Herpes Virus Shows Early Promise for Advanced Skin Cancer
The particular strain of herpes simplex virus used in the study, HSV1716, is a mutant type that lacks a gene that normally directs the virus to prevent the early death of the cells it invades. For a virus, which loves to hijack normal cells and take over their machinery so it can reproduce itself, causing the early death of those cells just doesn't make sense, because it stops the virus from spreading too far and thus being harmful to a much larger number of healthy cells.
But although this herpes virus is less lethal to normal cells than other strains of the virus, it appears to have lost none of its larcenous and reproductive capabilities when it comes to tumor cells.
Here's how it works: The mutant virus is allowed to replicate inside the tumor cells, because these cells carry their own life-preserving function and don't need to rely on help from the gene that was removed from the virus. So the virus in the meantime can spread and go about its business, which is to damage and ultimately destroy the cells it invades, in this case the tumor cells.
But "once the virus spreads to normal cells, those cells will crash and burn, and the virus can't prevent that because it's lacking this [life-preserving] gene," Cantin says. This self-limiting factor thus keeps the virus from spreading outside the tumor.