The Omicron BA.2 variant exhibits significantly higher infectivity and immune evasion compared to BA.1 and the wildtype strain. Structural analysis reveals that BA.2's spike trimer displays all three receptor-binding domains in an open conformation, facilitating ACE2 binding. While the therapeutic antibody JMB2002 effectively neutralizes both BA.1 and BA.2, the high binding affinity of both BA.1 and BA.2 spike trimers to mouse ACE2 suggests a potential evolutionary pathway involving a human-cat-mouse-human transmission cycle.
