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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 whichboththe 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.
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This content will become publicly available on April 1, 2026
How cells wrap around coronavirus-like particles using extracellular filamentous protein structures
Nanoparticles, such as viruses, can enter cells via endocytosis, a process by which the cell membrane wraps around them. The role of nanoparticle size and shape on endocytosis has been well studied, but the biophysical details of how extracellular proteins on the cell membrane surface mediate uptake are less clear. Motivated by recent discoveries regarding extracellular vimentin in viral and bacterial uptake and the structure of coronaviruses, we construct a computational model with a cell-like and virus-like construct containing filamentous protein structures protruding from their surfaces. We study the impact of these additional degrees of freedom on viral wrapping. The cell surface is modeled as a deformable sheet with bending rigidity, and extracellular vimentin as semiflexible polymers, or extracellular components (ECC), placed randomly on the sheet. The virus is modeled as a deformable shell that also has explicit, freely rotating spike filaments on its surface. Our results indicate that cells with optimally populated filaments are more susceptible to infection as they take up the virus more quickly and utilize a relatively smaller area of the cell surface. At optimal ECC density, the cell surface forms a fold around the virus, which is faster and more efficient at wrapping than localized crumples. Additionally, cell surface bending rigidity aids in the generation of folds by increasing force transmission across the surface. Changing other mechanical parameters, such as the stretching stiffness of filamentous ECC or virus spikes, can result in localized crumple formation on 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. Published by the American Physical Society2025
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- Award ID(s):
- 2019745
- PAR ID:
- 10597068
- Publisher / Repository:
- American Physical Society
- Date Published:
- Journal Name:
- Physical Review Research
- Volume:
- 7
- Issue:
- 2
- ISSN:
- 2643-1564
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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