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Global Properties of HIV-1 Dynamics Models with CTL Immune Impairment and Latent Cell-to-Cell Spread

Author

Listed:
  • Noura H. AlShamrani

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

  • Reham H. Halawani

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

  • Wafa Shammakh

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

  • Ahmed M. Elaiw

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

Abstract

This paper presents and analyzes two mathematical models for the human immunodeficiency virus type-1 (HIV-1) infection with Cytotoxic T Lymphocyte cell (CTL) immune impairment. These models describe the interactions between healthy CD 4 + T cells, latently and actively infected cells, HIV-1 particles, and CTLs. The healthy CD 4 + T cells might be infected when they make contact with: (i) HIV-1 particles due to virus-to-cell (VTC) contact; (ii) latently infected cells due to latent cell-to-cell (CTC) contact; and (iii) actively infected cells due to active CTC contact. Distributed time delays are considered in the second model. We show the nonnegativity and boundedness of the solutions of the systems. Further, we derive basic reproduction numbers ℜ 0 and ℜ ˜ 0 , that determine the existence and stability of equilibria of our proposed systems. We establish the global asymptotic stability of all equilibria by using the Lyapunov method together with LaSalle’s invariance principle. We confirm the theoretical results by numerical simulations. The effect of immune impairment, time delay and CTC transmission on the HIV-1 dynamics are discussed. It is found that weak immunity contributes significantly to the development of the disease. Further, we have established that the presence of time delay can significantly decrease the basic reproduction number and then suppress the HIV-1 replication. On the other hand, the presence of latent CTC spread increases the basic reproduction number and then enhances the viral progression. Thus, neglecting the latent CTC spread in the HIV-1 infection model will lead to an underestimation of the basic reproduction number. Consequently, the designed drug therapies will not be accurate or sufficient to eradicate the viruses from the body. These findings may help to improve the understanding of the dynamics of HIV-1 within a host.

Suggested Citation

  • Noura H. AlShamrani & Reham H. Halawani & Wafa Shammakh & Ahmed M. Elaiw, 2023. "Global Properties of HIV-1 Dynamics Models with CTL Immune Impairment and Latent Cell-to-Cell Spread," Mathematics, MDPI, vol. 11(17), pages 1-29, August.
    • Handle: RePEc:gam:jmathe:v:11:y:2023:i:17:p:3743-:d:1229778
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    References listed on IDEAS

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    1. AlShamrani, N.H., 2021. "Stability of a general adaptive immunity HIV infection model with silent infected cell-to-cell spread," Chaos, Solitons & Fractals, Elsevier, vol. 150(C).
    2. Liu, Huijuan & Zhang, Jia-Fang, 2019. "Dynamics of two time delays differential equation model to HIV latent infection," Physica A: Statistical Mechanics and its Applications, Elsevier, vol. 514(C), pages 384-395.
    3. Ahmed M. Elaiw & Afnan D. Al Agha, 2022. "Global Stability of a Reaction–Diffusion Malaria/COVID-19 Coinfection Dynamics Model," Mathematics, MDPI, vol. 10(22), pages 1-31, November.
    4. Hattaf, Khalid & Dutta, Hemen, 2020. "Modeling the dynamics of viral infections in presence of latently infected cells," Chaos, Solitons & Fractals, Elsevier, vol. 136(C).
    5. Alan S. Perelson & Avidan U. Neumann & Martin Markowitz & John M. Leonard & David D. Ho, 1996. "HIV-1 Dynamics In Vivo: Virion Clearance Rate, Infected Cell Lifespan, and Viral Generation Time," Working Papers 96-02-004, Santa Fe Institute.
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    Cited by:

    1. Miled El Hajji & Rahmah Mohammed Alnjrani, 2023. "Periodic Behaviour of HIV Dynamics with Three Infection Routes," Mathematics, MDPI, vol. 12(1), pages 1-23, December.

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