This work investigates the dynamics of a diffusive viral infection model that incorporates a nonlinear incidence and follicular dendritic cells (FDCs). First, the well-posedness is established. Then, We show that the basic reproduction number serves as a critical threshold for global stabilities: the infection-free steady state is globally asymptotically stable when the basic reproduction number is less than one, while the model exhibits a uniform persistence when the basic reproduction number is greater than one. Under the condition that the basic reproduction number equals to one, the infection-free steady state is shown to be globally asymptotically stable given certain additional assumptions. Furthermore, the global stability of the infected steady state is established for the homogeneous case. We find that ignoring the spatial heterogeneity in the infection capacity of viruses and infected cells may lead to an underestimation of the transmission risk. Although the spatial heterogeneity of a FDC does not affect the basic reproduction number, neglecting the infection originating from a FDC may lead to an underestimation of the infection risk.

In this paper, we propose a new viral infection model by incorporating a new compartment for follicular dendritic cell (FDC), nonlinear incidence, CTL immune response, and two intracellular delays. The main purpose of the paper is to make an improvement and supplement to the global dynamics of the model proposed by Callaway and Perelson (2002), in which global stability has not been studied. The global stabilities of equilibria are established by constructing corresponding Lyapunov functionals in terms of two threshold parameters, ${\mathfrak{R}}_0$ and ${\mathfrak{R}}_1$. The obtained results imply that both nonlinear incidence and intracellular time delays have no impact on the stability of the model.