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2.
Am J Pathol ; 191(12): 2064-2071, 2021 12.
Article in English | MEDLINE | ID: covidwho-1506649

ABSTRACT

Current understanding of coronavirus disease 2019 (COVID-19) pathophysiology is limited by disease heterogeneity, complexity, and a paucity of studies assessing patient tissues with advanced molecular tools. Rapid autopsy tissues were evaluated using multiscale, next-generation RNA-sequencing methods (bulk, single-nuclei, and spatial transcriptomics) to provide unprecedented molecular resolution of COVID-19-induced damage. Comparison of infected/uninfected tissues revealed four major regulatory pathways. Effectors within these pathways could constitute novel therapeutic targets, including the complement receptor C3AR1, calcitonin receptor-like receptor, or decorin. Single-nuclei RNA sequencing of olfactory bulb and prefrontal cortex highlighted remarkable diversity of coronavirus receptors. Angiotensin-converting enzyme 2 was rarely expressed, whereas basigin showed diffuse expression, and alanyl aminopeptidase, membrane, was associated with vascular/mesenchymal cell types. Comparison of lung and lymph node tissues from patients with different symptoms (one had died after a month-long hospitalization with multiorgan involvement, and the other had died after a few days of respiratory symptoms) with digital spatial profiling resulted in distinct molecular phenotypes. Evaluation of COVID-19 rapid autopsy tissues with advanced molecular techniques can identify pathways and effectors, map diverse receptors at the single-cell level, and help dissect differences driving diverging clinical courses among individual patients. Extension of this approach to larger data sets will substantially advance the understanding of the mechanisms behind COVID-19 pathophysiology.


Subject(s)
COVID-19/genetics , COVID-19/pathology , SARS-CoV-2/pathogenicity , Autopsy , Disease Progression , Gene Expression Profiling , Heart/virology , Host-Pathogen Interactions/genetics , Humans , Kidney/metabolism , Kidney/pathology , Kidney/virology , Liver/metabolism , Liver/pathology , Liver/virology , Male , Middle Aged , Myocardium/metabolism , Myocardium/pathology , Olfactory Bulb/metabolism , Olfactory Bulb/pathology , Olfactory Bulb/virology , Prefrontal Cortex/metabolism , Prefrontal Cortex/pathology , Prefrontal Cortex/virology , Respiratory System/metabolism , Respiratory System/pathology , Respiratory System/virology , Salivary Glands/metabolism , Salivary Glands/pathology , Salivary Glands/virology , Sequence Analysis, RNA , Signal Transduction/genetics
3.
Viruses ; 13(11)2021 11 04.
Article in English | MEDLINE | ID: covidwho-1502532

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative pathogen of coronavirus disease 2019 (COVID-19). It is known as a respiratory virus, but SARS-CoV-2 appears equally, or even more, infectious for the olfactory epithelium (OE) than for the respiratory epithelium in the nasal cavity. In light of the small area of the OE relative to the respiratory epithelium, the high prevalence of olfactory dysfunctions (ODs) in COVID-19 has been bewildering and has attracted much attention. This review aims to first examine the cytological and molecular biological characteristics of the OE, especially the microvillous apical surfaces of sustentacular cells and the abundant SARS-CoV-2 receptor molecules thereof, that may underlie the high susceptibility of this neuroepithelium to SARS-CoV-2 infection and damages. The possibility of SARS-CoV-2 neurotropism, or the lack of it, is then analyzed with regard to the expression of the receptor (angiotensin-converting enzyme 2) or priming protease (transmembrane serine protease 2), and cellular targets of infection. Neuropathology of COVID-19 in the OE, olfactory bulb, and other related neural structures are also reviewed. Toward the end, we present our perspectives regarding possible mechanisms of SARS-CoV-2 neuropathogenesis and ODs, in the absence of substantial viral infection of neurons. Plausible causes for persistent ODs in some COVID-19 convalescents are also examined.


