Interferon and oncolytic virus synergistically regulate the proliferation of tumor cells in oncolytic virotherapy

Oncolytic virotherapy achieves therapeutic effects through virus-mediated targeting of malignant cells, with treatment efficacy fundamentally determined by the dynamic equilibrium between viral propagation and tumor progression. This study establishes a mathematical framework incorporating exponential growth kinetics for tumor proliferation, while considering the combined antiviral effects of oncolytic viruses and interferon-mediated immune responses that collectively suppress tumor expansion thereby inducing a homeostatic state. Through rigorous stability analysis, we demonstrate the inherent instability of both tumor-free state and tumor-virus coexistence state. The analytical and numerical results demonstrate that adjusting system parameters enables the tumor cell population to approach a locally stable equilibrium. Systematic parameter sensitivity studies reveal two critical regulators of tumor burden: the viral budding rate from infected cells ([Formula: see text]) and interferon synthesis rate ([Formula: see text]). These findings provide crucial theoretical guidance for optimizing therapeutic strategies: enhancing viral cytolytic potential through [Formula: see text] modulation in viral engineering, as well as synergistically boosting interferon responses via [Formula: see text] potentiation in combined immunotherapy regimens. The established model offers a quantitative framework for predicting treatment outcomes and designing precision interventions in oncolytic virotherapy.