Table 1.

Role for Fc-dependent BnAb functions for protection from cell free virus in vivo

Aim of study	BnAb studied	Model	Outcome	References
Compare wild type b12 with b12 versions deficient for FcR binding and/or complement binding for protection of macaques from high-dose SHIV challenge	b12	Macaque high-dose SHIV	Elimination of the ability of b12 to engage FcR diminished the ability of the antibody to protect macaques from high-dose SHIV challenge	[5]
Compare low doses of wild type b12 and b12 deficient for FcR binding for protection of macaques from repeated low-dose SHIV challenge	b12	Macaque repeated low-dose SHIV	More challenges did not result in infection of animals infused with wild type b12, as compared to animals infused with b12 deficient in FcR binding	[35]
Assess if low doses of a non-fucosylated version of b12, with enhanced ADCC potential, are better than wild type b12 for protecting macaques from repeated low-dose SHIV challenge	b12	Macaque repeated low-dose SHIV	Non-fucosylated b12 did not provide enhanced protection from repeated low-dose SHIV challenge, as compared to wild type b12	[36]
Screen panel of BnAbs with enhanced of diminished FcR binding for ability to block viral entry in a murine model	BnAb panel	Murine HIV-1 entry	BnAbs with enhanced FcR binding demonstrated enhanced in vivo blocking of HIV-1 entry	[20]
Determine if modifying VRC01 to enhance binding to FcRn improves the ability of suboptimal doses of the BnAb to protect against SHIV challenge	VRC01	Macaque SHIV	Suboptimal doses of VRC01 with enhanced binding to FcRn protected more macaques from SHIV challenge than wild type VRC01	[31]