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Al-Tuwairqi2020 - Dynamics of cancer virotherapy with immune response

ABSTRACT: This ordinary differential equation model of the role of the immune response in cancer virotherapy dynamics is described in the publication: Al-Tuwairqi, S.M., Al-Johani, N.O., Simbawa, E.A. "Modeling dynamics of cancer virotherapy with immune response." Adv Differ Equ 2020, 438 (2020). DOI: 10.1186/s13662-020-02893-6 Comment: This model is represented by the system described in Equation 2 of the publication manuscript. Abstract: Virotherapy is a therapeutic treatment for cancer. It uses genetically engineered viruses to selectively infect, replicate in, and destroy cancer cells without damaging normal cells. In this paper, we present a modified model to include, within the dynamics of virotherapy, the interaction between uninfected tumor cells and immune response. The model is analyzed qualitatively to produce five equilibrium points. One of these equilibriums demonstrates the effect observed in virotherapy, where the immune system demolishes infected cells as well as viruses. Moreover, the existence and stability of the equilibrium points are established under certain criteria. Numerical simulations are performed to display the agreement with the analytical results. Finally, parameter analysis is carried out to illustrate which parameters in the model affect the outcome of virotherapy.

DISEASE(S): Cancer

SUBMITTER: Emilia Chen

PROVIDER: BIOMD0000001035 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000001035?filename=Al-Tuwairqi2020%20-%20Fig2(a)%20simulation.sedml	Other
	BIOMD0000001035?filename=Al-Tuwairqi2020%20-%20Fig2(b)%20simulation.sedml	Other
	BIOMD0000001035?filename=Al-Tuwairqi2020%20-%20Fig2(c)%20simulation.sedml	Other
	BIOMD0000001035?filename=Al-Tuwairqi2020%20-%20Fig7(a)%20simulation.sedml	Other
	BIOMD0000001035?filename=Al-Tuwairqi2020%20-%20Fig7(b)%20simulation.sedml	Other

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Project description:This ordinary differential equation model simulating the interactions between tumor and immune cells is detailed in the publication: Ahmed M. Makhlouf, Lamiaa El-Shennawy, Hesham A. Elkaranshawy, "Mathematical Modelling for the Role of CD4+T Cells in Tumor-Immune Interactions", Comput Math Methods Med. 2020 Feb 19;2020:7187602. doi: 10.1155/2020/7187602 Comment: This no treatment model is described by equations 1-7 of the publication manuscript. Abstract: Mathematical modelling has been used to study tumor-immune cell interaction. Some models were proposed to examine the effect of circulating lymphocytes, natural killer cells, and CD8+T cells, but they neglected the role of CD4+T cells. Other models were constructed to study the role of CD4+T cells but did not consider the role of other immune cells. In this study, we propose a mathematical model, in the form of a system of nonlinear ordinary differential equations, that predicts the interaction between tumor cells and natural killer cells, CD4+T cells, CD8+T cells, and circulating lymphocytes with or without immunotherapy and/or chemotherapy. This system is stiff, and the Runge–Kutta method failed to solve it. Consequently, the “Adams predictor-corrector” method is used. The results reveal that the patient’s immune system can overcome small tumors; however, if the tumor is large, adoptive therapy with CD4+T cells can be an alternative to both CD8+T cell therapy and cytokines in some cases. Moreover, CD4+T cell therapy could replace chemotherapy depending upon tumor size. Even if a combination of chemotherapy and immunotherapy is necessary, using CD4+T cell therapy can better reduce the dose of the associated chemotherapy compared to using combined CD8+T cells and cytokine therapy. Stability analysis is performed for the studied patients. It has been found that all equilibrium points are unstable, and a condition for preventing tumor recurrence after treatment has been deduced. Finally, a bifurcation analysis is performed to study the effect of varying system parameters on the stability, and bifurcation points are specified. New equilibrium points are created or demolished at some bifurcation points, and stability is changed at some others. Hence, for systems turning to be stable, tumors can be eradicated without the possibility of recurrence. The proposed mathematical model provides a valuable tool for designing patients’ treatment intervention strategies.

Project description:Replicating viruses have broad applications in biomedicine, notably in cancer virotherapy and in the design of attenuated vaccines, however uncontrolled virus replication in vulnerable tissues can give pathology and often restricts the use of potent strains. Increased knowledge of tissue-selective microRNA expression now affords the possibility of engineering replicating viruses that are attenuated at the RNA level in sites of potential pathology, but retain wild type replication activity at sites not expressing the relevant microRNA. To assess the usefulness of this approach for the DNA virus, adenovirus, we have engineered a hepatocyte-safe wild type adenovirus 5 (Ad5), which normally mediates significant toxicity and is potentially lethal in mice. To do this we have included binding sites for hepatocyte-selective microRNA122a within the 3' UTR of the E1A transcription cassette. Imaging versions of these viruses, produced by fusing E1A with luciferase, showed that inclusion of microRNA122a binding sites caused up to 80 fold decreased hepatic expression of E1A following intravenous delivery to mice. Animals administered a ten-times lethal dose of wild type Ad5 (5 x 1010 viral particles/mouse) showed substantial hepatic genome replication and extensive liver pathology, while inclusion of 4 microRNA binding sites decreased replication 50-fold and virtually abrogated liver toxicity. This modified wild type virus retained full activity within cancer cells and provides a potent, liver-safe oncolytic virus. In addition to providing many potent new viruses for cancer virotherapy, microRNA-control of virus replication should provide a new strategy for designing safe attenuated vaccines applied across a broad range of viral diseases. four groups which we had were: WT: RNA extracted from livers of mice treated with wild type Ad5, 3 Replicates miR: RNA extracted from livers of mice treated with wild type Ad5 bearing mir122-binding sites in the 3'UTR of E1A (3 Replicates) Luc: RNA extracted from livers of mice treated with non-replicating Ad5 (3 Replicates) PBS: RNA extracted from livers of mice treated with PBS only (3 Replicates)

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Al-Tuwairqi2020 - Dynamics of cancer virotherapy with immune response

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