CD4 and HIV-1 infection: In addition, viral and neutralizing antibody evolution data collected from longitudinal HIV-1 infection case studies, demonstrated that the development of bNAbs targeting either a complex epitope encompassing the V2 loop, CAP256-VRC26 (ref. 39), or the CD4-BS, CH103 (ref. 40), was dependent on the emergence of particular viral variants capable of activating the germline BCR forms of these antibodies and on the continuous evolution of variants capable of driving the mutation of BCRs along particular evolutionary pathways.