The recent spread of Zika virus stimulated extensive research on its structure, pathogenesis, and immunology, but mechanistic study of entry has lagged behind, in part due to the lack of a defined reconstituted system. Here, we report Zika membrane fusion measured using a platform that bypasses these barriers, enabling observation of single-virus fusion kinetics without receptor reconstitution. Surprisingly, target membrane binding and low pH are sufficient to trigger viral hemifusion to liposomes containing only neutral lipids. Second, although the extent of hemifusion strongly depends on pH, hemifusion rates are relatively insensitive to pH. Kinetic analysis shows that an off-pathway state is required to capture this pH-dependence and suggests this may be related to viral inactivation. Our surrogate-receptor approach thus yields new understanding of flaviviral entry mechanisms and should be applicable to many emerging viruses.

中文翻译：

---

Zika膜融合动力学的pH依赖性揭示了非通路状态。

寨卡病毒的最新传播激发了对其结构，发病机理和免疫学的广泛研究，但进入机制研究滞后，部分原因是缺乏确定的重组系统。在这里，我们报告使用绕过这些障碍的平台测量的Zika膜融合，可以观察到没有受体重构的单病毒融合动力学。令人惊讶地，靶膜结合和低pH足以触发病毒半融合至仅包含中性脂质的脂质体。其次，尽管半融合的程度很大程度上取决于pH值，但是半融合速率对pH相对不敏感。动力学分析表明捕获这种pH依赖性需要处于偏离路径状态，并暗示这可能与病毒灭活有关。