Real time adapting viruses are not really something that exists, unless I'm mistaken. They would be very hard to build not least because the problem is poorly specified and would introduce an unpredictable element which is undesirable for a medical therapy.
Yeah using viruses to potentiate anti-tumor immunity is an interesting idea. But returning to my main point, this is creating additional complexities. Most successful cancer therapies tend to do one thing well. Reliable synergy between treatments is actually quite rare. Peter Sorger has published some interesting stuff about this point. The reason combination therapies work better is because it is harder for a cancer cell to be resistant to everything, not because the drugs synergise to kill otherwise resistant cells.
MHC Class I mediated killing is done by effector T cells, not NK cells. Cancers of course learn to turn off peptide presentation via MHC, which stops anti-PD-1 drugs from working. Interestingly many real viruses stop the cells they infect from displaying peptides to escape T cell mediated destruction.
There are already studies of treatments which ramp up the immune response without killing off cancer cells much eg intratumoral STING agonists, mRNA compounds which induce manufacture of chemokines. They don't work that well, so I think the cancer killing capacity of the virus is important. Otherwise there are simpler more 'drug-like' ways to attract more effector cells to the tumor.
Sorry, I mis-remembered my immunology. NK cells kill in the absence of MHC Class I, which is something that would be really nice if it could be turned into therapy.
Yeah using viruses to potentiate anti-tumor immunity is an interesting idea. But returning to my main point, this is creating additional complexities. Most successful cancer therapies tend to do one thing well. Reliable synergy between treatments is actually quite rare. Peter Sorger has published some interesting stuff about this point. The reason combination therapies work better is because it is harder for a cancer cell to be resistant to everything, not because the drugs synergise to kill otherwise resistant cells.
MHC Class I mediated killing is done by effector T cells, not NK cells. Cancers of course learn to turn off peptide presentation via MHC, which stops anti-PD-1 drugs from working. Interestingly many real viruses stop the cells they infect from displaying peptides to escape T cell mediated destruction.
There are already studies of treatments which ramp up the immune response without killing off cancer cells much eg intratumoral STING agonists, mRNA compounds which induce manufacture of chemokines. They don't work that well, so I think the cancer killing capacity of the virus is important. Otherwise there are simpler more 'drug-like' ways to attract more effector cells to the tumor.