Speaker
Description
Predicting disease progression hinges on understanding how innate immune responses regulate viral spread at the tissue level. Type I interferon (IFN) induces local antiviral protection in epithelial cells, yet the combined effects of virion diffusion, IFN transport, and cellular heterogeneity remain difficult to capture in spatial models. We present a spatial agent-based model of influenza A virus infection in mouse lung epithelium that couples virion propagation with IFN transport. Cells transition between susceptible, refractory, infected, and IFN-producing infected states according to probabilistic rules governed by local viral load and IFN concentration. Viral replication and IFN secretion occur at the single-cell level, while extracellular virions and IFN diffuse through a heterogeneous tissue microenvironment characterized by irregular cell spacing and local density variations. Simulations reveal a competition between virion spread and IFN-mediated antiviral protection. IFN diffusion can halt infection by forming barriers of refractory cells when IFN diffusion exceeds virion diffusion. However, containment is probabilistic: under identical conditions some simulations produce effective barriers while others allow continued virion spread. The likelihood of containment depends strongly on the ratio of IFN to virion diffusion. This framework provides a stochastic spatial platform to study how innate immune responses regulate viral spread in heterogeneous tissues.
