Host proteases (TMPRSS2 and possibly others, such as furin) cleave the S protein to create a fusion protein that enables the virus to enter the cytoplasm.45,46 Although alveolar type I and AT2 cells express ACE2, productive infection probably occurs mainly in surfactant-producing AT2 cells, as shown for SARS-CoV.47 There may be alternate cell-entry mechanisms, such as Fc-receptor-mediated internalization of antibody-bound virions.48 Infected cells produce virions, which infect adjacent epithelial cells, endothelial cells, and macrophages. This evidence concerns the gene ACE2 and infection.