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COVID-19 and loss of sense of smell




2019 Coronavirus Disease (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2).one Symptoms of COVID-19 It is a sensory dysfunction, the ability to reduce or distort the sense of smell or the sense of smell during meals.

Recent reviews published in the journal virus We will investigate the high susceptibility of the olfactory epithelium, which is the protective layer in the nasal cavity that causes the sense of smell, to SARS-CoV-2 infection, and the plausible cause of persistent olfactory dysfunction during the recovery period of some COVID-19.

study: Anosmia: high prevalence of SARS-CoV-2, multiple neuropathogenic mechanisms, and poor neurotrophic? Image Credits: Design_Cells /

Smell dysfunction

Smell dysfunction is a common nasal disorder caused by nasal congestion, inflammation of the olfactory epithelium, infection, damage, or structural dysfunction of the olfactory nerve, olfactory bulb, or other central nervous system (CNS) structures.

COVID-19’s sensory dysfunction differs from the traditional sensation of these disorders because it may appear before other symptoms and may be the only symptom of the infection.

The incidence of olfactory and / or dysgeusia in COVID-19 patients varies. Studies have reported prevalence of 5% to 98%, depending on region, population, SARS-CoV-2 mutant, and diagnostic method. However, most studies report an incidence of sensory dysfunction between 20% and 80%. Most COVID-19-related sensory dysfunctions resolve in a few weeks. However, in some patients, these effects may persist long after the other COVID-19 symptoms have resolved.

Olfactory epithelium and SARS-CoV-2 sensitivity

The sense of smell or smell begins when odor molecules in the air bind to receptors on the surface of the olfactory epithelium of the nasal cavity. Odor substances elicit electrical signals that are transmitted to the olfactory bulb of the brain via the olfactory nerve.

The olfactory epithelium covers the nasal cavity near the entrance to the upper respiratory tract. This tissue helps in the early detection of important or potentially harmful odorants in the air. Importantly, the location of the olfactory epithelium is also vulnerable to pathogens or other types of damage.

The olfactory epithelium is like the respiratory epithelium that lines the nasal passages. However, careful examination reveals a slight structural difference between these two tissues.

Electron micrograph showing vertical (NS) And tangent / diagonal sections (NS) At the apex of rat OE. The dotted line on panel A shows the apical surface of the sustentacular cell (S) from the apical part of rat OE. The dotted line on panel A shows the apical surface of the sustentacular cells (S), from which the microvilli of long, thin sustentacular cells project approximately 2-3 μm into the nasal cavity. Microvilli of long, thin sustentacular cells project into the nasal cavity approximately 2-3 μm. The ORN dendrite knob (DN) and cilia (C) at the apex of the ORN dendrite (D) are mainly found with the ORN dendrite knob (DN) at the apex of the ORN dendrite (D) Cilia (C) are found primarily in supporting cells, most of the microvilli ((B) unlabeled small profile structures) and most of the supporting cell microvilli ((B) unlabeled small profile structures) )NS) And the area above the dotted line in (A).Human OE is organized in the same way [52–54].. Scale bar = 0.5 μm. (Dotted lineNS).Human OE is organized in the same way [52–54].. Scale bar = 0.5 μm.

For example, there are differences between the olfactory epithelium and the respiratory epithelium in the expression of the angiotensin converting enzyme 2 (ACE2) receptor that SARS-CoV-2 uses to invade host cells. In fact, ACE2 expression is hundreds of times higher in the olfactory epithelium than in the respiratory epithelium. In addition, the olfactory epithelium has cellular microvilli with increased cell surface area due to binding or absorption.

Neuropathology of SARS-CoV-2

Viruses can preferentially bind to and invade nerves, thereby exhibiting their neurotrophic nature. The majority of neurotropic viruses bind to neuronal receptors. ACE2 is present in specific cell types within the olfactory and respiratory epithelium. However, mature nerves in the sensory system have minimal or no ACE2.

Several studies have reported SARS-CoV-2 infection and / or pathology in human autopsy or biopsy samples and various cells, tissues, and organs of animal models.In addition, some studies have reported the presence of SARS-CoV-2. Spike protein In the olfactory epithelium and respiratory epithelium.

In one study, a biopsy of a patient who lost his sense of smell three months after recovering from COVID-19 showed extensive destruction and damage to the olfactory epithelium. SARS-CoV-2 was rarely detected in the cerebrospinal fluid (CSF) of patients with COVID-19. However, inflammation and immune response were commonly observed.

