Length of mucin-like domains enhances cell-Ebola virus adhesion by increasing binding probability.

The Ebola virus (EBOV) hijacks normal physiological processes by apoptotic mimicry to be taken up by the cell it infects. The initial adhesion of the virus to the cell is based on the interaction between T cell immunoglobulin and mucin domain protein, TIM, on the cell surface and phosphatidylserine (PS) on the viral outer surface. Therefore, it is important to understand the interaction between EBOV and PS and TIM, with selective blocking of the interaction as a potential therapy.

Adhesive contact between cylindrical (Ebola) and spherical (SARS-CoV-2) viral particles and a cell membrane.

A critical event during the process of cell infection by a viral particle is attachment, which is driven by adhesive interactions and resisted by bending and tension. The biophysics of this process has been studied extensively, but the additional role of externally applied force or displacement has generally been neglected. In this work, we study the adhesive force-displacement response of viral particles against a cell membrane.

A surface with stress, extensional elasticity, and bending stiffness.

We demonstrate that the surface of a commonly used polydimethylsiloxane formulation (PDMS, Sylgard 184) treated by ultraviolet ozonolysis (UVO) has significant surface stress, considerable extensional elasticity (the "Shuttleworth Effect"), and surface bending elasticity. For soft solids, phenomena such as wetting, contact, surface flattening, and stiffening by liquid inclusions are often governed by their surface, which is usually represented by a liquid-like constant surface stress. Whether the surfaces of soft solids can have more complex constitutive response is actively debated.