Abstract
We develop and analyse a mathematical model of tumour-immune interaction that explicitly incorporates heterogeneity in tumour cell cycle duration by using a distributed delay differential equation. We derive a necessary and sufficient condition for local stability of the cancer-free equilibrium in which the amount of tumour-immune interaction completely characterizes disease progression. Consistent with the immunoediting hypothesis, we show that decreasing tumour-immune interaction leads to tumour expansion. Finally, by simulating the mathematical model, we show that the strength of tumour-immune interaction determines the long-term success or failure of viral therapy.
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