Here, a decoy was created. It's the same set or proteins that HIV binds to in order to gain access to human cells. But the proteins are only tiny chunks from the original and are floating around on their own rather than acting as the keys to the cell. Not all that different from redirecting a heat seeking missile with a bunch of flares. But because the 'flares' are actually identical (in part) to the real proteins in a human, were HIV to mutate away from being able to bind to those chunks it too would become less virulent when attacking the real proteins. And if the strategy is effective, it takes less than a week of labwork to design and produce another similar tactic - very much unlike the small molecule variety.
Forgive my ignorance, but are there any indicators to predict whether a virus will evolve one way or another?
What I mean is, once it comes in contact with these mimic proteins, instead of mutating away from binding to these proteins, can it not mutate in such a way that it increases its virility so that it will bind onto more proteins in an effort to combat "false positives"? So it'll become even more virulent in individuals that have not received this treatment, and maintain its current virility in individuals receiving such treatments?
Back to your question - is there an indicator to predict whether a virus will evolve towards or away from its effectiveness. Ideally, you'd put such constraints on the virus in other ways (in addition to the above concept/treatment), that it wouldn't have the energy/time to get to that much more complicated state of binding more proteins. Every additional mechanism a virus uses is a significant penalty against something as compact and efficient as a virus. But in the end there is likely no way to make any treatment perfect and unovercomable. Best we can do is defend.
"Farzan’s team stitched the gene for eCD4-Ig into an adeno-associated virus (AAV) that is harmless to humans. Those viruses, injected into monkey muscles, continued to produce eCD4-Ig for the 40 weeks of the experiment. “Everyone expects with AAV that this can go on forever,” Farzan says."
Having the 'drug' produced by its host means it costs pennies to administer the first virus. It means the drug is continually produced over the time period. And frankly, it's easier than having to purify the protein from another source, figure out injection conditions/strengths, etc. Further, if it works, it's a great demonstration of gene therapy in addition to HIV treatment.
I see where you're going, but you don't avoid a lot of that work with gene therapy. You still need to produce and the test the virus, and then scale up product along with all the purification needed. The FDA will also ask you to test various doses to provide you're giving the right amount need for the desired efficacy.
In addition, gene therapy requires additional tests to prove that the inserted genes don't end up in some weird place that causes even more issues. Not a huge cost driver, but a concern that small molecules don't have (admitting they still need carcinogenicity testing).