Subject(s)
Anosmia/epidemiology , Anosmia/etiology , COVID-19/complications , Olfactory Mucosa/virology , SARS-CoV-2/physiology , Viral Tropism , Angiotensin-Converting Enzyme 2/metabolism , Anosmia/physiopathology , COVID-19/pathology , COVID-19/virology , Humans , Olfactory Bulb/pathology , Olfactory Bulb/virology , Olfactory Mucosa/metabolism , Olfactory Mucosa/ultrastructure , Prevalence , Receptors, Coronavirus/metabolism
4.
Semin Cell Dev Biol ; 129: 22-30, 2022 Sep.
Article in English | MEDLINE | ID: covidwho-1373267

ABSTRACT

Olfactory dysfunction is often the earliest indicator of disease in a range of neurological and psychiatric disorders. One tempting working hypothesis is that pathological changes in the peripheral olfactory system where the body is exposed to many adverse environmental stressors may have a causal role for the brain alteration. Whether and how the peripheral pathology spreads to more central brain regions may be effectively studied in rodent models, and there is successful precedence in experimental models for Parkinson's disease. It is of interest to study whether a similar mechanism may underlie the pathology of psychiatric illnesses, such as schizophrenia. However, direct comparison between rodent models and humans includes challenges under light of comparative neuroanatomy and experimental methodologies used in these two distinct species. We believe that neuroimaging modality that has been the main methodology of human brain studies may be a useful viewpoint to address and fill the knowledge gap between rodents and humans in this scientific question. Accordingly, in the present review article, we focus on brain imaging studies associated with olfaction in healthy humans and patients with neurological and psychiatric disorders, and if available those in rodents. We organize this review article at three levels: 1) olfactory bulb (OB) and peripheral structures of the olfactory system, 2) primary olfactory cortical and subcortical regions, and 3) associated higher-order cortical regions. This research area is still underdeveloped, and we acknowledge that further validation with independent cohorts may be needed for many studies presented here, in particular those with human subjects. Nevertheless, whether and how peripheral olfactory disturbance impacts brain function is becoming even a hotter topic in the ongoing COVID-19 pandemic, given the risk of long-term changes of mental status associated with olfactory infection of SARS-CoV-2. Together, in this review article, we introduce this underdeveloped but important research area focusing on its implications in neurological and psychiatric disorders, with several pioneered publications.


Subject(s)
COVID-19 , Olfaction Disorders , Humans , Neuroimaging/adverse effects , Olfaction Disorders/diagnostic imaging , Olfaction Disorders/etiology , Olfaction Disorders/pathology , Olfactory Bulb/anatomy & histology , Olfactory Bulb/pathology , Pandemics , SARS-CoV-2 , Smell
5.
Acta Otolaryngol ; 141(8): 786-790, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1319071

ABSTRACT

BACKGROUND: Although there are a limited number of studies investigating the changes in olfactory bulb volume (OBV) and olfactory sulcus depth (OSD) values in the acute and subacute periods after COVID-19 infection, there are no studies conducted in the chronic period. PURPOSE: The aim of this study is to reveal the changes in OBV and OSD after COVID-19 in the chronic period. MATERIAL AND METHODS: A total of 83 people were included in our study, including 42 normal healthy individuals (control group) and 41 patients with COVID-19 infection (10-12 months after infection). RESULTS: The COVID-19 group included 41 patients with the mean age 40.27 ± 14.5 years and the control group included 42 individuals with the mean age 40.27 ± 14.4. The mean OBV was 67.97 ± 14.27 mm3 in the COVID-19 group and 94.21 ± 7.56 mm3 in the control group. The mean OSD was 7.98 ± 0.37 mm in the COVID-19 group and 8.82 ± 0.74 mm in the control group. Left, right, and mean OBVs and OSD were significantly lower in patients with COVID- 19 than the control individuals (all p < .05). CONCLUSION: Our findings show that COVID-19 infection causes a significant decrease in the OBV and OSD measurements in the chronic period.


Subject(s)
COVID-19/complications , COVID-19/pathology , Olfaction Disorders/pathology , Olfaction Disorders/virology , Olfactory Bulb/pathology , Prefrontal Cortex/pathology , Aged , COVID-19/diagnostic imaging , Case-Control Studies , Female , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Olfaction Disorders/diagnostic imaging , Olfactory Bulb/diagnostic imaging , Organ Size , Prefrontal Cortex/diagnostic imaging , Prospective Studies
6.
Immunity ; 54(7): 1594-1610.e11, 2021 07 13.
Article in English | MEDLINE | ID: covidwho-1281436

