Wilcox-King Andrew, Wan Yu-Hsin, Scharffenberger Samuel C, Chhan Crystal B, Davis Amelia R, Homad Leah J, Seydoux Emilie, MacPhee Kellie J, Siddaramaiah Latha Kallur, Melo Mariane, Dosenovic Pia, Irvine Darrell J, Hyrien Ollivier, Stamatatos Leonidas, McGuire Andrew T
Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, WA, USA.
Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.
NPJ Vaccines. 2025 Aug 5;10(1):185. doi: 10.1038/s41541-025-01235-5.
VRC01-class antibodies are a genetically restricted class of antibodies capable of potently neutralizing diverse strains of HIV-1. Unmutated VRC01 precursors fail to recognize recombinant HIV-1 Envelope (Env) proteins, which necessitated the development of germline targeting vaccine immunogens capable of initiating VRC01-class B cell response. Among these, we developed an anti-idiotypic monoclonal antibody (ai-mAb)-derived VRC01 class targeting immunogen. Because it is distinct from Env, we speculated that the ai-mAb will selectively engage naive VRC01 class B cells while limiting B cell responses directed at off-target epitopes on Env during prime-boost regimens. Here, we evaluated the serum and B cell responses to ai-mAb prime/Env boost, and Env-prime/Env boost regimens in a murine adoptive transfer model where VRC01 precursor B cells are present at physiological levels. We found that the Env-Env regimen led to the greatest expansion of on-target VRC01 B cells, drove larger VRC01-class GC responses, and elicited higher titers of circulating antibodies despite also eliciting substantial off-target Env-specific responses. Single-cell sorting experiments revealed that the ai-mAb was driving off-track somatic mutations. IgG transfer experiments demonstrated that circulating off-target antibodies provide a positive feedback mechanism that potentiates on-target B cell responses. Collectively, the results suggest that non-Env immunogens are not ideal for priming VRC01-class B cells, where sequential boosting with Env will be required to drive maturation of neutralizing breadth.
VRC01类抗体是一类基因受限的抗体,能够有效中和多种HIV-1毒株。未发生突变的VRC01前体无法识别重组HIV-1包膜(Env)蛋白,这使得开发能够引发VRC01类B细胞反应的靶向胚系疫苗免疫原成为必要。在这些免疫原中,我们开发了一种源自抗独特型单克隆抗体(ai-mAb)的VRC01类靶向免疫原。由于它与Env不同,我们推测ai-mAb将选择性地激活幼稚的VRC01类B细胞,同时在初免-加强免疫方案中限制针对Env上非靶向表位的B细胞反应。在此,我们在一个小鼠过继转移模型中评估了对ai-mAb初免/Env加强免疫以及Env初免/Env加强免疫方案的血清和B细胞反应,该模型中VRC01前体B细胞以生理水平存在。我们发现,Env-Env方案导致靶向VRC01 B细胞的最大扩增,驱动更大的VRC01类生发中心反应,并引发更高滴度的循环抗体,尽管也引发了大量非靶向Env特异性反应。单细胞分选实验表明,ai-mAb正在驱动偏离轨道的体细胞突变。IgG转移实验证明,循环中的非靶向抗体提供了一种正反馈机制,可增强靶向B细胞反应。总体而言,结果表明非Env免疫原并非启动VRC01类B细胞的理想选择,其中需要用Env进行序贯加强免疫以驱动中和广度的成熟。