Anosmia in COVID-19 patients

Hornuß, Daniel; Lange, Berit; Schröter, Nils; Rieg, Siegbert; Kern, Winfried V.; Wagner, Dirk

doi:10.1016/j.cmi.2020.05.017

Cited by 151 publications

(131 citation statements)

References 5 publications

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“…The frequency of chemosensory disorders was significantly higher among COVID-19 patients, compared to the control group (p < 0.001). Similarly, Hornuss and colleagues [83] detected a significantly higher prevalence of anosmia in a sample of COVID-19 patients (40% of 45 patients) as compared to control group (p < 0.001).…”

Section: Effects Of Sars-cov-2 On Cnsmentioning

confidence: 75%

“…In total, 6890 patients were included in the studies. Among the 68 studies on the CNS effects, 46 were case reports [16,17,, followed by 10 retrospective studies [64][65][66][67][68][69][70][71][72][73], 4 observational cohort studies [74][75][76][77], 3 prospective studies [78][79][80], 3 case-control studies [81][82][83] and 2 cross-sectional studies [84,85]. Among the 21 studies regarding PNS disorders, there were 19 case reports [86][87][88][89][90][91][92][93][94][95][96][97][98][99][100][101][102][103][104], 1 prospective study [78] and 1 retrospective study [68].…”

Section: Categorization and Characteristics Of The Selected Studiesmentioning

confidence: 99%

“…The main neurologic conditions associated to SARS-CoV-2 were found to be stroke, STDs and encephalopathy. In particular, 41% of the studies reported stroke as neurological complication [20,[22][23][24][25][26][27]33,35,37,38,44,47,51,52,54,55,57,58,62,64,65,[67][68][69]71,74,78], 26% reported STDs [34,36,40,46,49,50,66,73,[75][76][77][79][80][81][82][83][84][85] and 18% reported encephalopathy [17,[30][31][32]…”

Section: Effects Of Sars-cov-2 On Cnsmentioning

confidence: 99%

See 2 more Smart Citations

Neurological Complications of COVID-19 and Possible Neuroinvasion Pathways: A Systematic Review

Orrù

Conversano

Malloggi

et al. 2020

IJERPH

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The Coronavirus Disease 2019 (COVID-19) outbreak has shocked the whole world with its unexpected rapid spread. The virus responsible for the disease, the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), enters host cells by means of the envelope spike protein, which binds to angiotensin-converting enzyme 2 receptors. These receptors are highly expressed in heart, lungs, respiratory tract epithelium, endothelial cells and brain. Since an increasing body of significant evidence is highlighting a possible neuroinvasion related to SARS-CoV-2, a state of the art on the neurological complications is needed. To identify suitable publications, our systematic review was carried out by searching relevant studies on PubMed and Scopus databases. We included studies investigating neurologic manifestations of SARS-CoV-2 in patients over 18. According to the analyzed studies, the most frequent disorders affecting central nervous system (CNS) seem to be the following: olfactory and taste disorders, ischemic/hemorrhagic stroke, meningoencephalitis and encephalopathy, including acute necrotizing encephalopathy, a rare type of encephalopathy. As regards the peripheral nervous system (PNS), Guillain-Barré and Miller Fisher syndromes are the most frequent manifestations reported in the literature. Important clinical information on the neurological manifestations of SARS-CoV-2 would help clinicians raise awareness and simultaneously improve the prognosis of critically ill patients.

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Section: Effects Of Sars-cov-2 On Cnsmentioning

confidence: 75%

Section: Categorization and Characteristics Of The Selected Studiesmentioning

confidence: 99%

Section: Effects Of Sars-cov-2 On Cnsmentioning

confidence: 99%

See 1 more Smart Citation

Neurological Complications of COVID-19 and Possible Neuroinvasion Pathways: A Systematic Review

Orrù

Conversano

Malloggi

et al. 2020

IJERPH

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“…While self-reported new onset loss of smell is important from an infection control perspective, as it allows patients to recognize COVID infection and self-isolate at an early stage; however, psychophysical testing has demonstrated that self-reporting underestimates the true prevalence of olfactory dysfunction [7,8]. Most self-reported questionnaires combine smell and taste disorders, due to the difficulty in distinguishing perception of true taste and flavor, Psychophysical gustatory tests confirm the presence of true gustatory dysfunction in nearly half of patients tested, but with mean scores returning to normal within 3 weeks of onset [9].…”

mentioning

confidence: 99%

Anosmia: an evolution of our understanding of its importance in COVID-19 and what questions remain to be answered

