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Anosmia in COVID-19: Underlying Mechanisms and Assessment of an Olfactory Route to Brain Infection.

ABSTRACT: In recent months it has emerged that the novel coronavirus-responsible for the COVID-19 pandemic-causes reduction of smell and taste in a large fraction of patients. The chemosensory deficits are often the earliest, and sometimes the only signs in otherwise asymptomatic carriers of the SARS-CoV-2 virus. The reasons for the surprisingly early and specific chemosensory dysfunction in COVID-19 are now beginning to be elucidated. In this hypothesis review, we discuss implications of the recent finding that the prevalence of smell and taste dysfunction in COVID-19 patients differs between populations, possibly because of differences in the spike protein of different virus strains or because of differences in the host proteins that enable virus entry, thus modifying infectivity. We review recent progress in defining underlying cellular and molecular mechanisms of the virus-induced anosmia, with a focus on the emerging crucial role of sustentacular cells in the olfactory epithelium. We critically examine the current evidence whether and how the SARS-CoV-2 virus can follow a route from the olfactory epithelium in the nose to the brain to achieve brain infection, and we discuss the prospects for using the smell and taste dysfunctions seen in COVID-19 as an early and rapid diagnostic screening tool.

SUBMITTER: Butowt R

PROVIDER: S-EPMC7488171 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia (scRNA-seq: olfactory mucosa)

Project description:A subset of COVID-19 patients exhibit altered olfactory function. Here we analyze bulk and single cell RNA-Seq datasets to identify cell types in the olfactory epithelium and olfactory bulb that express cell entry molecules that mediate infection by SARS-CoV-2 (CoV-2), the causal agent in COVID-19. We find that samples from whole olfactory mucosa in species including mouse and human express two key genes involved in CoV-2 entry, ACE2 and TMPRSS2. However, neither olfactory sensory neurons nor olfactory bulb neurons express these genes, which are instead expressed in support cells, stem cells, and perivascular cells. These findings suggest that CoV-2 infection of non-neuronal cell types leads to anosmia and related disturbances in odor perception in COVID-19 patients.

2020-07-30 | GSE151346 | GEO

Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia (scRNA-seq: olfactory bulb)

2020-07-30 | GSE148360 | GEO

Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia.

Project description:Altered olfactory function is a common symptom of COVID-19, but its etiology is unknown. A key question is whether SARS-CoV-2 (CoV-2) - the causal agent in COVID-19 - affects olfaction directly, by infecting olfactory sensory neurons or their targets in the olfactory bulb, or indirectly, through perturbation of supporting cells. Here we identify cell types in the olfactory epithelium and olfactory bulb that express SARS-CoV-2 cell entry molecules. Bulk sequencing demonstrated that mouse, non-human primate and human olfactory mucosa expresses two key genes involved in CoV-2 entry, ACE2 and TMPRSS2. However, single cell sequencing revealed that ACE2 is expressed in support cells, stem cells, and perivascular cells, rather than in neurons. Immunostaining confirmed these results and revealed pervasive expression of ACE2 protein in dorsally-located olfactory epithelial sustentacular cells and olfactory bulb pericytes in the mouse. These findings suggest that CoV-2 infection of non-neuronal cell types leads to anosmia and related disturbances in odor perception in COVID-19 patients.

| S-EPMC10715684 | biostudies-literature

Airborne aerosol olfactory deposition contributes to anosmia in COVID-19.

Project description:IntroductionOlfactory dysfunction (OD) affects a majority of COVID-19 patients, is atypical in duration and recovery, and is associated with focal opacification and inflammation of the olfactory epithelium. Given recent increased emphasis on airborne transmission of SARS-CoV-2, the purpose of the present study was to experimentally characterize aerosol dispersion within olfactory epithelium (OE) and respiratory epithelium (RE) in human subjects, to determine if small (sub 5μm) airborne aerosols selectively deposit in the OE.MethodsHealthy adult volunteers inhaled fluorescein-labeled nebulized 0.5-5μm airborne aerosol or atomized larger aerosolized droplets (30-100μm). Particulate deposition in the OE and RE was assessed by blue-light filter modified rigid endoscopic evaluation with subsequent image randomization, processing and quantification by a blinded reviewer.Results0.5-5μm airborne aerosol deposition, as assessed by fluorescence gray value, was significantly higher in the OE than the RE bilaterally, with minimal to no deposition observed in the RE (maximum fluorescence: OE 19.5(IQR 22.5), RE 1(IQR 3.2), p<0.001; average fluorescence: OE 2.3(IQR 4.5), RE 0.1(IQR 0.2), p<0.01). Conversely, larger 30-100μm aerosolized droplet deposition was significantly greater in the RE than the OE (maximum fluorescence: OE 13(IQR 14.3), RE 38(IQR 45.5), p<0.01; average fluorescence: OE 1.9(IQR 2.1), RE 5.9(IQR 5.9), p<0.01).ConclusionsOur data experimentally confirm that despite bypassing the majority of the upper airway, small-sized (0.5-5μm) airborne aerosols differentially deposit in significant concentrations within the olfactory epithelium. This provides a compelling aerodynamic mechanism to explain atypical OD in COVID-19.

| S-EPMC7864464 | biostudies-literature

Infection of Brain Pericytes Underlying Neuropathology of COVID-19 Patients.

