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Oncolytic virotherapy is an experimental cancer treatment that usesgenetically engineered viruses to target and kill cancer cells. One majorlimitation of this treatment is that virus particles are rapidly cleared by theimmune system, preventing them from arriving at the tumour site. To improvevirus survival and infectivity modified virus particles with the polymerpolyethylene glycol (PEG) and the monoclonal antibody herceptin. While PEGmodification appeared to improve plasma retention and initial infectivity italso increased the virus particle arrival time. We derive a mathematical modelthat describes the interaction between tumour cells and an oncolytic virus. Wetune our model to represent the experimental data by Kim et al. (2011) andobtain optimised parameters. Our model provides a platform from whichpredictions may be made about the response of cancer growth to other treatmentprotocols beyond those in the experiments. Through model simulations we findthat the treatment protocol affects the outcome dramatically. We quantify theeffects of dosage strategy as a function of tumour cell replication and tumourcarrying capacity on the outcome of oncolytic virotherapy as a treatment. Therelative significance of the modification of the virus and the crucial role itplays in optimising treatment efficacy is explored.

Mathematical modelling of the interaction between cancer cells and an oncolytic virus: insights into the effects of treatment protocols