HIV Immunology Goes Out On a Limb Nicole A. Doria-Rose, John R. Mascola  Immunity  Volume 44, Issue 5, Pages 1088-1090 (May 2016) DOI: 10.1016/j.immuni.2016.05.004 Copyright © 2016 Terms and Conditions

Figure 1 HIV Env Sites of Vulnerability to bNAbs (Top) Five sites are well described targets of bNAbs that have been isolated from multiple HIV-infected individuals. Antibody development pathways have been described for the Env CD4 binding site (Bonsignori et al., 2016; Gao et al., 2014; Liao et al., 2013) and V1-V2 apex (Bhiman et al., 2015; Doria-Rose et al., 2016; Doria-Rose et al., 2014). In this issue, MacLeod et al. delineate the development of antibodies to the high-mannose patch of gp120, also called the glycan-V3 supersite. (Bottom) Upon HIV infection, the naive version of a bNAb—the UCA— might engage the initial founder virus or a mutant thereof, termed the lineage-triggering virus. That virus mutates at the antibody epitope and escapes the early antibody. Some limbs of the antibody lineage will be unable to engage the mutated virus and will die out (dead-end limb). Others will diversify and mature to tolerate the escape mutants and other diverse viral variants, allowing neutralization of the escape variants and, fortuitously, heterologous viruses, thus producing bNAbs (multiple broad limbs). Immunity 2016 44, 1088-1090DOI: (10.1016/j.immuni.2016.05.004) Copyright © 2016 Terms and Conditions