The genetic analysis of SARS-CoV-2 revealed that this virus is a new Betacoronavirus in close proximity to bat-derived SARS-like coronaviruses, and that SARS-CoV-2 has clear zoonotic origins, probably arising through adaptations caused by genetic mutation and recombination between different strains of coronaviruses in pangolins whose scales are used in traditional Chinese medicine [5,6]. The genomic characterization also showed that SARS-CoV-2 shares angiotensin-converting enzyme 2 (ACE2) receptors with SARS-CoV, which was the Betacoronavirus responsible for the global outbreak in 2002 [1,2]. For both coronaviruses, binding to ACE2, which is expressed on ciliated bronchial epithelial cells and type II pneumocytes, may be a critical determinant not only for clinical manifestations (i.e., pulmonary involvement) but also for transmission capacity. In fact, a strain of SARS-CoV with higher affinity for ACE2 was proved to have higher efficiency of infection in human cells and transmission between humans [7]. The binding affinity for ACE2 may explain why SARS-CoV-2 is more easily transmissible than SARS-CoV and Middle East respiratory syndrome coronavirus (MERS-CoV). The basic reproduction number (R 0, the expected number of secondary cases produced by one infected case) for SARS-CoV-2 is estimated to be more than 2 [1,8].