Hi @Hrdwk. My 2c. Like so many medical procedures the messaging...

Hi @Hrdwk. My 2c. Like so many medical procedures the messaging gets dumbed down to the point where it doesn’t answer enough questions. CF33 infects all cells, however it has been engineered to replicate selectively in cancer cells (and stem cells and some liver cells) because a key enzyme it codes for normally has been deleted. The key there is selective replication, not selective infection. The directed evolution used to generate CF33 is a concoction of different pox virus strains that replicates and lyses cancer cells better than all parental viruses. The tightrope that must be crossed is to allow CF33 to infect and replicate before killing its host. When it replicates it has two types of progeny. The first type remains inside the cell which can lead to lysis and the second type escapes to infect other cells. Again the unknown (until now) aspect was whether that combo was working against a background of the immune system trying to clear it. The proposed maximum dose of 3e9 virus particles is the current maximum feasible dose based on the manufacturing process and purity constraints. Previous oncolytic viruses have tapped out before reaching that value, ie too toxic or not enough cancer killing at 3e9. This was another huge question mark cleared - therapeutic effect before maxing out at 3e9. It is interesting (perhaps) that pox viruses, like all viruses prefer that the host cell keeps replicating so another massive question put to bed is whether CF33 might actually help the cancer cells too much before the kill switch is hit. I’ve probably just added to the confusion. In simple terms, it works!