ABSTRACT

COVID-19 can cause severe neurological symptoms, but the underlying pathophysiological mechanisms are unclear. Here, we interrogated the brain stems and olfactory bulbs in postmortem patients who had COVID-19 using imaging mass cytometry to understand the local immune response at a spatially resolved, high-dimensional, single-cell level and compared their immune map to non-COVID respiratory failure, multiple sclerosis, and control patients. We observed substantial immune activation in the central nervous system with pronounced neuropathology (astrocytosis, axonal damage, and blood-brain-barrier leakage) and detected viral antigen in ACE2-receptor-positive cells enriched in the vascular compartment. Microglial nodules and the perivascular compartment represented COVID-19-specific, microanatomic-immune niches with context-specific cellular interactions enriched for activated CD8+ T cells. Altered brain T-cell-microglial interactions were linked to clinical measures of systemic inflammation and disturbed hemostasis. This study identifies profound neuroinflammation with activation of innate and adaptive immune cells as correlates of COVID-19 neuropathology, with implications for potential therapeutic strategies.


Subject(s)
Brain/immunology , CD8-Positive T-Lymphocytes/immunology , COVID-19/immunology , Microglia/immunology , Blood-Brain Barrier/immunology , Blood-Brain Barrier/metabolism , Blood-Brain Barrier/pathology , Brain/metabolism , Brain/pathology , CD8-Positive T-Lymphocytes/metabolism , COVID-19/pathology , Cell Communication , Central Nervous System/immunology , Central Nervous System/metabolism , Central Nervous System/pathology , Humans , Immune Checkpoint Proteins/metabolism , Inflammation , Lymphocyte Activation , Multiple Sclerosis/immunology , Multiple Sclerosis/pathology , Olfactory Bulb/immunology , Olfactory Bulb/metabolism , Olfactory Bulb/pathology , Respiratory Insufficiency/immunology , Respiratory Insufficiency/pathology , SARS-CoV-2 , Spike Glycoprotein, Coronavirus/metabolism , T-Lymphocyte Subsets/immunology , T-Lymphocyte Subsets/metabolism
7.
Signal Transduct Target Ther ; 6(1): 169, 2021 04 24.
Article in English | MEDLINE | ID: covidwho-1199270

ABSTRACT

Neurological manifestations are frequently reported in the COVID-19 patients. Neuromechanism of SARS-CoV-2 remains to be elucidated. In this study, we explored the mechanisms of SARS-CoV-2 neurotropism via our established non-human primate model of COVID-19. In rhesus monkey, SARS-CoV-2 invades the CNS primarily via the olfactory bulb. Thereafter, viruses rapidly spread to functional areas of the central nervous system, such as hippocampus, thalamus, and medulla oblongata. The infection of SARS-CoV-2 induces the inflammation possibly by targeting neurons, microglia, and astrocytes in the CNS. Consistently, SARS-CoV-2 infects neuro-derived SK-N-SH, glial-derived U251, and brain microvascular endothelial cells in vitro. To our knowledge, this is the first experimental evidence of SARS-CoV-2 neuroinvasion in the NHP model, which provides important insights into the CNS-related pathogenesis of SARS-CoV-2.


Subject(s)
Brain Diseases/metabolism , Brain/metabolism , COVID-19/metabolism , Olfactory Bulb/metabolism , SARS-CoV-2/metabolism , Animals , Astrocytes/metabolism , Astrocytes/pathology , Astrocytes/virology , Brain/pathology , Brain/virology , Brain Diseases/pathology , Brain Diseases/virology , COVID-19/pathology , Disease Models, Animal , Humans , Macaca mulatta , Microglia/metabolism , Microglia/pathology , Microglia/virology , Neurons/metabolism , Neurons/pathology , Neurons/virology , Olfactory Bulb/pathology , Olfactory Bulb/virology
8.
J Neurovirol ; 27(1): 171-177, 2021 02.
Article in English | MEDLINE | ID: covidwho-1064632

ABSTRACT

The complete features of the neurological complications of coronavirus disease 2019 (COVID-19) still need to be elucidated, including associated cranial nerve involvement. In the present study we describe cranial nerve lesions seen in magnetic resonance imaging (MRI) of six cases of confirmed COVID-19, involving the olfactory bulb, optic nerve, abducens nerve, and facial nerve. Cranial nerve involvement was associated with COVID-19, but whether by direct viral invasion or autoimmunity needs to be clarified. The development of neurological symptoms after initial respiratory symptoms and the absence of the virus in the cerebrospinal fluid (CSF) suggest the possibility of autoimmunity.


