Loss of smell is one of the syndromes characteristic of COVID-19 infections, especially its initial variants. According to a study published in the journal Cell, scientists were able to find out what causes the disturbance of this sense.
A study by scientists at NYU Grossman School of Medicine and Columbia University found that SARS-CoV-2 infection indirectly inhibits the action of olfactory receptors, proteins on the surface of nerve cells in the human nose that are smells of the molecule. According to experts, the new discovery could shed new light on the impact of COVID-19 on other neurological effects of the coronavirus transition.
Analyzes have shown that the presence of a virus in the area of olfactory tissue neurons causes the growth of immune cells, microglia and T lymphocytes, which are responsible for detecting and preventing infection. These cells release proteins called cytokines that experts say alter the genetic activity of olfactory nerve cells, even though the coronavirus cannot infect them.
The authors of the study argue that the activity of immune cells would fade quickly in other situations, however, according to their theory, the immune signaling persists in a way that reduces the activity of olfactory gene receptors.
- Our findings provide the first mechanistic explanation for loss of smell in COVID-19 and how it could underlie COVID-19's long biology, said one study author Dr Benjamin tenOever. What's more, the work also suggests how SARS-CoV-2 infects less than 1 percent. cells in the human body and can cause serious damage to many organs.
In the vast majority of cases, a patient who lost his sense of smell as a result of COVID-19 infection all returns to normal within a few weeks. However, 12 percent. of people, the olfactory dysfunction persists in the form of hyposmia, i.e. a reduced ability to sense and recognize smells, or a parosmia characterized by a change in the perception of smells.
To identify the mechanism behind this, a group of researchers conducted studies on hamsters and olfactory tissue collected from 23 human autopsies. Choiceanimals for analysis was not accidental. Hamsters are mammals that are more dependent on their sense of smell than humans. This makes them more prone to various types of nasal cavity infections.
Experiments have confirmed that COVID-19 infection and the resulting immune response reduce the ability of the DNA chains in the chromosomes to influence the formation of olfactory receptors. It turned out that in both animal and human tissues, the research team discovered a persistent and extensive regulation of the structure of the olfactory receptors.
Earlier research work on Long COVID by the same authors showed that olfactory neurons are closely correlated with sensitive areas of the brain, and that ongoing immune cell responses in the nasal cavity can affect clear thinking and emotions.
Further scientific analysis has shown that COVID-19 causes longer disruptions in the chromosomal regulation of gene expression, representing a form of "nuclear memory". Thus, it prevents the restoration of the olfactory receptor transcription even after removing SARS-CoV-2.
- The realization that the sense of smell is based on "fragile" genomic interactions between chromosomes has important implications, explained Dr. tenOever. In his opinion, "COVID-19 damages brain tissue before other symptoms appear and suggests new treatments for it."
In the next stage of the research, scientists want to see whether treating hamsters suffering from the long-term effects of COVID-19 with steroids can restore the inhibition of harmful immune reactions, such as the appearance of inflammation.