There is no direct evidence that SARS-CoV-2 infects the brain. Autopsy of COVID-19 shows extensive inflammation of the brain region and damage to the olfactory bulb.

COVID-19 Mechanism of neuropathogenesis

SARS-CoV-2 primarily infects the olfactory sustentacular cells of the olfactory epithelium, which express high levels of ACE2. Persistent cell infection and damage can lead to inflammation, immune response, cytokine release, and signal transduction that can lead to sensory dysfunction and damage to the nerves of the sensory system.

For persistent sensory dysfunction after COVID-19, pathogenic mechanisms may include damage to specific cells, persistent inflammation, or chronic SARS-CoV-2 infection in the olfactory epithelium. Transport of pathogenic molecules from the olfactory epithelium to the olfactory bulb via nerves can cause nerve dysfunction and degeneration of the olfactory bulb. SARS-CoV-2 infection of cells within the capillaries of the brain can endanger the blood-brain barrier and cause neuropathology and dysfunction in various brain regions.

In patients with COVID-19 who have obvious stuffy nose, blocking the airflow through the nasal passages also adversely affects the sense of smell and enhances the sense of dysfunction.

The schematic which shows the possible mechanism of the pathogenesis of the sensory nerve in COVID-19. (((NS) Schematic diagram to explain the relationship between the nasal cavity, olfactory epithelium (OE), olfactory nerve (ON), olfactory bulb (OB), and brain (OB)NSIn OE, SARS-CoV-2 primarily infects sensory sustentacular cells (OSCs) that express high levels of SARS-CoV-2 receptor ACE2 on the surface of the lumen. Persistent cell infection and damage can lead to inflammation, SARS-CoV-2 receptor ACE2 on the surface of the lumen. Persistent cell infections and damage are mediated by inflammation, immune response, cytokine release, and signal transduction via pathogen-associated molecular patterns (PAMP), injured immune responses, cytokine release, and pathogen-associated molecular patterns (PAMP). It can lead to signaling. Damage-associated molecular patterns (DAMP), pattern recognition receptors (PRR) can cause dysfunction of related molecular patterns (DAMP), and pattern recognition receptors (PRR) can cause dysfunction (anosmia and hypoosmolarity). Etc.) can be caused. Damage to olfactory receptor neurons (ORN) and / or anterograde degeneration. In the case of persistent sensory dysfunction after COVID-19, pathogenic mechanisms may include damage to the basal degeneration of the OB’s neural structure. (D) SARS-CoV-2 infection of endothelial or pericytes, and microthrombotic transport of pathogenic molecules from OE to OB along ORN axons can cause capillary dysfunction and synapses. Yes, it can compromise the blood-brain barrier. Causes hematogenous neuropathology and degeneration of neural structures in OBs. (((NS) SARS-CoV-2 infection of endothelial or pericytes, and microthrombogenic dysfunction in various brain regions, including OB. Capillaries can impair the blood-brain barrier and cause hematogenous neuropathology and dysfunction in various brain regions, including OBs.

Long-term sensory dysfunction after COVID-19

The olfactory epithelium undergoes regular aging and self-replacement throughout life. In addition, this tissue is easily repaired or regenerated after damage.

Lack or slow recovery from COVID-19 sensory dysfunction in a particular individual means severe or persistent damage to the olfactory epithelium by the virus. Another possible explanation is the persistent presence of SARS-CoV-2, chronic inflammation, immune response, or increased cell death in the olfactory epithelium. Interestingly, chronic inflammation can switch the function of certain cells in the olfactory epithelium from regeneration to inflammatory signaling and immune cell proliferation.


There is no evidence that SARS-CoV-2 is infected with nerves. SARS-CoV-2 infection causes olfactory dysfunction and damage. Probably by indirect means such as deprivation of support or inflammatory or immune response. These processes add to the many pathogenic mechanisms of COVID-19 neurological symptoms and complications.

In summary, it is essential to investigate the causes and treatment of chronic SARS-CoV-2 infection of the olfactory epithelium and persistent post-COVID-19 olfactory dysfunction during some COVID-19 convalescent periods.

Journal reference:

  • Liang, F. , And Wang, DY (2021). COVID-19 Anosmia: High prevalence of SARS-CoV-2, multiple neuropathogenic mechanisms, and poor neurotrophic? virus, 13(11), 2225. doi: 10.3390 / v13112225..





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