Expression of ACE2 and TMPRSS2 proteins in the upper and lower aerodigestive tracts of rats

Ueha, Rumi; Sato, Taku; Goto, Takao; Yamauchi, Akio; Kondo, Kenji; Yamasoba, Tatsuya

doi:10.1101/2020.05.14.097204

Cited by 18 publications

(23 citation statements)

References 18 publications

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“…Furthermore, ACE2 high expression was demonstrated in the taste buds of rats and was associated with angiotensin II production in mice taste buds. These findings might also suggest the inability of ACE2 to degrade this protein during COVID-19 infection, resulting in disorderly taste responses (Shigemura et al 2019; Mariz et al 2020; Sato et al 2020).…”

Section: Discussionmentioning

confidence: 99%

Oral Manifestations in Patients with COVID-19: A Living Systematic Review

et al. 2020

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This living systematic review aims to summarize evidence on the prevalence of oral signs and symptoms in patients with COVID-19. The review was reported per the PRISMA checklist, and the literature search was conducted in 6 databases and in gray literature. Studies published in any language mentioning oral symptoms and signs in patients with COVID-19 were included. The risk of bias was assessed by the Joanna Briggs Institute appraisal tools. The certainty of evidence was evaluated through GRADE assessment. After a 2-step selection, 40 studies were included: 33 cross-sectional and 7 case reports. Overall, 10,228 patients (4,288 males, 5,770 females, and 170 unknown) from 19 countries were assessed. Gustatory impairment was the most common oral manifestation, with a prevalence of 45% (95% CI, 34% to 55%; I2 = 99%). The pooled eligible data for different taste disorders were 38% for dysgeusia and 35% for hypogeusia, while ageusia had a prevalence of 24%. Taste disorders were associated with COVID-19 (odds ratio [OR], 12.68; 95% CI, 6.41 to 25.10; I2 = 63%; P < 0.00001), mild/moderate severity (OR, 2.09; 95% CI, 1.25 to 3.49; I2 = 66%; P = 0.005), and female patients (OR, 1.64; 95% CI, 1.23 to 2.17; I2 = 70%; P = 0.0007). Oral mucosal lesions presented multiple clinical aspects, including white and erythematous plaques, irregular ulcers, small blisters, petechiae, and desquamative gingivitis. Tongue, palate, lips, gingiva, and buccal mucosa were affected. In mild cases, oral mucosal lesions developed before or at the same time as the initial respiratory symptoms; however, in those who required medication and hospitalization, the lesions developed approximately 7 to 24 d after onset symptoms. Therefore, taste disorders may be common symptoms in patients with COVID-19 and should be considered in the scope of the disease’s onset and progression. Oral mucosal lesions are more likely to present as coinfections and secondary manifestations with multiple clinical aspects (PROSPERO CRD42020184468).

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Section: Discussionmentioning

confidence: 99%

Oral Manifestations in Patients with COVID-19: A Living Systematic Review

et al. 2020

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“…While ACE2 is expressed in the bronchial epithelium and in type 2 pneumocytes, TMPRSS2 results strongly expressed in the cytoplasm of bronchioles and alveolar epithelial cells (144). Since ACE2 was found to exist on alveolar epithelial cells at approximately similar level as in the whole lung, Sato et al found that the expression level of TMPRSS2 was considerably different between the peripheral and central parts of the lung (145). Thus, since that peripheral parts of the lung strongly express TMPRSS2, along with ACE2, the SARS-CoV-2 may be considered to damage the peripheral area at the beginning of infection.…”

Section: Lungsmentioning

confidence: 99%

Body Localization of ACE-2: On the Trail of the Keyhole of SARS-CoV-2

et al. 2020

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The explosion of the new coronavirus (SARS-CoV-2) pandemic has brought the role of the angiotensin converting enzyme 2 (ACE2) back into the scientific limelight. Since SARS-CoV-2 must bind the ACE2 for entering the host cells in humans, its expression and body localization are critical to track the potential target organ of this infection and to outline disease progression and clinical outcomes. Here, we mapped the physiological body distribution, expression, and activities of ACE2 and discussed its potential correlations and mutal interactions with the disparate symptoms present in SARS-CoV-2 patients at the level of different organs. We highlighted that despite during SARS-CoV-2 infection ACE2-expressing organs may become direct targets, leading to severe pathological manifestations, and subsequent multiple organ failures, the exact mechanism and the potential interactions through which ACE2 acts in these organs is still heavily debated. Further scientific efforts, also considering a personalized approach aimed to consider specific patient differences in the mutual interactions ACE2-SARS-CoV-2 and the long-term health effects associated with COVID-19 are currently mandatory.

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“…Much less is known about the underlying mechanisms that may explain taste reduction in COVID-19. ACE2 is expressed in epithelial cells of the tongue ( Sato and others 2020 ; Vaira and others 2020c ; Xu and others 2020 ; Cooper and others 2020 ), but probably not in taste buds ( Wang and others 2020e ), yet ACE2 inhibitor drugs are known to induce taste (and smell) disorders ( Irvin and Viau 1986 ; Naik and others 2010 ; Bertlich and others 2020 ). In the olfactory epithelium, the evidence suggests a distinct cascade of cellular events that can explain the transient anosmia in COVID-19.…”

Section: Introductionmentioning

confidence: 99%

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

2020

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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.

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Expression of ACE2 and TMPRSS2 proteins in the upper and lower aerodigestive tracts of rats

Cited by 18 publications

References 18 publications

Oral Manifestations in Patients with COVID-19: A Living Systematic Review

Oral Manifestations in Patients with COVID-19: A Living Systematic Review

Body Localization of ACE-2: On the Trail of the Keyhole of SARS-CoV-2

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

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