The lack of efficacy in previous studies was likely because of the use of soluble CD4 as a ligand, which binds with low affinity compared with the aggregated receptors that engage in the immune synapse formed during infection, or the use of anti-HIV-1 antibodies with restricted strain specificity16, 17, 19, that is, previous bispecific proteins had neither the specificity nor activation potential required to activate and redirect T-cell killing. This evidence concerns the gene CD4 and infection.