Project description:A wide range of neurological manifestations have been associated with the development of COVID-19 following SARS-CoV-2 infection. However, the etiology of the neurological symptomatology is still largely unexplored. Here, we used state-of-the-art multiplexed immunostaining of human brains (n = 6 COVID-19, median age = 69.5 years; n = 7 control, median age = 68 years) and demonstrated that expression of the SARS-CoV-2 receptor ACE2 is restricted to a subset of neurovascular pericytes. Strikingly, neurological symptoms were exclusive to, and ubiquitous in, patients that exhibited moderate to high ACE2 expression in perivascular cells. Viral dsRNA was identified in the vascular wall and paralleled by perivascular inflammation, as signified by T cell and macrophage infiltration. Furthermore, fibrinogen leakage indicated compromised integrity of the blood-brain barrier. Notably, cerebrospinal fluid from additional 16 individuals (n = 8 COVID-19, median age = 67 years; n = 8 control, median age = 69.5 years) exhibited significantly lower levels of the pericyte marker PDGFRβ in SARS-CoV-2-infected cases, indicative of disrupted pericyte homeostasis. We conclude that pericyte infection by SARS-CoV-2 underlies virus entry into the privileged central nervous system space, as well as neurological symptomatology due to perivascular inflammation and a locally compromised blood-brain barrier.

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Cohort survey of healthcare workers with COVID-19 infection

Project description: Not available

| S-BSST563 | biostudies-other

Anosmia and ageusia associated with coronavirus infection (COVID-19) - what is known?

Project description:In 2020 a new pandemic caused by the SARS-CoV-2 coronavirus is affecting the lives of millions of patients and healthcare workers worldwide. The clinical picture of this infection is in a dynamic process of discovery, and more symptoms emerge as the clinicians observe and diagnose manifestations that affect multiple organs. Anosmia (loss of smell), and ageusia (loss of taste) become more frequently cited as independent symptoms or in association with the most common manifestations of the disease, such as fever, cough and dyspnea. A thorough screening program will prevent most nosocomial and community-acquired infections by promoting efficient triage and specific measures such as isolation of the patients. Therefore, it is important to include frequent symptoms in the anamnesis and questionnaires to select those patients who might benefit from testing, isolation, and treatment. This study summarizes the existing data regarding the association of anosmia and ageusia with the SARS-CoV-2 infection. It also aims to describe manifestations of these, particularly in the clinical picture of all symptomatic patients.

| S-EPMC7401831 | biostudies-literature

Epidemiological Observations on the Association Between Anosmia and COVID-19 Infection: Analysis of Data From a Self-Assessment Web Application.

Project description:BackgroundWe developed a self-assessment and participatory surveillance web application for coronavirus disease (COVID-19), which was launched in France in March 2020.ObjectiveOur objective was to determine if self-reported symptoms could help monitor the dynamics of the COVID-19 outbreak in France.MethodsUsers were asked questions about underlying conditions, sociodemographic status, zip code, and COVID-19 symptoms. Depending on the symptoms reported and the presence of coexisting disorders, users were told to either stay at home, contact a general practitioner (GP), or call an emergency phone number. Data regarding COVID-19-related hospitalizations were retrieved from the Ministry of Health.ResultsAs of March 29, 2020, the application was opened 4,126,789 times; 3,799,535 electronic questionnaires were filled out; and 2,477,174 users had at least one symptom. In total, 34.8% (n=1,322,361) reported no symptoms. The remaining users were directed to self-monitoring (n=858,878, 22.6%), GP visit or teleconsultation (n=1,033,922, 27.2%), or an emergency phone call (n=584,374, 15.4%). Emergency warning signs were reported by 39.1% of participants with anosmia, a loss of the sense of smell (n=127,586) versus 22.7% of participants without anosmia (n=1,597,289). Anosmia and fever and/or cough were correlated with hospitalizations for COVID-19 (Spearman correlation coefficients=0.87 and 0.82, respectively; P<.001 for both).ConclusionsThis study suggests that anosmia may be strongly associated with COVID-19 and its severity. Despite a lack of medical assessment and virological confirmation, self-checking application data could be a relevant tool to monitor outbreak trends.Trial registrationClinicalTrials.gov NCT04331171; https://clinicaltrials.gov/ct2/show/NCT04331171.

| S-EPMC7295000 | biostudies-literature

Mechanisms Underlying Potential Therapeutic Approaches for COVID-19.

Project description:Coronavirus disease (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is a betacoronavirus, and is associated with cytokine storm inflammation and lung injury, leading to respiratory distress. The transmission of the virus is mediated by human contact. To control and prevent the spread of this virus, the majority of people worldwide are facing quarantine; patients are being subjected to non-specific treatments under isolation. To prevent and stop the COVID-19 pandemic, several clinical trials are in the pipeline. The current clinical trials either target the intracellular replication and spread of the virus or the cytokine storm inflammation seen in COVID-19 cases during the later stages of the disease. Since both targeting strategies are different, the window drug administration plays a crucial role in the efficacy of the treatment. Here, we review the mechanism underlying SARS-CoV-2 cell infection and potential future therapeutic approaches.

| S-EPMC7385230 | biostudies-literature

COVID-19 and anosmia in Tehran, Iran.

Project description:Patients with acute olfactory disorders typically present to the otolaryngologist with both acute hyposmia and less often with anosmia. With the onset of COVID-19 we have noticed an increase in the number of patients who have presented with new onset of complete smell loss to the senior author's practice in Tehran, Iran. This anosmia and the frequency with which patients present is highly unusual. Coronaviruses have been known to cause common cold symptoms. COVID-19 infections have been described as causing more severe respiratory infections and the symptoms reported by authors from Wuhan, China have not specifically included anosmia. We describe patients who have presented during a two-week period of the COVID-19 pandemic with complete loss of sense of smell. Most had either no symptoms or mild respiratory symptoms. Many had a normal otolaryngologic exam. A relationship between COVID-19 and anosmia should be considered during the pandemic. We hypothesize that the mechanism of injury is similar to that of other coronavirus infections that cause central and peripheral neurologic deficits.

| S-EPMC7177057 | biostudies-literature

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