Institute of Molecular Life Science, University of Zürich, Winterthurerstrasse, Switzerland.
Cell Host Microbe. 2011 Aug 18;10(2):105-17. doi: 10.1016/j.chom.2011.07.006.
Viral particle binding to plasma membrane receptors elicits virus motions, recruits signaling proteins, and triggers membrane bending and fission, finally resulting in endocytic virus uptake. Here we analyze how human adenovirus engages its receptor coxsackievirus adenovirus receptor (CAR) and coreceptor αv integrin to move on the plasma membrane. Virus binding to CAR through fiber knobs gave rise to diffusive motions and actomyosin-2-dependent drifts, while integrin-targeted viruses were spatially more confined. Diffusions, drifts, and confined motions were specifically observed with viral particles that were subsequently internalized. CAR-mediated drifts together with integrin binding supported fiber shedding from adenovirus particles, leading to exposure of the membrane-lytic internal virion protein VI and enhanced viral escape from endosomes. Our results show that adenovirus uncoating is initiated at the plasma membrane by CAR drifting motion and binding to immobile integrins.
病毒粒子与质膜受体结合会引发病毒运动，募集信号蛋白，并触发膜弯曲和裂变，最终导致内吞作用摄取病毒。在这里，我们分析了人类腺病毒如何与它的受体柯萨奇病毒腺病毒受体 (CAR) 和辅助受体αv 整合素在质膜上移动。病毒通过纤维球与 CAR 结合引起弥散运动和肌动球蛋白-2 依赖性漂移，而整合素靶向的病毒在空间上受到更大的限制。与随后被内化的病毒颗粒一起，特异性地观察到扩散、漂移和受限运动。CAR 介导的漂移与整合素结合共同支持纤维从腺病毒颗粒上脱落，导致膜裂解内部病毒蛋白 VI 暴露，并增强病毒从内涵体中的逃逸。我们的结果表明，腺病毒脱壳是由 CAR 漂移运动和与固定整合素的结合在质膜上启动的。
