Can ACE2 expression explain SARS-CoV-2 infection of the respiratory epithelia in COVID-19?
Martijn C NawijnWim TimensPublished in: Molecular systems biology (2020)
Infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) leads to coronavirus disease 2019 (COVID-19), which poses an unprecedented worldwide health crisis, and has been declared a pandemic by the World Health Organization (WHO) on March 11, 2020. The angiotensin converting enzyme 2 (ACE2) has been suggested to be the key protein used by SARS-CoV-2 for host cell entry. In their recent work, Lindskog and colleagues (Hikmet et al, 2020) report that ACE2 is expressed at very low protein levels-if at all-in respiratory epithelial cells. Severe COVID-19, however, is characterized by acute respiratory distress syndrome and extensive damage to the alveoli in the lung parenchyma. Then, what is the role of the airway epithelium in the early stages of COVID-19, and which cells need to be studied to characterize the biological mechanisms responsible for the progression to severe disease after initial infection by the novel coronavirus?
Keyphrases
- respiratory syndrome coronavirus
- angiotensin converting enzyme
- sars cov
- coronavirus disease
- angiotensin ii
- acute respiratory distress syndrome
- public health
- extracorporeal membrane oxygenation
- mechanical ventilation
- healthcare
- binding protein
- early onset
- induced apoptosis
- oxidative stress
- single cell
- intensive care unit
- bone marrow
- cell cycle arrest
- drug induced
- cell therapy
- signaling pathway
- pi k akt
- climate change