  Nanoparticles, such as viruses, can enter cells via endocytosis. During
endocytosis, the cell surface wraps around the nanoparticle to effectively eat
it. Prior focus has been on how nanoparticle size and shape impacts
endocytosis. However, inspired by the noted presence of extracellular vimentin
affecting viral and bacteria uptake, as well as the structure of coronaviruses,
we construct a computational model in which both the cell-like construct and
the virus-like construct contain filamentous protein structures protruding from
their surfaces. We then study the impact of these additional degrees of freedom
on viral wrapping. We find that cells with an optimal density of filamentous
extracellular components (ECCs) are more likely to be infected as they uptake
the virus faster and use relatively less cell surface area per individual
virus. At the optimal density, the cell surface folds around the virus, and
folds are faster and more efficient at wrapping the virus than crumple-like
wrapping. We also find that cell surface bending rigidity helps generate folds,
as bending rigidity enhances force transmission across the surface. However,
changing other mechanical parameters, such as the stretching stiffness of
filamentous ECCs or virus spikes, can drive crumple-like formation of the cell
surface. We conclude with the implications of our study on the evolutionary
pressures of virus-like particles, with a particular focus on the cellular
microenvironment that may include filamentous ECCs.

Soft Condensed Matter;Biological Physics;Cell Behavior