key: cord-0747556-709ofj86
authors: Othman, Banw Anwar; Maulud, Sazan Qadir; Jalal, Paywast Jamal; Abdulkareem, Saman Muhsin; Ahmed, Jivan Qasim; Dhawan, Manish; Priyanka; Choudhary, Om Prakash
title: Olfactory dysfunction as a post-infectious symptom of SARS-CoV-2 infection
date: 2022-02-11
journal: Ann Med Surg (Lond)
DOI: 10.1016/j.amsu.2022.103352
sha: c30a531704b9cc9edb738d94b7628e632e578b1a
doc_id: 747556
cord_uid: 709ofj86

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.

On December 31, 2019, a novel coronavirus (COVID-19) was discovered in Wuhan, Hubei 25

Province, China, as a severe respiratory disease of humans (1-2). SARS-CoV-2, like SARS-26

CoV and MERS-CoV, is a member of the Coronaviridae family. That has a single-stranded 27 RNA genome (a positive-sense single-stranded RNA, enveloped virus). The genome size is the 28 largest among RNA viruses (3). The invasion of coronavirus to the target cells is intermediated 29 by a spike glycoproteins' transmembrane (S), which is made up of two subunits: S1, which has 30 responsibility for attaching to hosts' cell receptors, and S2, which is responsible for fusion with 31 the hosts' cell membrane. Since cleavage by a particular protease, these subunits will stay in a 32 of signs that can occur 2 to 14 days after COVID-19 exposure (1). 75 76 One of the five primary humans' senses is olfaction, which performs a multitude of vital health-77 related functions such as the detection of health risks such as fire or poisonous gases and the 78 capacity to enjoy food does have psychosocial implications (11), which might have a 79 detrimental impact on one's quality of life (22). It has been reported that olfactory disorder is The capacity of the olfactory neuron system to restore damaged olfactory neurons in the 86 olfactory epithelium is well known, and it has offered that olfactory training might enhance 87 this regeneration (11, 22, 24) . The present study aims to illustrate the relationship between OD 88 and COVID-19. Nevertheless, it enhances our understanding of olfactory circuits' dysfunction 89 physiology and offers additional information on the causes of odour issues. 90 substantial neural circuitry has been dedicated to processing olfaction and multisensory 100 integration (25). The odorant receptor is composed of coupled G-protein receptors that will activate Golf. By 106

Golf activation, adenylyl cyclase will stimulate after it comes to the formation of cyclic 107 adenosine monophosphate. Adenosine monophosphate results in action potential via the 108 opening of chloride channels and then an efflux of chloride ions (28). OSNs of the olfactory 109 bulb are bipolar neurons with axons that form synapses. Also, they had many projections called 110 dendrites that protrude out from the nasal cavity and are enclosed by sustentacular cells. Each 111 dendritic knob has 10-30 cilia that emerge into the mucus layer (29). Every OSN represents a 112 distinct OR type and all OR-specific OSNs send their axons to the glomeruli, then in the 113 olfactory bulb, they synapse with mitral and tufted cells. Second-order olfactory neurons 114 

By using spike glycoprotein (S protein), which is the initial target for antibody neutralization, 157 coronaviruses connect to the hosts' receptor and promote entry of the virus by membrane 158 fusion. The strong virulence of SARS-CoV-2 S protein, which has significantly greater 159 affinities than SARS-CoV and a lower thermostability factor than SARS-CoV, is indeed a vital 

More Than Smell

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Myeloid Cells during Viral Infections 492 and Inflammation. Viruses

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CoronaVirus (CoV) and SARS-CoV-2. Would a rose by another name smell as sweet?

Olfactory training changes 517 electrophysiological responses at the level of the olfactory epithelium

Counting the zinc-proteins 520 encoded in the human genome

Zn (2+) inhibits coronavirus and arterivirus RNA polymerase 523 activity in vitro and zinc ionophores block the replication of these viruses in cell culture