The subsequent binding of ACE2 receptor to the spike glycoprotein triggers both the ADAM17-mediated ACE2 shedding and dissociation of S1 fragments by exogenous (furin-related or other) proteases from the spike trimer, which leads on one hand to one S1-ACE2 complex and two S1 free fragments, and on the other hand to fusion of S2 viral trimers and cellular membrane structures, finally producing cell infection.