Designing and building oncolytic viruses

Maroun, Justin; Muñoz-Alía, Miguel; Ammayappan, Arun; Schulze, Autumn; Peng, Kah-Whye; Russell, Stephen

Another factor that significantly impacts the kinetics of virus spread is the burst size, or the number of progeny viruses released by a productively infected cell, which varies widely between viral families. Picornaviruses, VSV and vaccinia virus can release up to 10,000 progeny from a single infected cell after a delay of only 6-18 h [131] [132] [133] . In addition to innate antiviral immunity, adaptive cell-mediated immune responses are typically required for the complete elimination of a viral infection and act by eliminating infected cells before progeny can be released. Oncolytic virotherapy can therefore be viewed as a race between the spreading virus and the responding immune system. For this reason, faster moving viral infections are often considered capable of inflicting greater damage to an infected tumor before they can be contained by the immune system [134] . However, in defense of the viruses with smaller burst sizes, or which release progeny by budding, they tend to be less review Maroun, Muñoz-Alía, Ammayappan, Schulze, Peng & Russell future science group rapidly controlled both by the innate and adaptive host immune responses [135] . Therefore, as with the classic race between the hare and the tortoise, it is very difficult to predict whether a fast or slow replicating virus will show superior efficacy in a given preclinical cancer model.