A new detailed mathematical model for dynamics of immune response to hepatitis B is proposed, which takes into account contributions from innate and adaptive immune responses, as well as cytokines. Stability analysis of different steady states is performed to identify parameter regions where the model exhibits clearance of infection, maintenance of a chronic infection, or periodic oscillations. Effects of nucleoside analogues and interferon treatments are analysed, and the critical drug efficiency is determined.

Abstract:A major contribution to the onset and development of autoimmune disease is known to come from infections. An important practical problem is identifying the precise mechanism by which the breakdown of immune tolerance as a result of immune response to infection leads to autoimmunity. In this paper, we develop a mathematical model of immune response to a viral infection, which includes T cells with different activation thresholds, regulatory T cells (Tregs), and a cytokine mediating immune dynamics. Particular emphasis is made on the role of time delays associated with the processes of infection and mounting the immune response. Stability analysis of various steady states of the model allows us to identify parameter regions associated with different types of immune behaviour, such as, normal clearance of infection, chronic infection, and autoimmune dynamics. Numerical simulations are used to illustrate different dynamical regimes, and to identify basins of attraction of different dynamical states. An important result of the analysis is that not only the parameters of the system, but also the initial level of infection and the initial state of the immune system determine the progress and outcome of the dynamics.