Wang Jiajun, Ziarnik Matthew, Zhang X Frank, Jagota Anand
Department of Bioengineering, Lehigh University, Bethlehem, Pennsylvania 18015, United States.
Department of Biomedical Engineering, University of Massachusetts Amherst, Amherst, Massachusetts 01003, United States.
J Phys Chem B. 2024 Nov 28;128(47):11546-11553. doi: 10.1021/acs.jpcb.4c04527. Epub 2024 Sep 24.
We present a model for virus-cell adhesion that can be used for quantitative extraction of adhesive properties from atomic force microscopy (AFM)-based force spectroscopy measurements. We extend a previously reported continuum model of viral cell interactions based on a single parameter representing adhesive energy density by using a cohesive zone model in which adhesion is represented by two parameters, a pull-off stress and associated characteristic displacement. This approach accounts for the deformability of the adhesive receptors, such as the Spike protein and transmembrane immunoglobulin and mucin domain (TIM) family that mediate adhesion of SARS-CoV-2 and Ebola viruses, and the omnipresent glycocalyx. Our model represents receptors as a Winkler foundation and aims to predict the pull-off force needed to break the adhesion between the virus and the cell. By comparing the force-separation curves simulated by the model and experimental data, we found that the model can effectively explain the AFM pull-off force trace, thus allowing quantification of the adhesion parameters. Our model provides a more refined understanding of viral cell adhesion and also establishes a framework for interpreting and predicting AFM force spectroscopy measurements.
我们提出了一种病毒 - 细胞粘附模型,该模型可用于从基于原子力显微镜(AFM)的力谱测量中定量提取粘附特性。我们扩展了先前报道的基于表示粘附能量密度的单个参数的病毒 - 细胞相互作用连续模型,采用了内聚区模型,其中粘附由两个参数表示,即拉脱应力和相关的特征位移。这种方法考虑了粘附受体的可变形性,例如介导SARS-CoV-2和埃博拉病毒粘附的刺突蛋白、跨膜免疫球蛋白和粘蛋白结构域(TIM)家族,以及普遍存在的糖萼。我们的模型将受体表示为温克勒地基,旨在预测破坏病毒与细胞之间粘附所需的拉脱力。通过比较模型模拟的力 - 分离曲线和实验数据,我们发现该模型可以有效地解释AFM拉脱力曲线,从而实现粘附参数的量化。我们的模型为病毒 - 细胞粘附提供了更精确的理解,也为解释和预测AFM力谱测量建立了一个框架。