RT Journal Article SR Electronic T1 Modelling the within-host spread of SARS-CoV-2 infection, and the subsequent immune response, using a hybrid, multiscale, individual-based model. Part I: Macrophages JF bioRxiv FD Cold Spring Harbor Laboratory SP 2022.05.06.490883 DO 10.1101/2022.05.06.490883 A1 C. F. Rowlatt A1 M. A. J. Chaplain A1 D. J. Hughes A1 S. H. Gillespie A1 D. H. Dockrell A1 I. Johannessen A1 R. Bowness YR 2022 UL http://biorxiv.org/content/early/2022/05/06/2022.05.06.490883.abstract AB Individual responses to SARS-CoV-2 infection vary significantly, ranging from mild courses of infection that do not require hospitalisation to the development of disease which not only requires hospitalisation but can be fatal. Whilst many immunological studies have revealed fundamental insights into SARS-CoV-2 infection and COVID-19, mathematical and computational modelling can offer an additional perspective and enhance understanding. The majority of mathematical models for the within-host spread of SARS-CoV-2 infection are ordinary differential equations, which neglect spatial variation. In this article, we present a hybrid, multiscale, individual-based model to study the within-host spread of SARS-CoV-2 infection. The model incorporates epithelial cells (each containing a dynamical model for viral entry and replication), macrophages and a subset of cytokines. We investigate the role of increasing initial viral deposition, increasing delay in type I interferon secretion from epithelial cells (as well as the magnitude of secretion), increasing macrophage virus internalisation rate and macrophage activation, on the spread of infection.Competing Interest StatementThe authors have declared no competing interest.