Some people with Covid-19 have a special symptom: anosmia, which is a total loss of smell. By dint of investigating the subject, researchers have finally understood why the Covid-19 is at the origin of this phenomenon.
A different anosmia in case of Covid-19
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 certain colds caused by non-fatal coronaviruses. Most of the time, anosmia occurs due to congestion of the nasal passages. This prevents the aroma molecules from reaching the olfactory receptors. With the disappearance of the stuffy nose, smell logically returns, except in very rare cases.
After the appearance of Covid-19, researchers have mentioned nervous system damage. Later, the loss of smell but also of taste have been added to the symptom list. The fact is that not all Covid-19 patients with anosmia have a stuffy nose! In addition, even after recovery, some people testify to prolongation of anosmia over time. As an article published by The Conversation on June 24, 2020, the anosmia linked to Covid-19 was different from that from other respiratory infections.
In reality, these people are affected by the olfactory cleft syndrome, the part of the nose responsible for the perception of odors. More specifically, the olfactory cleft is blocked by swelling of the soft tissues as well as the appearance of mucus. However, the other organs and sinuses remain normal, which is why patients do not have a stuffy nose.
The basic hypothesis questioned
Today we know that SARS-CoV-2 (Covid-19) infects our bodies by binding to ACE2 receptors. These receptors are located on the surface of cells in the upper airways. Then the protein TMPRSS2 promotes the invasion of these cells by the virus. Inside, the body undergoes replication of the virus and the problems begin.
Originally, the hypothesis was that Covid-19 could infect and destroy olfactory neurons. But some research tends to demonstrate (pre-publication) that ACE2 receptors favoring the entry of the virus into the cells are absent from the surface of olfactory neurons.
Olfactory neurons victims of collateral damage
However, these ACE2 receptors have been identified in so-called “sustentacular” cells. These represent a structural support for 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 leave the neurons free again. This therefore brings us to the question of cases where the sense of smell extends over time.
Remember that inflammation is the body’s immune response to infection. However, the chemicals produced by this response are capable of destroying the tissues or even the cells located nearby. In the case of very severe inflammations, the olfactory neurons would therefore could have suffered this kind of damage. Thus, the return of smell would take time since the olfactory neurons must first regenerate.