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http://conacyt.repositorioinstitucional.mx/jspui/handle/1000/8440| Self-inhibiting percolation and viral spreading in epithelial tissue | |
| Xiaochan Xu Bjarke Frost Nielsen Kim Sneppen | |
| Acceso Abierto | |
| Atribución-NoComercial-SinDerivadas | |
| https://doi.org/10.1101/2023.12.12.571279 | |
| https://www.biorxiv.org/content/10.1101/2023.12.12.571279v1 | |
| SARS-CoV-2 induces delayed type-I/III interferon production, allowing it to escape the early innate immune response. The delay has been attributed to a deficiency in the ability of cells to sense viral replication upon infection, which in turn hampers activation of the antiviral state in bystander cells. Here, we introduce a cellular automaton model to investigate the spatiotemporal spreading of viral infection as a function of virus and host-dependent parameters. The model suggests that the considerable person-to-person heterogeneity in SARS-CoV-2 infections is a consequence of high sensitivity to slight variations in biological parameters near a critical threshold. It further suggests that within-host viral proliferation can be curtailed by the presence of remarkably few cells that are primed for IFN production. Thus the observed heterogeneity in defense readiness of cells reflects a remarkably cost-efficient strategy for protection. | |
| bioRxiv | |
| 13-12-2023 | |
| Preimpreso | |
| Inglés | |
| Público en general | |
| VIRUS RESPIRATORIOS | |
| Aparece en las colecciones: | Materiales de Consulta y Comunicados Técnicos |
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| Self-inhibiting percolation and viral spreading in epithelial tissue.pdf | 2.2 MB | Adobe PDF | Visualizar/Abrir |