Viral Infection Dynamics with Immune Chemokines and CTL Mobility Modulated by the Infected Cell Density

We study a viral infection model incorporating both cell-to-cell infection and immune chemokines. Based on experimental results in the literature, we make a standing assumption that the cytotoxic T lymphocytes (CTL) will move toward the location with more infected cells, while the diffusion rate of CTL is a decreasing function of the density of infected cells. We first establish the global existence and ultimate boundedness of the solution via a priori energy estimates. We then define the basic reproduction number of viral infection R_0 and prove (by the uniform persistence theory, Lyapunov function technique and LaSalle invariance principle) that the infection-free steady state E_0 is globally asymptotically stable if R_0<1 . When R_0>1 , then E_0 becomes unstable, and another basic reproduction number of CTL response R_1 becomes the dynamic threshold in the sense that if R_1<1 , then the CTL-inactivated steady state E_1 is globally asymptotically stable; and if R_1>1 , then the immune response is uniform persistent and, under an additional technical condition the CTL-activated steady state E_2 is globally asymptotically stable. To establish the global stability results, we need to prove point dissipativity, obtain uniform persistence, construct suitable Lyapunov functions, and apply the LaSalle invariance principle.