Systemic diseases and disorders

Doty, Richard L.

doi:10.1016/b978-0-444-63855-7.00021-6

Cited by 12 publications

(9 citation statements)

References 227 publications

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“…A possible association between olfactory dysfunction and CoV-2 is consistent with a case report describing a patient with SARS with long term anosmia after recovery from respiratory distress 14 , with the observation that olfactory function is commonly altered after infection with endemic coronaviruses 7,[15][16][17] , and with data demonstrating that intentional experimental infection of humans with hCoV-299E raises the thresholds at which odors can be detected 18 . Although definitive reports of pervasive CoV-2-associated anosmia have not yet been published in the literature (but see 19 ), these collective findings raise the question of how CoV-2 might influence odor processing mechanisms to change smell perception in COVID-19 patients.…”

Section: Introductionsupporting

confidence: 86%

“…Many possible mechanisms have been proposed through which viruses can alter olfactory function, including inflammation-related deficits in odor conduction and primary damage to the olfactory epithelium 15,16 . Viral injury has been extensively modeled in rodents, which has revealed substantial diversity among viruses (and even within different types of coronaviruses) in the nature and extent of damage to the OE 16,[58][59][60][61] . Intriguingly, infection of the rat with the SDAV coronavirus appears to cause denuding of ciliary cells in the RE, reduction in the number of goblet cells in the RE, and focal infection of subsets of sustentacular cells in the OE.…”

Section: Discussionmentioning

confidence: 99%

“…However, viral-induced deficits in olfactory function may also be caused by central dysfunction in higher-order olfactory structures. Many viruses, including coronaviruses, have been shown to propagate from the nasal epithelium past the cribriform plate to infect the olfactory bulb and downstream areas like piriform cortex; this form of central infection has been suggested to mediate olfactory deficits, even in the absence of lasting OE damage 16,40,59,61,[67][68][69] . Coronoviral RNA has been identified in the brains of patients, suggesting this possibility as a pathophysiological mechanism in the case of COVID-19 67,70 .…”

Section: Discussionmentioning

confidence: 99%

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

Brann

Tsukahara

Weinreb

et al. 2020

Preprint

282

343

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Recent reports suggest an association between COVID-19 and altered olfactory function. Here we analyze bulk and single cell RNA-Seq datasets to identify cell types in the olfactory epithelium that express molecules that mediate infection by SARS-CoV-2 (CoV-2), the causal agent in COVID-19. We find in both mouse and human datasets that olfactory sensory neurons do not express two key genes involved in CoV-2 entry, ACE2 and TMPRSS2. In contrast, olfactory epithelial support cells and stem cells express both of these genes, as do cells in the nasal respiratory epithelium. Taken together, these findings suggest possible mechanisms through which CoV-2 infection could lead to anosmia or other forms of olfactory dysfunction.

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Section: Introductionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

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

Brann

Tsukahara

Weinreb

et al. 2020

Preprint

282

343

View full text Add to dashboard Cite

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“…Two anosmic patients with COVID-19 have presented with functional magnetic resonance imaging-identified hyperintensity in both OBs that reverted to normal after resolution of the anosmia (58,59), consistent with central involvement in at least some cases. Many viruses, including coronaviruses, have been shown to propagate from the nasal epithelium past the cribriform plate to infect the OB; this form of central infection has been suggested to mediate olfactory deficits, even in the absence of lasting OE damage (60)(61)(62)(63)(64)(65). The rodent coronavirus MHV (mouse hepatitis virus) passes from the nose to the bulb, although rodent OSNs do not express Ceacam1, the main MHV receptor (figs.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2020

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Abstract: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.

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“…Olfactory loss can be devastating to patients, significantly altering the flavor of foods and beverages, their nutrition, and their safety. Although loss of smell function can arise from head trauma, 1 exposures to toxic agents, 2 and a number of diseases, 3 including Alzheimer's and Parkinson's, 4 acute viral upper respiratory infections that damage the olfactory neuroepithelium are the major cause of chronic olfactory dysfunction, a condition termed postviral olfactory disorder (PVOD) 5‐7 . Importantly, a number of viruses have the propensity to invade the brain via the olfactory fila 8,9 …”

mentioning

confidence: 99%

Olfactory dysfunction from acute upper respiratory infections: relationship to season of onset

Potter

Chen

Lobban

et al. 2020

Int Forum Allergy Rhinol

Self Cite

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Background: Acute viral upper respiratory tract infections are the most common cause of chronic olfactory dysfunction. In light of the seasonality of numerous viruses, the question arises as to whether the frequency and magnitude of postviral olfactory disorders (PVODs) are similarly seasonal. We sought to determine whether olfactory deficits due to influenza and non-influenza-related viruses (I-PVODs and NI-PVODs) vary in frequency or magnitude across seasons in a North American population and whether they are more prevalent or produce more severe olfactory dysfunction during colder months when host susceptibility may be increased. Methods:This was a retrospective study of 587 patients presenting to an academic smell and taste center with either I-PVOD-related or NI-PVOD-related olfactory deficits. Chi-square and analysis of covariance (age = covariate) compared dysfunction prevalence frequencies and scores on the University of Pennsylvania Smell Identification Test (UPSIT) across calendar months and between months with the coldest and warmest air temperatures. Results:For I-PVOD-related cases, both the prevalence and magnitude of smell dysfunction were highest in the colder months. However, for NI-PVOD-related cases, prevalence was higher in warmer months but, paradoxically, the magnitude of dysfunction was higher in colder months. Conclusion:This study shows that seasonal variations occur in both the prevalence and magnitude of PVOD-related olfactory deficits in a North American population, and that such variations differ between NI-PVOD and I-PVOD cases. The findings suggest multiple viruses are involved in producing PVOD-related olfactory deficits. C 2020 ARS-AAOA, LLC. How to Cite this Article:Po er MR, Chen JH, Lobban N-S, Doty RL. Olfactory dysfunction from acute upper respiratory infections: relationship to season of onset. Int Forum Allergy Rhinol. 2020;10:706-712.

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Systemic diseases and disorders

Cited by 12 publications

References 227 publications

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

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

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

Olfactory dysfunction from acute upper respiratory infections: relationship to season of onset

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