ACE2 and infection: In particular, mutations in the receptor-binding domain (RBD) of the spike (S1) protein have demonstrated increased transmissibility through multiple mechanisms, including by i) increasing the affinity of the RBD for its cognate receptor, angiotensin-converting enzyme 2 (ACE2) [2–5] and ii) reducing RBD binding to human serum antibodies elicited by natural infection or vaccination [6–9].