Author: Sharif-Askari, Narjes Saheb; Sharif-Askari, Fatemeh Saheb; Alabed, Mashael; Temsah, Mohamed-Hani; Alheialy, Saba; Hamid, Qutayba; Halwani, Rabih
Title: Expression of SARS-CoV-2 receptor, ACE2, and TMPRSS2 in the lung airways is lower in children compared to adults and increases due to smoking and COPD Cord-id: 7bf53y6s Document date: 2020_5_22
ID: 7bf53y6s
Snippet: Abstract It has been reported that ACE2 and TMPRSS2 are the main cell entry proteins for SARS-CoV-2 and play a critical role in causing COVID-19. To investigate the expression level of these SARS-CoV-2 host cell entry genes in lung airway, public gene expression datasets were used. We have found a differential expression of ACE2 and TMPRSS2 in nasal and bronchial airways relative to age and diseases status. Children were found to have significantly lower expression of COVID-19 receptors in the u
Document: Abstract It has been reported that ACE2 and TMPRSS2 are the main cell entry proteins for SARS-CoV-2 and play a critical role in causing COVID-19. To investigate the expression level of these SARS-CoV-2 host cell entry genes in lung airway, public gene expression datasets were used. We have found a differential expression of ACE2 and TMPRSS2 in nasal and bronchial airways relative to age and diseases status. Children were found to have significantly lower expression of COVID-19 receptors in the upper and lower airways (nasal and bronchial). Moreover, the lung airway expression of both ACE2 and TMPRSS2 was found to be significantly upregulated in smokers compared to non-smokers; and in patients with COPD compared to healthy. No difference was observed in the blood expression levels of ACE2 and TMPRSS2 between children and adults, or in COPD or diabetic patients. However, a significant increase in blood expression levels of these genes was observed in patients with essential hypertension; while only ACE2 was upregulated in the blood of asthmatic. These results suggest that the observed difference in COVID-19 severity between children and adults could, in part, be attributed to the difference in ACE2 and TMPRSS2 airways tissue expression levels.
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