The pandemic COVID-19 has caused an immense disaster throughout the world. Coronavirus cases continue to surge worldwide. Ephemeral loss of taste, smell, or anosmia is the foremost neurological indications, and one of the earliest and most often reported symptoms of coronavirus. Studies have shown that it predicts the infection better than other well-known symptoms (such as fever and cough), but the underlying mechanisms of the loss of taste, smell, or anosmia in COVID-19 patients are unclear.
Now, in another development related to coronavirus symptoms, an international team of researchers found that there is no protein in the taste buds that the COVID-19 virus uses to enter host tissues.
In other words, researchers have identified the types of olfactory cells most vulnerable to SARS-CoV-2 disease (the virus that causes Corona).
Surprisingly, sensory neuron cells that can identify and transmit the sense of odor to the brain are not among the cell types that are vulnerable.
According to experts on July 24, the research team discovered that olfactory sensory neurons don’t express the encoded gene for the ACE2 receptor protein that SARS-CoV-2 uses to enter human cells. In contrast, ACE2 is expressed in cells that produce metabolic and structural supports for olfactory sensory neurons and certain vascular cell and stem cell populations.
These findings indicate that infections of non-neuronal cell types may be the cause of loss of taste, smell, or anosmia in coronavirus patients, and help to better understand the progression of the diseases.
Sandeep Robert Datta, an author and associate professor of neurobiology at the HMS Blavatnik Institute, stated that our findings show that the pandemic coronavirus does not directly infect neurons but changes the patient’s sense of taste and smell by affecting the function of supporting cells.
Datta further said: this means that in most cases, the SARS-CoV-2 virus is unlikely to permanently disable the olfactory neural circuit and cause persistent anosmia. This condition is related to various psychological and social health problems, especially anxiety and depression.
Besides this, the scientists analyzed the oral cells of the mice and concluded that the loss of odors reported by many COVID-19 patients may be due to inflammation caused by the disease rather than directly caused by viral contamination.
According to the study published in the journal ACS Pharmacology and translational science, although the ACE2 receptor protein used by the coronavirus SARS-CoV-2 pandemic to enter the host tissues, is enhanced in cells that give the tongue a bumpy surface, they cannot be detected in the taste buds’ cells.
Researchers, including those from the Georgia University in the United States, also unveiled that other viruses that influence the taste, including influenza viruses, may infect different tongue cell types, adding that these viruses can cause infections by invading precise cells in the body. In the process of reproduction, these cells are often damaged or killed.
Although previous studies have recognized the symptoms of coronavirus, it has been shown that SARS-CoV-2 enters human cells through ACE2 receptors on the surface of certain cells (including the surface of the human tongue), but recent studies have shown that this protein was not expressed specifically in taste bud cells. The mice were used as model organisms to study and express this protein specifically in taste bud cells.
Moreover, the mouse versions of ACE2 is not susceptive to SARS-CoV-2 disease, scientists asserted that considering where ACE2 is expressed in mice could help explain what happens when people are infected and lose their sense of taste or smell.
When they examined data on mouse buccal cells at three developmental stages, the researchers found ACE2 in infant mice, but not in fetuses. According to the researchers, former studies on humans did not focus on oral cells, which suggests that ACE2 can be expressed in the early stages of the fetus and then again at a later stage.
They speculated that the fetus may have different susceptibility to SARS-CoV-2 infection at various stages, and added that more extra work is needed to determine the timing and location of human ACE2 expression.
Therefore, the olfactory system that enables humans and other animals to smell is actually a significant way to decode chemical information. When someone sniffs, molecules flow up from the nose to the olfactory epithelium, a small piece of tissue behind the nasal cavity.
These molecules attach to olfactory sensory neurons and then burst out signals through the axon, which passes through the skull and transmits the information to the brain, which records these molecules, like coffee, leather, or rotting lettuce.
In addition to this, according to emerging data, most COVID-19 patients experience a certain degree of anosmia, which in most cases is temporary. The analysis of electronic health records shows that as compared with patients without COVID-19, patients with COVID-19 are 28 times more likely to have the odor disappear, while the probability of fever, cough or breathing difficulties is only 2.3 to 2.7 times higher.
Some studies have shown that the loss of taste, smell, or anosmia in COVID-19 patients is different from the sense of taste or smell caused by other viral infections.
For example, COVID-19 patients usually recover their sense of taste or smell within a few weeks, which is faster than months of recovering from anosmia caused by other viral infections that are known to directly damage many parts of the olfactory sensory neurons.
Furthermore, many viruses can cause temporary loss of taste or smell by triggering upper respiratory problems. However, some COVID-19 patients experienced anosmia without any nasal congestion.
The authors said these data together indicate that the loss of taste, smell, or anosmia associated with COVID-19 may be caused by the temporary loss of support cells function in the olfactory epithelium, which indirectly leads to changes in olfactory sensory neurons.
However, we do not fully know what these changes are yet, Datta said. Sertoli cell or a cell of the olfactory epithelium are largely ignored. It seems that we need to pay attention to them, just as we are more aware of glial cells’ vital role play in the brain.