Some people affected by Covid-19 have a particular symptom:anosmia, that is to say a total loss of smell. By dint of investigating the subject, researchers have finally understood why Covid-19 is at the origin of this phenomenon.
Anosmia is characterized by a total loss of smell temporary or permanent. In respiratory infections like the flu, anosmia is quite common. This is also the case for some colds caused by non-fatal coronaviruses. Most of the time, anosmia occurs due to clogging of the nasal passages . This prevents the aroma molecules from reaching the olfactory receptors. With the disappearance of the blocked nose, the sense of smell logically returns, except in very rare cases.
After the appearance of Covid-19, researchers spoke of damage to the nervous system. Later, the loss of smell but also of taste were added to the list of symptoms. However, the fact is that patients with Covid-19 and presenting with anosmia do not all have a stuffy nose! Moreover, even after their recovery, some people testify to a prolongation of anosmia over time . As stated in an article published by The Conversation June 24, 2020, anosmia from Covid-19 is different from that from other respiratory infections.
In reality, these people have olfactory cleft syndrome , the part of the nose responsible for the perception of odors. Specifically, the olfactory cleft is blocked by swelling of the soft tissues as well as the appearance of mucus. However, other organs and the sinuses remain normal, which explains why patients do not have a stuffy nose.
Today we know that SARS-CoV-2 (Covid-19) infects our body by binding to ACE2 receptors. However, these receptors are located on the surface of the cells of the upper airways. Then, the TMPRSS2 protein promotes the invasion of these cells by the virus. Inside, the organism undergoes virus replication and the problems begin.
Originally, the hypothesis was that Covid-19 could infect and destroy olfactory neurons. But some research tends to show (pre-publication) that the ACE2 receptors promoting the entry of the virus into cells are absent from the surface of olfactory neurons.
On the other hand, these ACE2 receptors have been identified at the level of the so-called "sustentacular" cells. The latter represent a structural support for the olfactory neurons . Thus, it seems that the infection attacks these cells by causing edema without destroying the neurons. After recovery, the edema is therefore supposed to shrink and again leave the field open to the neurons. This brings us to the question of cases where the sense of smell is prolonged over time.
Remember that inflammation is the body's immune response to an infection. However, the chemical substances produced by this response are capable of destroying the tissues and even the cells located nearby. In the case of very severe inflammation, the olfactory neurons could have suffered this kind of damage . Thus, the return of the sense of smell would take time since the olfactory neurons must first regenerate.
