In this paper, we propose and investigate a fractional diffusive model for hepatitis B virus (HBV) infection with capsids and immune response presented by cytotoxic T lymphocyte (CTL) cells. We derive the conditions for global asymptotic stability of the steady states of the model in terms of the basic reproduction number R0 and the immune response reproduction number R1. By constructing appropriate Lyapunov functionals, it is shown that the infection-free equilibrium is globally asymptotically stable when R0 ≤ 1, the immune-free infection equilibrium is globally asymptotically stable when R1 ≤ 1 < R0 and the infection equilibrium with CTL immune response is globally asymptotically stable when R1 > 1. Numerical simulations are performed to illustrate the analytical results.

In this paper, we propose a fractional reaction-diffusion model in order to better understand the mechanisms and dynamics of hepatitis B virus (HBV) infection in human body. The infection transmission is modeled by Hattaf–Yousfi functional response, and the fractional derivative is in the sense of Caputo. The global stability of the model equilibria is analyzed by means of Lyapunov functionals. Finally, numerical simulations are presented to support our analytical results.

Modeling by fractional order differential equations has more advantages to describe the dynamics of phenomena with memory which exists in many biological systems. In this paper, we propose a fractional order model for human immunodeficiency virus (HIV) infection by including a class of infected cells that are not yet producing virus, i.e., cells in the eclipse stage. We first prove the positivity and bound-edness of solutions in order to ensure the well-posedness of the proposed model. By constructing appropriate Lyapunov functionals, the global stability of the disease-free equilibrium and the chronic infection equilibrium is established. Numerical simulations are presented in order to validate our theoretical results.

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This paper deals with a fractional optimal control problem model that describes the interactions between hepatitis B virus (HBV) with HBV DNA-containing capsids, liver cells (hepatocytes), and the cytotoxic T-cell immune response. Optimal controls represent the effectiveness of drug therapy in inhibiting viral production and preventing new infections. The optimality system is derived and solved numerically. Our results also show that optimal treatment strategies reduce viral load and increase the number of uninfected cells, which improves the patient's quality of life.