Stability of Impaired Humoral Immunity HIV-1 Models with Active and Latent Cellular Infections

Author:

AlShamrani Noura H.1ORCID,Halawani Reham H.1ORCID,Shammakh Wafa1ORCID,Elaiw Ahmed M.2ORCID

Affiliation:

1. Department of Mathematics, Faculty of Science, University of Jeddah, P.O. Box 80327, Jeddah 21589, Saudi Arabia

2. Department of Mathematics, Faculty of Science, King Abdulaziz University, P.O. Box 80203, Jeddah 21589, Saudi Arabia

Abstract

This research aims to formulate and analyze two mathematical models describing the within-host dynamics of human immunodeficiency virus type-1 (HIV-1) in case of impaired humoral immunity. These models consist of five compartments, including healthy CD4+ T cells, (HIV-1)-latently infected cells, (HIV-1)-actively infected cells, HIV-1 particles, and B-cells. We make the assumption that healthy cells can become infected when exposed to: (i) HIV-1 particles resulting from viral infection (VI), (ii) (HIV-1)-latently infected cells due to latent cellular infection (CI), and (iii) (HIV-1)-actively infected cells due to active CI. In the second model, we introduce distributed time-delays. For each of these systems, we demonstrate the non-negativity and boundedness of the solutions, calculate the basic reproductive number, identify all possible equilibrium states, and establish the global asymptotic stability of these equilibria. We employ the Lyapunov method in combination with LaSalle’s invariance principle to investigate the global stability of these equilibrium points. Theoretical findings are subsequently validated through numerical simulations. Additionally, we explore the impact of B-cell impairment, time-delays, and CI on HIV-1 dynamics. Our results indicate that weakened immunity significantly contributes to disease progression. Furthermore, the presence of time-delays can markedly decrease the basic reproductive number, thereby suppressing HIV-1 replication. Conversely, the existence of latent CI spread increases the basic reproductive number, intensifying the progression of HIV-1. Consequently, neglecting latent CI spread in the HIV-1 dynamics model can lead to an underestimation of the basic reproductive number, potentially resulting in inaccurate or insufficient drug therapies for eradicating HIV-1 from the body. These findings offer valuable insights that can enhance the understanding of HIV-1 dynamics within a host.

Funder

University of Jeddah, Jeddah, Saudi Arabia

Publisher

MDPI AG

Subject

Applied Mathematics,Modeling and Simulation,General Computer Science,Theoretical Computer Science

Reference53 articles.

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