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

IF 1.9 Q2 MATHEMATICS, INTERDISCIPLINARY APPLICATIONS
Noura H. AlShamrani, Reham H. Halawani, Wafa Shammakh, Ahmed M. Elaiw
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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.
具有活性和潜伏细胞感染的体液免疫受损HIV-1模型的稳定性
本研究旨在建立和分析体液免疫受损情况下人类免疫缺陷病毒1型(HIV-1)在宿主内动态的两个数学模型。这些模型由五个区室组成,包括健康的CD4+ T细胞、(HIV-1)-潜伏感染细胞、(HIV-1)-活跃感染细胞、HIV-1颗粒和b细胞。我们假设健康细胞在暴露于以下情况时可能被感染:(i)由病毒感染引起的HIV-1颗粒(VI), (ii)由于潜伏细胞感染(CI)而被潜伏感染的HIV-1细胞,以及(iii)由于活跃CI而被活跃感染的HIV-1细胞。在第二个模型中,我们引入了分布式时滞。对于每一个系统,我们证明了解的非负性和有界性,计算了基本再生数,识别了所有可能的平衡状态,并建立了这些平衡的全局渐近稳定性。我们采用Lyapunov方法结合LaSalle不变性原理来研究这些平衡点的全局稳定性。理论结果随后通过数值模拟得到验证。此外,我们探讨了b细胞损伤、时间延迟和CI对HIV-1动力学的影响。我们的研究结果表明,免疫力的减弱显著地促进了疾病的进展。此外,时间延迟的存在可以显著减少基本繁殖数量,从而抑制HIV-1的复制。相反,潜伏CI传播的存在增加了基本繁殖数,加剧了HIV-1的进展。因此,在HIV-1动力学模型中忽略潜伏CI传播可能会导致对基本繁殖数量的低估,从而可能导致不准确或不充分的药物治疗来从体内根除HIV-1。这些发现提供了有价值的见解,可以加强对宿主内HIV-1动态的理解。
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来源期刊
Computation
Computation Mathematics-Applied Mathematics
CiteScore
3.50
自引率
4.50%
发文量
201
审稿时长
8 weeks
期刊介绍: Computation a journal of computational science and engineering. Topics: computational biology, including, but not limited to: bioinformatics mathematical modeling, simulation and prediction of nucleic acid (DNA/RNA) and protein sequences, structure and functions mathematical modeling of pathways and genetic interactions neuroscience computation including neural modeling, brain theory and neural networks computational chemistry, including, but not limited to: new theories and methodology including their applications in molecular dynamics computation of electronic structure density functional theory designing and characterization of materials with computation method computation in engineering, including, but not limited to: new theories, methodology and the application of computational fluid dynamics (CFD) optimisation techniques and/or application of optimisation to multidisciplinary systems system identification and reduced order modelling of engineering systems parallel algorithms and high performance computing in engineering.
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