Actually after this trial described in the power point presentation, the more successful things which involved HSV were done in 2004. Those trials used the virus as a vector...essentially a vehicle for carrying something into the cell, and something desirable not a negative. Since viruses can get past our immune system's cellular defenses, the question became, if we wish to alter the genetics of a cell we have to get into it first, and viruses became the most obvious means. Then they decided that gene p53 which controls apoptosis, or normal cellular death, was going to be the target. One commonality in cancer cells is that they are immortal. This is because gene-p53 is damaged in the dysplastic phase to malignancy. The switch (p53) that tells the cell to die on schedule, (our entire body is full of normal cells with programmed lifespans) or if the immune system senses that it is abnormal in some way is not there. So a novel idea was to attach a healthy version of gene p53 to a benign viral vector (HSV1), and infect a cancer-containing animal with it. Sure as anything, the virus did what it was supposed to do and got into the malignant and healthy cells, carrying p53 with it, which was reinstated in place, and the cell died as it was originally supposed to. This worked really well in the cancer cells, and of course in the cells that already had p53 it didn't do anything. (The virus infected both.) For sure this is a different perspective than you are describing in which the virus is the bad guy. But we are on the threshold of understanding more and more of all this. We thought that mapping the human genome was going to give us all the answers to which genes did what. We were ill prepared for the task still at hand, and that is figuring all that out. We actually ended up with more questions than we started with. It is not just the gene sequences, but also the various proteins (of which there are many) that interact with them. That makes the questions at hand tens of thousands of different variables more difficult to answer. We now know that cancer is not one disease, but many, hundreds or more. We are looking at the proteins that have to interact with a particular gene sequence to cause any one of them (cancers). We are moving towards targeted therapy, of which Iressa was one of the first. It was very effective, but only in certain patients, with certain genetic sequences, that were involved with certain proteins. This is all a gross over simplification of the whole thing. But we are looking now at therapies and cures that work for a particular sequence and eventually a cure that can be custom tailored to a specific cancer's genetic identity, following that a specific individual's genetic make up. Cancer is after all a genetic disease. But we are talking about two distinctly different things here