to persistent olfactory dysfunction.

Olfactory impairment is also common in common upper respiratory tract infections. However, unlike the coronavirus, it is associated with nasal congestion and copious, watery secretions that isolate olfactory neurons from odor sources.

A runny nose with COVID-19 is a less common symptom than seasonal colds. Therefore, the loss of smell with COVID-19 is not nasal congestion. In addition, the coronavirus does not infect olfactory neurons since their surface lacks the ACE2 and TMPRSS2 proteins necessary for SARS-CoV-2 to enter the cell. Therefore, the coronavirus does not directly affect olfactory neurons.

American scientists have learned what mechanisms lead to loss of smell in COVID-19. The study was carried out on hamsters and humans.

Scientists have found that the coronavirus infects and depletes the supporting cells of the olfactory epithelium. Support cells structurally support sensory neurons, destroy or neutralize potentially hazardous substances, maintain water-salt balance, and are also involved in delivering odor to olfactory sensory neurons. The supporting cells secrete mucus, which contains odor-binding proteins. These proteins carry odor molecules to the olfactory receptors of sensory neurons. Typically, supporting cells are restored 10 days after infection with coronavirus.

In addition, the coronavirus suppresses the olfactory receptor genes and other genes necessary for the perception of a smell. Suppression of these genes leads to changes in the structure of the cell nucleus of olfactory neurons. Therefore, even though the coronavirus does not infect olfactory neurons, it leads to a violation of their functions.

Output

The loss of smell in COVID-19 is that the coronavirus suppresses the genes for olfactory receptors and their signaling pathways, alerting the physiology and function of the olfactory neurons, which the coronavirus cannot infect.

Suppression of olfactory receptor genes can lead to irreversible damage to mature sensory neurons. If sensory neurons fail to restore the synthesis of olfactory receptors, the sense of smell in patients with COVID-19 will be restored only after replacing these sensory neurons, which takes weeks to months.

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Reference

Non-cell-autonomous disruption of nuclear architecture as a potential cause of COVID-19-induced anosmia

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