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  DOI Prefix   10.20431


 

International Journal of Scientific and Innovative Mathematical Research
Volume 5, Issue 6, 2017, Page No: 1-19

Quantum Optimal Control Dynamics for Delay Intracellular and Multiple Chemotherapy Treatment (MCT) of Dual Delayed HIV - Pathogen Infections

Bassey E.Bassey

Department of Mathematics /Statistics, Cross River University of Technology, Calabar, Nigeria.

Citation :Bassey E.Bassey, Quantum Optimal Control Dynamics for Delay Intracellular and Multiple Chemotherapy Treatment (MCT) of Dual Delayed HIV - Pathogen Infections International Journal of Scientific and Innovative Mathematical Research 2017,5(6) : 1-19

Abstract

In furtherance to the pursuit for the advent of more precised and acceptable preventive and suppressive approach to the continual de-replication of viral load and parasitoid-pathogen with presupposed maximization of both CD4+ T-lymphocytes and cytotoxic T-lymphocytes (CTLs), this present study using ordinary differential equation, formulated a set of nonlinear complex 10-Dimensional mathematical dynamic dual HIV-pathogen model. In addition to the embedded dual infectivity, the novelty of this present work is in the incorporation of the crucial role of delay intracellular and immune effectors response in the presence of multiple chemotherapeutic treatments. Presenting the model as an optimal control problem and saddle with terminal time objective functional, classical Hamilton-Pontryagin function was explored in the analysis of derived quantum locally optimal algorithm of successive approximation for healthy CD4+ T cells concentration. Using Runge-Kutter of order of precision 4 in a Mathcad surface, numerical validity of the model was conducted. Results of accompanying numerical simulations indicated the maximization of both healthy CD4+ T-lymphocytes and CTLs as a function of multiple chemotherapies with high toxicity and the presence of boosted immune effectors response under reduced systemic cost. Furthermore, maximal suppression of sensitive (infected T-cells and virions) state variables, which are daunted by persistent resistive infectious components suggests for a more articulated dual infectivity model.


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