Texas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, United States of America.
Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang, China.
PLoS Pathog. 2020 Aug 3;16(8):e1008736. doi: 10.1371/journal.ppat.1008736. eCollection 2020 Aug.
Human cytomegalovirus (HCMV) is one of the main causative agents of congenital viral infection in neonates. HCMV infection also causes serious morbidity and mortality among organ transplant patients. Glycoprotein B (gB) is a major target for HCMV neutralizing antibodies, yet the underlying neutralization mechanisms remain largely unknown. Here we report that 3-25, a gB-specific monoclonal antibody previously isolated from a healthy HCMV-positive donor, efficiently neutralized 14 HCMV strains in both ARPE-19 cells and MRC-5 cells. The core epitope of 3-25 was mapped to a highly conserved linear epitope on antigenic domain 2 (AD-2) of gB. A 1.8 Å crystal structure of 3-25 Fab in complex with the peptide epitope revealed the molecular determinants of 3-25 binding to gB at atomic resolution. Negative-staining electron microscopy (EM) 3D reconstruction of 3-25 Fab in complex with de-glycosylated postfusion gB showed that 3-25 Fab fully occupied the gB trimer at the N-terminus with flexible binding angles. Functionally, 3-25 efficiently inhibited HCMV infection at a post-attachment step by interfering with viral membrane fusion, and restricted post-infection viral spreading in ARPE-19 cells. Interestingly, bivalency was required for HCMV neutralization by AD-2 specific antibody 3-25 but not the AD-4 specific antibody LJP538. In contrast, bivalency was not required for HCMV binding by both antibodies. Taken together, our results reveal the structural basis of gB recognition by 3-25 and demonstrate that inhibition of viral membrane fusion and a requirement of bivalency may be common for gB AD-2 specific neutralizing antibody.
人巨细胞病毒(HCMV)是导致新生儿先天性病毒感染的主要病原体之一。HCMV 感染也是器官移植患者严重发病率和死亡率的原因。糖蛋白 B(gB)是 HCMV 中和抗体的主要靶标,但潜在的中和机制在很大程度上仍不清楚。在这里,我们报告先前从健康的 HCMV 阳性供体中分离出的 gB 特异性单克隆抗体 3-25 能够有效中和 ARPE-19 细胞和 MRC-5 细胞中的 14 株 HCMV 株。3-25 的核心表位被映射到 gB 抗原域 2(AD-2)上的一个高度保守的线性表位。3-25 Fab 与肽表位复合物的 1.8 Å 晶体结构揭示了 3-25 与 gB 结合的分子决定因素,达到原子分辨率。3-25 Fab 与去糖基化融合后 gB 的负染电子显微镜(EM)3D 重建显示,3-25 Fab 以灵活的结合角度完全占据 gB 三聚体的 N 端。功能上,3-25 通过干扰病毒膜融合,在附着后步骤有效抑制 HCMV 感染,并限制 ARPE-19 细胞中的感染后病毒扩散。有趣的是,AD-2 特异性抗体 3-25 中和 HCMV 需要二价性,但 AD-4 特异性抗体 LJP538 不需要。相比之下,两种抗体都不需要 HCMV 结合的二价性。总之,我们的结果揭示了 3-25 识别 gB 的结构基础,并表明抑制病毒膜融合和二价性的要求可能是 gB AD-2 特异性中和抗体的共同特征。