Saussez

Lechien

Hopkins

2020

Eur Arch Otorhinolaryngol

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Background From the start of the pandemic, many European otolaryngologists observed an unprecendented number of anosmic patients. Early reports proposed that anosmia could be the first or even the only symptom of COVID-19 infection, prompting calls for self-isolation in affected patients. Methods In the present article, we review the COVID-19 anosmia literature and try to answer the following two questions: first, why is COVID-19 infection responsible for such a high incidence of anosmia? Second, in patients with more severe forms is anosmia really less prevalent and why? Results In terms of the etiology of olfactory dysfunction, several hypotheses were proposed at the outset of the pandemic; that olfactory cleft inflammation and obstruction caused a localized conductive loss, that there was injury to the sustentacular supporting cells in the olfactory epithelium or, given the known neurotropic potential of coronavirus, that the virus could invade and damage the olfactory bulb. Olfactory cleft obstruction may contribute to the olfactory dysfunction in some patients, perhaps most likely in those that show very early resolution, it cannot account for the loss in all patients. Moreover, disordered regrowth and a predominance of immature neurons have been shown to be associated with parosmia, which is a common finding amongst patients with Covid-related anosmia. A central mechanism therefore certainly seems to be consistent with the group of patients with more prolonged olfactory deficits. Sustentacular cells showing ACE-2 immunohistochemical expression 200 to 700 times greater than nasal or tracheal epithelia seem to be the main SARS-CoV-2 gateway. As the pathophysiology of COVID-19 anosmia seems to be better understood, the question of why patients with a moderate to severe form of COVID-19 infection have less olfactory involvement remains unresolved. Different potential explanations are discussed in this review. Conclusions The last 5 months have benefited from great international collaborative research, first highlighting and then proving the value of loss of smell and taste as a symptom of COVID-19. Adoption of loss of smell into the case definition by international public health bodies will facilitate control of disease transmission.

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“…The clinical manifestations of the disease caused by SARS-CoV-2, coronavirus disease 2019 include fever, dry cough, breathing difficulties (dyspnoea), headache and fatigue (Lima, 2020;CDC, 2019). Other symptoms observed in some patients are sore throat in the prominent upper respiratory tract, sneezing, anosmia and rhinorrhoea (Huang et al, 2020, Hornuss et al, 2020Lee et al, 2020;Lechien et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Transcriptomic dysregulations associated with SARS-CoV-2 infection in human nasopharyngeal and peripheral blood mononuclear cells

Melo

Bhuiyan

Gatua

et al. 2020

Preprint

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IntroductionOver 24 million people have been infected globally with the novel coronavirus, SARS-CoV-2, with more than 820,000 succumbing to the resulting COVID-19 disease as of the end of August 2020. The molecular mechanisms underlying the pathogenesis of the disease are not completely elucidated. Thus, we aim to understand host response to SARS-CoV-2 infection by comparing samples collected from two distinct compartments (infection site and blood), obtained from COVID-19 subjects and healthy controls.MethodsWe used two publicly available gene expression datasets generated via RNA sequencing in two different samples; nasopharyngeal swabs and peripheral blood mononuclear cells (PBMCs). We performed a differential gene expression analysis between COVID-19 subjects and healthy controls in the two datasets and then functionally profiled their differentially expressed genes (DEGs). The genes involved in innate immunity were also determined.ResultsWe found a clear difference in the host response to SARS-CoV-2 infection between the two sample groups. In COVID-19 subjects, the nasopharyngeal sample group indicated upregulation of genes involved in cytokine activity and interferon signalling pathway, as well as downregulation of genes involved in oxidative phosphorylation and viral transcription. Host response in COVID-19 subjects for the PBMC group, involved upregulation of genes involved in the complement system and immunoglobulin mediated immune response. CXCL13, GABRE, IFITM3 were upregulated and HSPA1B was downregulated in COVID-19 subjects in both sample groups.ConclusionOur results indicate the host response to SARS-CoV-2 is compartmentalized and suggests potential biomarkers of response to SARS-CoV-2 infection.HighlightsTranscriptomic profiling from publicly available RNA-seq count data revealed a site-specific immune response in COVID-19.Host response was found cellular-mediated in nasopharyngeal samples and humoral-mediated in PBMCs samples.CXCL13, GABRE and IFITM3 commonly upregulated and HSPA1B downregulated in both sample groups highlights the potential of these molecules as markers of response to SARS-CoV-2 infection.

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Anosmia in COVID-19 patients

Cited by 151 publications

References 5 publications

Neurological Complications of COVID-19 and Possible Neuroinvasion Pathways: A Systematic Review

Neurological Complications of COVID-19 and Possible Neuroinvasion Pathways: A Systematic Review

Anosmia: an evolution of our understanding of its importance in COVID-19 and what questions remain to be answered

Transcriptomic dysregulations associated with SARS-CoV-2 infection in human nasopharyngeal and peripheral blood mononuclear cells

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