Considering the similarity between SARS-CoV-1 and SARS-CoV-2, it is likely that their biochemical interactions and pathogenesis are also similar (80, 81). Once SARS-CoV-2 was reported to use ACE2 to enter host cells, it is suggested that the virus may target a cell spectrum similar to SARS-CoV-1 (38, 82, 83). SARS-CoV-1 is known to mainly infect macrophages and pneumocytes in the lungs, as well as other extrapulmonary tissues that express ACE2, which can also be expected for SARS-CoV-2 (82–84). However, the affinity of SARS-CoV-2 to ACE2 is 10–20-fold higher than that of SARS-CoV-1, which could explain its higher transmissibility and demonstrate that it can bind more efficiently to host cells, having a robust infection in ACE2+ cells in the upper respiratory tract (7).