Global dynamics of a SARS-CoV-2 infection model with interferons, spatial heterogeneity and nonlocal diffusion

The global pandemic of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) highlights the critical need to understand its complex within-host dynamics. To investigate the roles of interferons (IFNs), spatial heterogeneity, and nonlocal diffusion in SARS-CoV-2 infection, we propose a novel within-host dynamics model incorporating these factors. The well-posedness of the system is first proved, and the basic reproduction number (ℛ0) of the system is defined. We then analyze global dynamics of the system based on ℛ0: when ℛ0<1, infection-free steady state is globally asymptotically stable; the system is uniformly persistent when ℛ0>1. In addition, for a special case, an appropriate Lyapunov function is constructed to prove global asymptotic stability of the unique infection steady state for ℛ0>1. Numerical simulations validate our theoretical findings and reveal that enhancing the antiviral potency of IFNs and maintaining the antiviral state are effective strategies to limit SARS-CoV-2 infection in its early stages. Moreover, our findings suggest that increasing the diffusion rates of cells and viruses can reduce ℛ0 and control viral transmission, with the diffusion of productively infected cells and viruses being particularly crucial. Our study provides theoretical insights for designing antiviral therapies and understanding SARS-CoV-2 persistence.