Tumours are extremely heterogeneous environments that contain a legion of cancerous and non-cancerous cell types with different characteristics. This variety of phenotypes contributes to tumour resistance against traditional therapies. Therefore, novel cancer therapies are being investigated to target these highly variable tumours. One therapy is the use of oncolytic viruses to prey upon the weakened antiviral response pathways and efficient metabolism of cancer cells. These viruses can be genetically engineered to stimulate the body’s natural immune responses and instigate endogenous tumour destruction. Some mathematical models of tumour growth explicitly model a constant cell cycle length using discrete delay differential equations. In this work, we present a mathematical model of tumour growth that explicitly incorporates tumour cell cycle length heterogeneity by modelling cell cycle length via distributed delay differential equations. By modelling the relationship between oncolytic viruses and immune cell recruitment, we show that immune involvement is necessary for tumour extinction. Specifically, we characterize the local stability of the cancer free equilibrium as a function of cell cycle length heterogeneity and show that the disease free equilibrium gains stability through a transcritical bifurcation. Our modelling framework clarifies the therapeutic benefit of oncolytic viruses when compared with standard immunotherapy and provides an explicit bound on immune efficiency to ensure sustained complete remission.