Alexandria Engineering Journal (Nov 2024)
Analysis of general HIV-1 infection models with weakened adaptive immunity and three transmission modalities
Abstract
Current medical research suggests that latently infected cells are the primary source of the virus’s resistance to elimination. Moreover, these cells can participate in cell–cell transmission. Human immunodeficiency virus type 1 (HIV-1) can transmit to CD4+T cells by three transmission modes, cell-free, latent cell–cell and active cell–cell. Incorporating the effect of latent infection, weakened humoral and CTL responses as well as three transmission modes, we investigate two generalized HIV-1 dynamics models. Three general incidence functions are used to represent the three viral transmission modes. Our proposed models extend and generalize many viral infection models presented in the virology literature. We begin by demonstrating the solutions’ boundedness and nonnegativity which guarantee the model’s wellposedness. We calculate the model’s basic reproduction ratio (ℜ0). We establish that the model admits two steady-states, namely, virus-free steady-state and virus-persistence steady-state. Through application of Lyapunov’s approach and LaSalle’s invariance principle, we demonstrate the global stability of each state-state. For two special forms of the general incidence functions, Holling type-II incidence and Crowley–Martin incidence, we provide numerical simulations to validate our theoretical findings. We illustrate how time delay and weakened adaptive immunity affect HIV-1 dynamics. More specifically, numerical data support our theoretical conclusions on the stability of steady-states. To demonstrate the impact of the parameter values on ℜ0, we examine the sensitivity analysis. We have demonstrated that each of the three viral transmission modes adds to ℜ0, and that ℜ0 would be underestimated if any one of them were ignored. This might lead to inadequate medication effectiveness that aims to remove the viruses from the body. The effects of weakened adaptive immunity and time delay on HIV-1 progression are examined. As per our findings, reduced adaptive immunity plays a crucial role in the proliferation of the infection. Weaken adaptive immunity can lead to the acquired immune deficiency syndrome (AIDS) and give a chance for opportunistic infections. We showed that ℜ0 fall as a function of both medication efficacy and delay parameter. If a model with time delays is used, fewer treatment efficacies will be required to maintain the system at the virus-free steady-state and eradicate HIV-1 from the body. Our study’s findings can help us better understand HIV-1 dynamics in the host and can also guide the development of new pharmacological therapies.
