Noura H. AlShamrani, Reham H. Halawani, Wafa Shammakh, Ahmed M. Elaiw
{"title":"Stability of Impaired Humoral Immunity HIV-1 Models with Active and Latent Cellular Infections","authors":"Noura H. AlShamrani, Reham H. Halawani, Wafa Shammakh, Ahmed M. Elaiw","doi":"10.3390/computation11100207","DOIUrl":null,"url":null,"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.","PeriodicalId":52148,"journal":{"name":"Computation","volume":"19 1","pages":"0"},"PeriodicalIF":1.9000,"publicationDate":"2023-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Computation","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3390/computation11100207","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATHEMATICS, INTERDISCIPLINARY APPLICATIONS","Score":null,"Total":0}
引用次数: 0
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.
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.