Spot on. Some OVs such as that developed by Oncarlytics...

Spot on. Some OVs such as that developed by Oncarlytics (cavatak) seek specific receptors on the cell membrane. Pox viruses are far less discerning but evolution gives them a taste for a host that will replicate without dying too early. CF33 include genes that code for inhibitors of cell death to keep the host going. IMU are also going down the specific receptor track with CD19. The CD19 coding gene is inserted as an early expression gene so the immune system will be alerted early after infection. It remains to be seen if it’s expressed too early but we all have our fingers crossed - again CF33 works by itself and that is a mighty relief.
Exploding cells are just PR imagery. Lysis can occur if the cell membrane simply increases permeability (as a result of a replicating virus in the cytosol), ie as purely a volume problem (yeah OK let’s call it an explosion). The CF33 progeny that exits the cell is by a process called exocytosis which is just like bubble membranes joining and then budding off - it can do this without lysing the cell. The progeny replicating inside the cell are not viable if the cell membrane breaks because those progeny are not protected by a suitable coating. They are more exposed to detection by the immune system. Cell death can be triggered by many viral factors both with and without involvement of the immune system. I find it helps to think about how the microbes and our immune systems have evolved together. The immunity language of attackers and defenders leads to many misconceptions, as does the notion that all viruses are bad. Reading this back it’s easy to see why the message must be simplified and told with vivid imagery but I’d encourage as much reading as possible so if you need to panic you’re one of the first.