Abstract
Mathematical models have been considered as a robust tool to support biological and medical studies of human viral infections. The global stability of viral infection models remains an important and largely open research problem. Such results are necessary to evaluate treatment strategies for infections and to establish thresholds for treatment rates. Human T-lymphotropic virus class I (HTLV-I) is a retrovirus which infects the CD4+T cells and causes chronic and deadly diseases. In this article, we developed a general nonlinear system of ODEs which describes the within-host dynamics of HTLV-I under the effect Cytotoxic T-Lymphocytes (CTLs) immunity. The mitotic division of actively infected cells are modeled. We consider general nonlinear functions for the generation, proliferation and clearancerates for all types of cells. The incidence rate of infection is also modeled by a general nonlinear function. These general functions are assumed to satisfy a set of suitable conditions and include several forms presented in the literature. We determine a bounded domain for the system’s solutions. We prove the existence of the system’s equilibrium points and determine two threshold numbers, the basic reproductive number R0 and the CTL immunity stimulation number R1. We establish the global stability of all equilibrium points by constructing Lyapunov function and applying Lyapunov-LaSalle asymptotic stability theorem. Under certain conditions it is shown that ifR0≤1, then the infection-free equilibrium point is globally asymptotically stable (GAS) and the HTLV-I infection is cleared. If R1≤1<R0, then the infected equilibrium point without CTL immunity is GAS and the HTLV-I infection becomes chronic with no sustained CTL immune response. If R1>1, then the infected equilibrium point with CTL immunity is GAS and the infection becomes chronic with persistent CTL immune response. We present numerical simulations for the system by choosing special shapes of the general functions. The effect of Crowley-Martin functional response and mitotic division of actively infected cells on the HTLV-I progression are studied. Our results cover and improve several ones presented in the literature.