Single-cell analysis of human lung epithelia reveals concomitant expression of the SARS-CoV-2 receptor ACE2 with multiple virus receptors and scavengers in alveolar type II cells

Guangchun Han; Ansam Sinjab; Warapen Treekitkarnmongkol; Patrick Brennan; Kieko Hara; Kyle Chang; Elena Bogatenkova; Beatriz Sanchez-Espiridion; Carmen Behrens; Boning Gao; Luc Girard; Jianjun Zhang; Boris Sepesi; Tina Cascone; Lauren Byers; Don L. Gibbons; Jichao Chen; Seyed Javad Moghaddam; Edwin J. Ostrin; Junya Fujimoto; Jerry Shay; John V. Heymach; John D. Minna; Steven Dubinett; Paul A. Scheet; Ignacio I. Wistuba; Edward Hill; Shannon Telesco; Christopher Stevenson; Avrum E. Spira; Linghua Wang; Humam Kadara

Upon SARS-CoV-2 infection, the clinical presentation of COVID-19 is diverse, ranging from asymptomatic infection and mild upper respiratory illness to pneumonia, acute respiratory distress syndrome (ARDS), respiratory failure and death 1 . Recent clinical reports have suggested that old age and comorbidities such as cardiovascular disease, chronic inflammatory lung disease and cancer are risk factors for COVID-19-associated severe pneumonia and death 1 . Recent analyses reported that COVID-19 patients who were smokers required more aggressive clinical interventions and that smoking possibly elevates the risk of COVID-19 associated pneumonia and death 4, 5 . These findings suggest that limiting inflammatory responses by intercepting pathways involved pulmonary (and perhaps cardiac) pathobiology may represent viable strategies to improve COVID-19 patient outcomes. lung injury mediated by SARS-CoV infection which was also alleviated by targeting the RAS 15 . A large body of literature suggests that the ACE2-mediated RAS axis plays important roles in lung function 14 , susceptibility to the SARS virus 8 , and inhibition of angiogenesis in lung cancer 16 .