中山大学钱军团队的研究显示，2018-2020年埃博拉病毒糖蛋白V75A取代的分子特征。该项研究成果发表在2026年1月22日出版的《细胞》上。
该团队发现埃博拉病毒（EBOV）糖蛋白V75A （GP-V75A）替代是疫情期间的显性变异。这种位于受体结合结构域内的替代在疫情早期出现，并迅速达到高流行率。GP-V75A在多种细胞系和小鼠模型中表现出增强的传染性。在机制上，GP- v75a增加了病毒GP与宿主受体尼曼-匹克C1 （NPC1）的结合亲和力，减少了对内体半胱氨酸蛋白酶进入的依赖。值得注意的是，GP-V75A还显著降低了NPC1靶向化合物和中和抗体的功效。流行病学分析表明，GP-V75A流行率的上升与疫情期间病例数的增加相吻合。这些发现为EBOV在大规模暴发期间的进化适应提供了重要见解，并强调了实时基因组监测对改善流行病防范的重要性。
据悉，2018-2020年埃博拉病毒病（EVD）流行促进了病毒突变的出现，在持续的人类传播过程中增强了宿主适应的可能性。
附：英文原文
Title: Molecular characterization of Ebola virus glycoprotein V75A substitution in the 2018–2020 epidemic
Author: Linjin Fan, Yulong Wang, Yinghao Wang, Zequn Wang, Xiaofeng Yang, Chudan Liang, Chongguang Yang, Nan Liu, Jun Zheng, Weifang Kang, Pengfei Ye, Pei Sun, Wendi Shi, Xinyi Guo, Weijian Wu, Jian-Rong Yang, Quan Liu, Linna Liu, Jun Qian
Issue&Volume: 2026-01-22
Abstract: The 2018–2020 Ebola virus disease (EVD) epidemic facilitated the emergence of viral mutations, enhancing the potential for host adaptation during sustained human transmission. Here, we identified the Ebola virus (EBOV) glycoprotein V75A (GP-V75A) substitution as a dominant variant during the epidemic. This substitution, located within the receptor-binding domain, emerged early in the outbreak and rapidly reached high prevalence. GP-V75A demonstrated enhanced infectivity in multiple cell lines and murine models. Mechanistically, GP-V75A increased viral GP binding affinity to the host receptor Niemann-Pick C1 (NPC1) and reduced the dependency on endosomal cysteine proteases for entry. Notably, GP-V75A also significantly reduced the efficacy of NPC1-targeting compounds and neutralizing antibodies. Epidemiological analysis indicated that the rise in GP-V75A prevalence coincided with the increase in case number during the outbreak. These findings provide crucial insights into the evolutionary adaptation of EBOV during large-scale outbreaks and underscore the importance of real-time genomic surveillance for improving epidemic preparedness.
DOI: 10.1016/j.cell.2025.12.022
Source: https://www.cell.com/cell/abstract/S0092-8674(25)01435-7