Subject(s)
Abducens Nerve/diagnostic imaging , COVID-19/diagnostic imaging , Cranial Nerve Diseases/diagnostic imaging , Facial Nerve/diagnostic imaging , Olfactory Bulb/diagnostic imaging , Optic Nerve/diagnostic imaging , Abducens Nerve/immunology , Abducens Nerve/pathology , Abducens Nerve/virology , Adult , Aged , Autoimmunity , COVID-19/immunology , COVID-19/pathology , COVID-19/virology , Cranial Nerve Diseases/immunology , Cranial Nerve Diseases/pathology , Cranial Nerve Diseases/virology , Facial Nerve/immunology , Facial Nerve/pathology , Facial Nerve/virology , Female , Humans , Magnetic Resonance Imaging , Male , Neuroimaging , Olfactory Bulb/immunology , Olfactory Bulb/pathology , Olfactory Bulb/virology , Optic Nerve/immunology , Optic Nerve/pathology , Optic Nerve/virology , SARS-CoV-2/pathogenicity
9.
Cells Tissues Organs ; 209(4-6): 155-164, 2020.
Article in English | MEDLINE | ID: covidwho-1042717

ABSTRACT

Usually, pandemic COVID-19 disease, caused by SARS-CoV2, presents with mild respiratory symptoms such as fever, cough, but frequently also with anosmia and neurological symptoms. Virus-cell fusion is mediated by angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) with their organ expression pattern determining viral tropism. Clinical presentation suggests rapid viral dissemination to the central nervous system leading frequently to severe symptoms including viral meningitis. Here, we provide a comprehensive expression landscape of ACE2 and TMPRSS2 proteins across human postmortem nasal and olfactory tissue. Sagittal sections through the human nose complemented with immunolabelling of respective cell types represent different anatomically defined regions including olfactory epithelium, respiratory epithelium of the nasal conchae and the paranasal sinuses along with the hardly accessible human olfactory bulb. ACE2 can be detected in the olfactory epithelium as well as in the respiratory epithelium of the nasal septum, the nasal conchae, and the paranasal sinuses. ACE2 is located in the sustentacular cells and in the glandular cells in the olfactory epithelium as well as in the basal cells, glandular cells, and epithelial cells of the respiratory epithelium. Intriguingly, ACE2 is not expressed in mature or immature olfactory receptor neurons and basal cells in the olfactory epithelium. Similarly, ACE2 is not localized in the olfactory receptor neurons albeit the olfactory bulb is positive. Vice versa, TMPRSS2 can also be detected in the sustentacular cells and the glandular cells of the olfactory epithelium. Our findings provide the basic anatomical evidence for the expression of ACE2 and TMPRSS2 in the human nose, olfactory epithelium, and olfactory bulb. Thus, they are substantial for future studies that aim to elucidate the symptom of SARS-CoV2 induced anosmia via the olfactory pathway.


Subject(s)
Angiotensin-Converting Enzyme 2/analysis , COVID-19/pathology , Nasal Mucosa/pathology , Olfactory Bulb/pathology , SARS-CoV-2/isolation & purification , Serine Endopeptidases/analysis , COVID-19/diagnosis , Humans , Nasal Mucosa/virology , Nose/pathology , Nose/virology , Olfactory Bulb/virology , Olfactory Mucosa/pathology , Olfactory Mucosa/virology
10.
PLoS Pathog ; 17(1): e1009153, 2021 01.
Article in English | MEDLINE | ID: covidwho-1006381

ABSTRACT

Neuropilin-1 (NRP-1), a member of a family of signaling proteins, was shown to serve as an entry factor and potentiate SARS Coronavirus 2 (SARS-CoV-2) infectivity in vitro. This cell surface receptor with its disseminated expression is important in angiogenesis, tumor progression, viral entry, axonal guidance, and immune function. NRP-1 is implicated in several aspects of a SARS-CoV-2 infection including possible spread through the olfactory bulb and into the central nervous system and increased NRP-1 RNA expression in lungs of severe Coronavirus Disease 2019 (COVID-19). Up-regulation of NRP-1 protein in diabetic kidney cells hint at its importance in a population at risk of severe COVID-19. Involvement of NRP-1 in immune function is compelling, given the role of an exaggerated immune response in disease severity and deaths due to COVID-19. NRP-1 has been suggested to be an immune checkpoint of T cell memory. It is unknown whether involvement and up-regulation of NRP-1 in COVID-19 may translate into disease outcome and long-term consequences, including possible immune dysfunction. It is prudent to further research NRP-1 and its possibility of serving as a therapeutic target in SARS-CoV-2 infections. We anticipate that widespread expression, abundance in the respiratory and olfactory epithelium, and the functionalities of NRP-1 factor into the multiple systemic effects of COVID-19 and challenges we face in management of disease and potential long-term sequelae.


