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Global dynamics of a cytokine-enhanced viral infection model with distributed delays and optimal control analysis
AIMS Mathematics 2025, 10(4): 9493-9515
Published: 15 April 2025
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This paper analyzed a cytokine-enhanced viral infection model incorporating three distributed delays: ( 1 ) Intracellular delays in infected C D 4 + T cells induced by inflammatory cytokines and viruses, ( 2 ) delays in C D 4 + T cell activation at inflammatory sites and subsequent cytokine production, and ( 3 ) viral replication delays. By using Lyapunov functionals and LaSalle's invariance principle, we established that each equilibrium exhibits global asymptotic stability under certain conditions. Furthermore, we formulated an optimality system that incorporates delays and then characterized it using Pontryagin's Maximum Principle. Numerical simulations have confirmed the global asymptotic stability of all equilibrium points in the system. Furthermore, for the optimal control system, our simulations not only justified the necessity of incorporating time delay in modeling inflammatory cytokine production but also highlighted the critical importance of tailoring precise HIV treatment strategies according to specific time-delay values.

Open Access Research Article Issue
Global properties of an HIV model with cytokine enhancement, saturated incidence and distributed delays
AIMS Mathematics 2026, 11(5): 14457-14473
Published: 15 May 2026
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This paper analyzes the global dynamics of an Human Immunodeficiency Virus (HIV) delay model which incorporates cytokine enhancement and three saturated incidence rates. Based on the distinct thresholds of two reproduction numbers, we establish the existence of both immunity-inactivated and immunity-activated equilibria. Furthermore, the global attractivity of all three equilibria is rigorously established through constructing Lyapunov functionals. Our simulations demonstrate the following: (i) enhanced virus-cell saturation demonstrates a superior efficacy over the saturation effect of inflammatory cytokines in driving systemic parameters toward Acquired Immunodeficiency Syndrome (AIDS) amelioration; (ii) immune saturation can critically impair anti-HIV defense mechanisms; (iii) increasing the virus-cell saturation levels significantly neutralizes the adverse effects of immune saturation on disease progression; and (iv) time delays exhibit therapeutic benefits within an optimal range, with diminishing returns beyond this threshold. These results suggest both saturation parameters and time delays represent potential therapeutic targets for HIV treatment.

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