The Global Dynamics of HIV Latency Model Including Cell-to-Cell Viral Transmission

Abstract

HIV spreads by cell-to-cell transfer and the release of cell-free particles. A slightly more effective method of retroviral transmission is the direct cell-to-cell transfer of HIV, according to recent reports. Intracellular interaction between unhealthy and healthy cells, in combination with cytokine discharged by the cells included, may affect the susceptibility of a target resting CD4+T cell to HIV infection and the formation of latent infection. We suggest a class of HIV latency mathematical model, integrating both cell-free virus transmission and direct cell-to-cell diffusion to improve the understanding of the dynamics of the latent reservoirs. We incorporate four components in our model: the uninfected T cells, the latently infected T cells, the active-infected T cells and the HIV viruses. We examine the latency model by introducing the basic reproduction number. We first establish the non-negativity and boundedness of the solutions of the system, and then we investigate the global stability of the steady states. The diseased-free equilibrium is globally stable when the basic reproduction number is less than 1 and if the basic reproduction number is greater than 1, the diseased equilibrium exists and is globally stable. Numerical simulations are executed to interpret the theoretical outcomes and evaluate the relative contribution of latency fractions in the virus production and the HIV latent reservoir by providing estimates.