Subject(s)
COVID-19/immunology , Neuropilin-1/immunology , SARS-CoV-2/immunology , Virus Internalization , COVID-19/pathology , Diabetic Nephropathies/immunology , Diabetic Nephropathies/pathology , Diabetic Nephropathies/virology , Humans , Immunologic Memory , Olfactory Bulb/immunology , Olfactory Bulb/pathology , Olfactory Bulb/virology , Respiratory Mucosa/immunology , Respiratory Mucosa/pathology , Respiratory Mucosa/virology , T-Lymphocytes/immunology , T-Lymphocytes/pathology
11.
Otolaryngol Head Neck Surg ; 164(6): 1337-1344, 2021 06.
Article in English | MEDLINE | ID: covidwho-852952

ABSTRACT

OBJECTIVE: This study aimed to investigate the differences in olfactory cleft (OC) morphology in coronavirus disease 2019 (COVID-19) anosmia compared to control subjects and postviral anosmia related to infection other than severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). STUDY DESIGN: Prospective. SETTING: This study comprises 91 cases, including 24 cases with anosmia due to SARS-CoV-2, 38 patients with olfactory dysfunction (OD) due to viral infection other than SARS-CoV-2, and a control group of 29 normosmic cases. METHODS: All cases had paranasal sinus computed tomography (CT), and cases with OD had magnetic resonance imaging (MRI) dedicated to the olfactory nerve. The OC width and volumes were measured on CT, and T2-weighted signal intensity (SI), olfactory bulb volumes, and olfactory sulcus depths were assessed on MRI. RESULTS: This study showed 3 major findings: the right and left OC widths were significantly wider in anosmic patients due to SARS-CoV-2 (group 1) or OD due to non-SARS-CoV-2 viral infection (group 2) when compared to healthy controls. OC volumes were significantly higher in group 1 or 2 than in healthy controls, and T2 SI of OC area was higher in groups 1 and 2 than in healthy controls. There was no significant difference in olfactory bulb volumes and olfactory sulcus depths on MRI among groups 1 and 2. CONCLUSION: In this study, patients with COVID-19 anosmia had higher OC widths and volumes compared to control subjects. In addition, there was higher T2 SI of the olfactory bulb in COVID-19 anosmia compared to control subjects, suggesting underlying inflammatory changes. There was a significant negative correlation between these morphological findings and threshold discrimination identification scores. LEVEL OF EVIDENCE: Level 4.


Subject(s)
Anosmia/pathology , Anosmia/virology , COVID-19/complications , Nasal Cavity/pathology , Olfactory Bulb/pathology , Adult , Anosmia/diagnostic imaging , COVID-19/diagnostic imaging , COVID-19/pathology , Case-Control Studies , Female , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Nasal Cavity/diagnostic imaging , Olfactory Bulb/diagnostic imaging , Olfactory Mucosa/diagnostic imaging , Olfactory Mucosa/pathology , Organ Size , Prospective Studies , Tomography, X-Ray Computed
12.
Am J Rhinol Allergy ; 35(3): 323-333, 2021 May.
Article in English | MEDLINE | ID: covidwho-760510

ABSTRACT

BACKGROUND: Post-viral olfactory dysfunction is a common cause of both short- and long-term smell alteration. The coronavirus pandemic further highlights the importance of post-viral olfactory dysfunction. Currently, a comprehensive review of the neural mechanism underpinning post-viral olfactory dysfunction is lacking. OBJECTIVES: To synthesize the existing primary literature related to olfactory dysfunction secondary to viral infection, detail the underlying pathophysiological mechanisms, highlight relevance for the current COVID-19 pandemic, and identify high impact areas of future research. METHODS: PubMed and Embase were searched to identify studies reporting primary scientific data on post-viral olfactory dysfunction. Results were supplemented by manual searches. Studies were categorized into animal and human studies for final analysis and summary. RESULTS: A total of 38 animal studies and 7 human studies met inclusion criteria and were analyzed. There was significant variability in study design, experimental model, and outcome measured. Viral effects on the olfactory system varies significantly based on viral substrain but generally include damage or alteration in components of the olfactory epithelium and/or the olfactory bulb. CONCLUSIONS: The mechanism of post-viral olfactory dysfunction is highly complex, virus-dependent, and involves a combination of insults at multiple levels of the olfactory pathway. This will have important implications for future diagnostic and therapeutic developments for patients infected with COVID-19.


