SARS-CoV-2 infects host cells mainly through the interaction between the virus's Spike protein and the viral receptors namely Angiotensin-Converting Enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2). Both are highly expressed in the gastrointestinal tract, in the nasal and bronchial epithelium, as well as in the type II alveolar epithelial cells. The aim of this review is to report the evidences from the scientific literature on the pathophysiology and the available treatments for olfactory-gustatory disorders in patients with COVID-19. The mechanisms involved in these disorders are still unclear and studies on specific therapies are scarce. However, it has been hypothesized that a decrease in the sensitivity of the sensory neurons as well as the co-expression of ACE2 and TMPRSS2 in the alveolar epithelial cells are the main causes of olfactory-gustatory disorders. The possible mechanisms described in the literature for changes in taste perception in patients with COVID-19 include olfactory disorders and a competitive activity of COVID-19 on ACE2 receptors in the taste buds. In addition, SARS-CoV-2 can bind to sialic acid receptors in the taste buds. In general, evidences show that there is no specific treatment for olfactory-taste disorders induced by SARS-CoV-2, even though some treatments have been used and have shown some promising results, such as olfactory training, intranasal application of sodium citrate and vitamin A, as well as systemic use of omega-3 and zinc. Corticosteroids have also been used as a pharmacological approach to treat patients with olfactory dysfunction with some contradictory results. The knowledge of the mechanisms by which SARS-CoV-2 influences the sensory systems and how effective therapies can treat the loss of smell and taste will have important implications on the understanding and clinical management of olfactory-taste disorders.

Pathophysiology and possible treatments for olfactory-gustatory disorders in patients affected by COVID-19

In nearly a year since the first reported cases of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a lot has been established about the virus. Correlates in regards to the biology and cellular effects of SARS-CoV-2 have brought a lot of explanations to the clinical manifestations of the disease and possible therapeutic modalities. However, despite the discoveries made, the tropism of SARS-CoV-2 has not yet been fully established, nor have all the clinical aspects of COVID-19. Herein we report the gross and histological findings in two diseased patients. Apart from the already established pulmonary and vascular changes caused by SARS-CoV-2, we report the presence of histological changes of the olfactory bulbs and frontal lobes of the brain, which may present as a correlate for COVID-19 related anosmia. The olfactory bulbs histologically showed necrotizing olfactory bulbitis. As both the olfactory bulb and frontal lobe of the cerebrum are key areas of olfaction, we believe that this tropism of SARS-CoV-2 may be key to the development of anosmia and not changes within the nasal cavity.

/pdf/gross-and-histopathology-of-covid-19-with-first-histology-1l1f4irlne.pdf

Gross and Histopathology of COVID-19 With First Histology Report of Olfactory Bulb Changes

The unexpected onset smell and taste disability was being recognized as a COVID-19 related symptom. Loss of smell might occur alone or be followed by other COVID-19 symptoms, such as a dry cough, fever, headache, and shortness of breath. Other virus infections have been linked to anosmia (parainfluenza, rhinovirus, SARS, and others), affecting up to 20% of the adult population, which is much less common than SARS-CoV-2 infection. A hypothesis about the pathophysiology of post-infectious olfactory loss is that viruses could make an inflammatory response of the nasal mucosa or directly damage the olfactory neuroepithelium. However, in patients with COVID-19, loss of smell may occur without other rhino logic symptoms or suggestive nasal inflammation. According to evidence, anosmia-related SARS-CoV-2 could be a new viral syndrome unique to COVID-19. Furthermore, through experimental intranasal inoculation in mice, SARS-CoV-2 can be inoculated into the olfactory neural circuitry. This disease has not had the required focus, most likely because it is not life-threatening in and of itself. Though patients' quality of living is significantly reduced as their olfactory ability is lost, resulting in lowering and inadequate appetite, excessive or unbalanced food consumption, as well as an overall sense of insecurity. This review aims to give a quick overview of the latest epidemiological research, pathological mechanisms for the dysfunction of smell, and taste in patients infected with SARS-CoV-2. In addition, the initial diagnosis and treatment options for dysfunction are also discussed. 

https://doi.org/10.1016/j.amsu.2022.103352

Olfactory dysfunction as a post-infectious symptom of SARS-CoV-2 infection

Smell/Taste alteration in COVID-19 may reflect zinc deficiency

Clinical outcomes of multiple sclerosis (MS) patients affected by coronavirus disease 2019 (COVID‐19) have been thoroughly investigated, but a further analysis on main signs and symptoms and their risk factors still needs attention. The objective of this study was to group together and describe based on similarity the most common signs and symptoms of COVID‐19 in MS patients and identify all factors associated with their manifestation.

/pdf/signs-and-symptoms-of-covid-19-in-patients-with-multiple-1blt6mt9.pdf

Signs and symptoms of COVID‐19 in patients with multiple sclerosis

/pdf/proposed-mechanism-for-anosmia-during-covid-19-the-role-of-30cmydektb.pdf

Proposed mechanism for anosmia during COVID-19: The role of local zinc distribution

Anosmia is common among COVID-19 patients and anosmia assessment is proposed to be useful in the early diagnosis and prognosis of patients. Data on the pathogenesis of anosmia during COVID-19 suggest potential olfactory nerve involvement. Zinc is an essential micronutrient that regulates the immune responses, and zinc deficiency is known to induce anosmia and ageusia. We previously proposed that a drop in nasal zinc level is a normal nasal immune response to acute viral infections, including SARS-CoV-2 infection, and play a role in the pathogenesis of anosmia. The drop in the local zinc level in response to SARS-CoV-2 may lead to lower type 1 interferons and shift toward Th2 immune responses; if prolonged, it may lead to increased viral replication and more severe disease. In people who are at risk for baseline systemic zinc deficiency, such as the elderly and those with chronic diseases such as, chronic lung disease, diabetes, cardiovascular disease, and cancer, SARS-CoV-2 infection-induced drop in nasal zinc level may be more severe and prolonged and lead to an insufficient anti-viral nasal immune response and control the spread of the virus systemically and to the lungs. A better understanding of the clinical implications of baseline systemic zinc deficiency on anosmia and nasal immune responses may allow the development of new treatment strategies to slow down or stop the systemic invasion of SARS-CoV-2.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/lio2.513

Intra-nasal zinc level relationship to COVID-19 anosmia and type 1 interferon response: A proposal.

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Proposed mechanism for anosmia during COVID-19: The role of local zinc distribution

Intra-nasal zinc level relationship to COVID-19 anosmia and type 1 interferon response: A proposal.