Rita de Almeida Slides

Rita de Almeida Video

James Faeder Slides

James Faeder Video

James Faeder Abstract: Most intrahost models of viral infections track virus are built on ordinary differential equations that track viral and cell population but that simplify processes at the intracellular level. While these models have yielded key insights into the factors that affect viral load kinetics and have identified how factor such as timing and mechanism can determine treatment efficacy, there are several questions that require more detailed modeling of interactions at the molecular level. In particular, viral replication products and host signaling pathways interact in numerous ways that determine both the quantitative and qualitative outcomes of infection. Here, I will describe our initial attempts to model viral replication and to embed more detailed kinetic models inside a larger multiscale framework called PhysiCell, that models viral dynamics in a multicellular context. These efforts have been carried in collaboration with a large group of scientists led by Paul Macklin at the University of Indiana. While that effort has been largely concerned with modeling the complex array of cell types that are recruited to the site of infection over the course of several days, we are also interested in modeling the cell type specific induction of interferon responses at the intracellular level and its potential effects for both the local and systemic control of viral infection. This work is in collaboration with Caroline Larkin, William Klimstra, Penelope Morel, Ali Sinan Saglam, Jason Shoemaker, and other investigators in the SARS-CoV-2 Tissue Simulation Coalition.