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by jerojero
323 days ago
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It depends on the drug but generally the principle is trying to target a part of the virus that is so fundamental to its structure that it simply cannot adapt to function without it. The redundancy on a bacteria is degrees higher than on viruses which are extremely efficient so they're more prepared to survive if that were to happen. But it also depends on the way you're doing the drug. That doesn't mean virus can't adapt, they do. But if you manage to hit the right pieces it might just not be possible for them to do so fast enough. Obviously finding that particular protein and figuring out a mechanism to target it while at the same time for your drug not to have undesirable side effects on the host is an expensive, long and difficult process. For this drug in particular, it doesn't function the same way PrEP does; this targets a different protein which previously was thought to be too difficult to target but new research on it showed that perhaps there was an easier way to do it and that's how this drug (lenacapavir) came to be. However that was not the end of the story as there was also a problem on how to actually deliver the drug to the cells as the drug is relatively insoluble and isn't easily absorbed by the body so although the drug was promising when it comes to affecting the virus it didn't seem to be possible to develop a drug that could be deliverable to people. Eventually though they did figure this part out and that's how we got where we are. But generally, to answer your question, finding the right molecule to target; a right way to target it and a right way to deliver it is really the problem when it comes to drug development, being so targeted and specific makes it extremely unlikely for the virus to develop a resistance because it would mean it has to become a whole new virus basically. |
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