2012
DOI: 10.5402/2012/215124
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Optimal Control of a Delayed HIV Infection Model with Immune Response Using an Efficient Numerical Method

Abstract: We present a delay-differential equation model with optimal control that describes the interactions between human immunodeficiency virus (HIV), CD4 + T cells, and cell-mediated immune response. Both the treatment and the intracellular delay are incorporated into the model in order to improve therapies to cure HIV infection. The optimal controls represent the efficiency of drug treatment in inhibiting viral production and preventing new infections. Existence for the optimal control pair is established, Pontryag… Show more

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Cited by 77 publications
(67 citation statements)
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References 12 publications
(15 reference statements)
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“…Hence, equation (27) has no positive roots. Thus, equation (26) has no positive roots as F R (0) = α 3 > 0.…”
Section: Length Of Delay and Stability Of The Systemmentioning
confidence: 99%
“…Hence, equation (27) has no positive roots. Thus, equation (26) has no positive roots as F R (0) = α 3 > 0.…”
Section: Length Of Delay and Stability Of The Systemmentioning
confidence: 99%
“…Cytotoxic lymphocytes are often subdivided into precursors (CTLp) and effectors (CTLe). Other considered state components includes: critical role of time-delay immunity period (or delay intracellular) and the functioning capacities of therapeutic chemotherapies, which are generally classified into two families of HAART -reverse transcriptase inhibitors (RTI) and protease inhibitors (PIs) [11][12][13][14][15][16]. In most recent dimensions, indepth evaluations of viral load have resulted to the inclusion of viral aggressiveness index denoted as r state  variable.…”
Section: Introductionmentioning
confidence: 99%
“…The amiable quest of tackling this life threatening disease -HIV/AIDS infection has been through the application of mathematical modeling, which allows the utilization of significant knowledge of numerical methods for the optimization of host target immune system cells and the minimization of systemic cost, while suppressing viral victors below detectable clinical assay, see for examples the studies of models [1][2][3][4].…”
Section: Introductionmentioning
confidence: 99%
“…Articulating the above seeming silent but unavoidable epidemiological constraints and motivated by the studies [1,5], the present paper proposes and formulates using ordinary differential equations, an improved complex nonlinear 10-Dimensional dual HIV-pathogen dynamic delay-differential model, prime with the task of not only overcoming the lapses of model [16] but also to account for the methodological application of multiple chemotherapy treatment (MCT) in dual delay HIV-pathogen infections incorporated with delay intracellular and immune effectors response. Therefore, the present model is studied under the auspices of 10-subpopulations, which includes the critical roles of immune effectors response and two treatment functions 1 () t  and 2 () t …”
Section: Introductionmentioning
confidence: 99%
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