Subject(s)
COVID-19/complications , Olfaction Disorders/physiopathology , Animals , COVID-19/epidemiology , COVID-19/pathology , COVID-19/physiopathology , Humans , Olfaction Disorders/epidemiology , Olfaction Disorders/pathology , Olfactory Bulb/pathology , Olfactory Mucosa/pathology , Olfactory Pathways/pathology , SARS-CoV-2/genetics , SARS-CoV-2/pathogenicity , Species Specificity
13.
Neuroradiology ; 63(1): 147-148, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-757901

ABSTRACT

As the global COVID-19 pandemic evolves, our knowledge of the respiratory and non-respiratory symptoms continues to grow. One such symptom, anosmia, may be a neurologic marker of coronavirus infection and the initial presentation of infected patients. Because this symptom is not routinely investigated by imaging, there is conflicting literature on neuroimaging abnormalities related to COVID-19-related anosmia. We present a novel case of COVID-19 anosmia with definitive olfactory bulb atrophy compared with pre-COVID imaging. The patient had prior MR imaging related to a history of prolactinoma that provided baseline volumes of her olfactory bulbs. After a positive diagnosis of COVID-19 and approximately 2 months duration of anosmia, an MRI was performed that showed clear interval olfactory bulb atrophy. This diagnostic finding is of prognostic importance and indicates that the olfactory entry point to the brain should be further investigated to improve our understanding of COVID infectious pathophysiology.


Subject(s)
Anosmia/etiology , COVID-19/complications , Olfactory Bulb/pathology , Atrophy/diagnostic imaging , Atrophy/etiology , Female , Humans , Magnetic Resonance Imaging , Olfactory Bulb/diagnostic imaging , Young Adult
14.
Brain Behav Immun ; 89: 579-586, 2020 10.
Article in English | MEDLINE | ID: covidwho-656807

ABSTRACT

Anosmia is one of the most prevalent symptoms of SARS-CoV-2 infection during the COVID-19 pandemic. However, the cellular mechanism behind the sudden loss of smell has not yet been investigated. The initial step of odour detection takes place in the pseudostratified olfactory epithelium (OE) mainly composed of olfactory sensory neurons surrounded by supporting cells known as sustentacular cells. The olfactory neurons project their axons to the olfactory bulb in the central nervous system offering a potential pathway for pathogens to enter the central nervous system by bypassing the blood brain barrier. In the present study, we explored the impact of SARS-CoV-2 infection on the olfactory system in golden Syrian hamsters. We observed massive damage of the OE as early as 2 days post nasal instillation of SARS-CoV-2, resulting in a major loss of cilia necessary for odour detection. These damages were associated with infection of a large proportion of sustentacular cells but not of olfactory neurons, and we did not detect any presence of the virus in the olfactory bulbs. We observed massive infiltration of immune cells in the OE and lamina propria of infected animals, which may contribute to the desquamation of the OE. The OE was partially restored 14 days post infection. Anosmia observed in COVID-19 patient is therefore likely to be linked to a massive and fast desquamation of the OE following sustentacular cells infection with SARS-CoV-2 and subsequent recruitment of immune cells in the OE and lamina propria.


Subject(s)
Coronavirus Infections/pathology , Olfactory Bulb/pathology , Olfactory Mucosa/pathology , Pneumonia, Viral/pathology , Animals , Betacoronavirus , COVID-19 , Cilia/pathology , Coronavirus Infections/physiopathology , Mesocricetus , Olfaction Disorders/pathology , Olfaction Disorders/physiopathology , Olfactory Bulb/virology , Olfactory Mucosa/virology , Olfactory Receptor Neurons/pathology , Olfactory Receptor Neurons/virology , Pandemics , Pneumonia, Viral/physiopathology , SARS-CoV-2
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