Expression Pattern of the SARS-CoV-2 Entry Genes ACE2 and TMPRSS2 in the Respiratory Tract

Abstract

To address the expression pattern of the SARS-CoV-2 receptor ACE2 and the viral priming protease TMPRSS2 in the respiratory tract, this study investigated RNA sequencing transcriptome profiling of samples of airway and oral mucosa. As shown, ACE2 has medium levels of expression in both small airway epithelium and masticatory mucosa, and high levels of expression in nasal epithelium. The expression of ACE2 is low in mucosal-associated invariant T (MAIT) cells and cannot be detected in alveolar macrophages. TMPRSS2 is highly expressed in small airway epithelium and nasal epithelium and has lower expression in masticatory mucosa. Our results provide the molecular basis that the nasal mucosa is the most susceptible locus in the respiratory tract for SARS-CoV-2 infection and consequently for subsequent droplet transmission and should be the focus for protection against SARS-CoV-2 infection.

Impact of COVID-19 on Mitochondrial-Based Immunity in Aging and Age-Related Diseases

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Integrated human/SARS-CoV-2 metabolic models present novel treatment strategies against COVID-19

“…Previous studies have also demonstrated the role of the ACE2 as the receptor for both the SARS-CoV and the SARS-CoV-2. The ACE2 cells are expressed in the human airway epithelial cells ( Hamming et al, 2004 ; Liu et al, 2020 ). In this study, we have constructed an integrated human epithelial cell and SARS-CoV-2 to provide insight into the infection patterns of the virus in the human body.…”

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Multifunctional angiotensin converting enzyme 2, the SARS-CoV-2 entry receptor, and critical appraisal of its role in acute lung injury

“…Interestingly, recent investigations studying ACE2 expression in the respiratory system indicate that ACE2 is highly expressed in the nasal epithelium, that its expression decreases to medium levels in the epithelium of the small airways and that it cannot be detected in alveolar macrophages [ 207 ]. In agreement with this study, a gradient of decreasing ACE2 expression from nasal to intrapulmonary bronchial regions was reported [ 208 ].…”