About $ 1.5\% $ of all cancers worldwide are attributed to the Epstein-Barr Virus (EBV). Mathematical models have been used to support clinical trials in identifying potential treatments for many diseases. This paper proposes a delayed within-host model of EBV oncovirus dynamics. The model analyzes the interactions between uninfected B cells, actively infected B cells, latently infected B cells, cancerous infected B cells, EBV particles, and cytotoxic T lymphocytes (CTLs). We establish the nonnegativity and boundedness of the model solutions. We derive all equilibrium points and demonstrate their local stability. We execute sensitivity analyses of the reproduction numbers $ \mathcal{R}_{V} $ and $ \mathcal{R}_{I} $. We conduct several numerical simulations. Based on our results, increasing the value of $ a_{1} $, which measures the role of the EBV in weakening the ability of CTLs to kill infected cells, raises the concentration of infected B cells in the body. This can lead to more severe EBV infections. Moreover, increasing the value of $ a_{2} $, which measures the role of the EBV in impairing the natural death of cancer cells, increases the concentration of cancer cells in the body. In addition, increasing the values of the time delays in the absence of CTLs increases the concentration of healthy cells and reduces the concentrations of actively infected cells and cancer cells. Additionally, the results show that the basic reproduction number $ \mathcal{R}_{V} $ is sensitive to the proliferation rate of the EBV, the production rate of uninfected cells, the infection rate, and the death rates of uninfected and actively infected cells. Thus, the values of these parameters should be carefully estimated.
Citation: Azizah Alrajhi, Afnan D. Al Agha. Analysis of a delayed EBV oncovirus dynamics model[J]. AIMS Mathematics, 2026, 11(8): 23847-23867. doi: 10.3934/math.2026960
About $ 1.5\% $ of all cancers worldwide are attributed to the Epstein-Barr Virus (EBV). Mathematical models have been used to support clinical trials in identifying potential treatments for many diseases. This paper proposes a delayed within-host model of EBV oncovirus dynamics. The model analyzes the interactions between uninfected B cells, actively infected B cells, latently infected B cells, cancerous infected B cells, EBV particles, and cytotoxic T lymphocytes (CTLs). We establish the nonnegativity and boundedness of the model solutions. We derive all equilibrium points and demonstrate their local stability. We execute sensitivity analyses of the reproduction numbers $ \mathcal{R}_{V} $ and $ \mathcal{R}_{I} $. We conduct several numerical simulations. Based on our results, increasing the value of $ a_{1} $, which measures the role of the EBV in weakening the ability of CTLs to kill infected cells, raises the concentration of infected B cells in the body. This can lead to more severe EBV infections. Moreover, increasing the value of $ a_{2} $, which measures the role of the EBV in impairing the natural death of cancer cells, increases the concentration of cancer cells in the body. In addition, increasing the values of the time delays in the absence of CTLs increases the concentration of healthy cells and reduces the concentrations of actively infected cells and cancer cells. Additionally, the results show that the basic reproduction number $ \mathcal{R}_{V} $ is sensitive to the proliferation rate of the EBV, the production rate of uninfected cells, the infection rate, and the death rates of uninfected and actively infected cells. Thus, the values of these parameters should be carefully estimated.
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