It is important to analyze to what extent these random or designed mutations abrogate viral replication in normal cells because a tightly controlled vector could be injected at higher doses intratumorally or even systemically. On the other hand, it is also important to analyze to what extent these mutations affect the amount of virus produced per infected tumor cell (burst size) compared to wild-type virus because lower yields will result in a slower propagation throughout the tumor. Finally, as concluded from the clinical trials with wildtype
