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Wang2016/3 - oncolytic efficacy of M1 virus-SN model

ABSTRACT: The paper describes a basic model of oncolytic virotherapy. Created by COPASI 4.25 (Build 207) This model is described in the article: A mathematical model verifying potent oncolytic efficacy of M1 virus Zizi Wang, Zhiming Guo, Huaqin Peng Mathematical Biosciences 276 (2016) 19–27 Abstract: Motivated by the latest findings in a recent medical experiment [19] which identify a naturally occurring alphavirus (M1) as a novel selective killer targeting zinc-finger antiviral protein (ZAP)-deficient cancer cells, we propose a mathematical model to illustrate the growth of normal cells, tumor cells and the M1 virus with limited nutrient. In order to better understand biological mechanisms, we discuss two cases of the model: without competition and with competition. In the first part, the explicit threshold condi- tions for the persistence of normal cells (or tumor cells) is obtained accompanying with the biological explanations. The second part indicates that when competing with tumor cells, the normal cells will ex- tinct if M1 virus is ignored; Whereas, when M1 virus is considered, the growth trend of normal cells is similar to the one without competition. And by using uniformly strong repeller theorem, the minimum effective dosage of medication is explicitly found which is not reported in [19]. Furthermore, numerical simulations and corresponding biological interpretations are given to support our results. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

SUBMITTER: Jinghao Men

PROVIDER: BIOMD0000000782 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000000782?filename=Wang2016:3.cps	Other
	BIOMD0000000782?filename=Wang2016:3.sedml	Other
	BIOMD0000000782?filename=Wang2016:3.xml	Xml

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A mathematical model verifying potent oncolytic efficacy of M1 virus.

Wang Zizi Z Guo Zhiming Z Peng Huaqin H

Mathematical biosciences 20160311

Motivated by the latest findings in a recent medical experiment [19] which identify a naturally occurring alphavirus (M1) as a novel selective killer targeting zinc-finger antiviral protein (ZAP)-deficient cancer cells, we propose a mathematical model to illustrate the growth of normal cells, tumor cells and the M1 virus with limited nutrient. In order to better understand biological mechanisms, we discuss two cases of the model: without competition and with competition. In the first part, the e ...[more]

PMID: 26976483

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Project description:This mathematical model of the role of the innate immune responses generated by macrophages in the context of anti-tumour oncolytic viral therapies is described in the publication: Nada Almuallem, Dumitru Trucu, Raluca Eftimie. "Oncolytic viral therapies and the delicate balance between virus-macrophage-tumour interactions: A mathematical approach". Mathematical Biosciences and Engineering, 2021, 18(1): 764-799. doi: 10.3934/mbe.2021041 Comment: This model is represented by Equations 2.1a-f of the publication manuscript. Abstract: The success of oncolytic virotherapies depends on the tumour microenvironment, which contains a large number of infiltrating immune cells. In this theoretical study, we derive an ODE model to investigate the interactions between breast cancer tumour cells, an oncolytic virus (Vesicular Stomatitis Virus), and tumour-infiltrating macrophages with different phenotypes which can impact the dynamics of oncolytic viruses. The complexity of the model requires a combined analytical-numerical approach to understand the transient and asymptotic dynamics of this model. We use this model to propose new biological hypotheses regarding the impact on tumour elimination/relapse/persistence of: (i) different macrophage polarisation/re-polarisation rates; (ii) different infection rates of macrophages and tumour cells with the oncolytic virus; (iii) different viral burst sizes for macrophages and tumour cells. We show that increasing the rate at which the oncolytic virus infects the tumour cells can delay tumour relapse and even eliminate tumour. Increasing the rate at which the oncolytic virus particles infect the macrophages can trigger transitions between steady-state dynamics and oscillatory dynamics, but it does not lead to tumour elimination unless the tumour infection rate is also very large. Moreover, we confirm numerically that a large tumour-induced M1→M2 polarisation leads to fast tumour growth and fast relapse (if the tumour was reduced before by a strong anti-tumour immune and viral response). The increase in viral-induced M2→M1 re-polarisation reduces temporarily the tumour size, but does not lead to tumour elimination. Finally, we show numerically that the tumour size is more sensitive to the production of viruses by the infected macrophages.