So a bunch of test subjects right now have heavily mutated HIV of a strain that apparently did not get affected by this drug, and could possibly be spreading it. The approach is wrong - if half the clinical patients show no difference, but they now have a randomized sequence of deadly DNA, then this is not a cure, it's a new disease.
I recall hearing in a documentary that only the un-mutated form of HIV is any good at slipping though the gap in human defenses it uses. So as a consequence, once it gets to mutating, those changed viruses only work inside the current victim. Sorry my memory is not more precise.
Consider, it already mutates a lot, and hasn't turned itself into something more deadly.
I'm probably overly paranoid and certainly under-educated (possibly even to the point of the level of believing in "magic"), but accelerating the mutation rate of something like this just scares me. As I said though, that's an emotionally based feeling and not logical. I'd be VERY happy to have someone scientifically show me I'm full of #$!#.
From my understanding, HIV is already near the max mutation rate that is sustainable, this is what makes it so hard to kill. But it's on the edge of the cliff, if it mutates any faster then too many of the mutated cells aren't viable and not enough live on to the next generation to maintain the population.
You have to understand that most mutations are harmful, beneficial mutation are extremely rare so there is a maximum rate of mutation before mutation itself becomes deadly to the virus. Pushing it over this limit by hijacking its replication process and damaging the DNA is brilliant.
Consider how long the human race would survive if our mutation rate was 80%, things like mental retardation, autism, physical deformity, infant death, etc. would sky rocket, it wouldn't be long before most people couldn't take care of themselves.
HIV's mutation rate occurs after entry. This is due to the fact that HIV seems utterly incapable of fighting the human body without making itself weak in the process. HIV beats the human immune system by changing itself quicker than the human body can adapt.
It's like one day you're fighting the Nazi's, the next day its the USSR, then it's Mussolini's Italy, then it's Saddam and then some Aztec warriors with machine guns. Each day you're expecting to wake up and see more Nazi's, you're not expecting the Iraqi army. Each of these armies is on the retreat, it's just that they win by attrition because every mutation they have they get to swarm your immune system.
It is true that the virus can spread during this time, it's just far less likely. The drug they're proposing is that they make the HIV virus switch its uniform (surface markers in the biological sense) faster, say every 6 hours. Well the problem with this is that you're potentially going to kill the cells through ware, or you're going to end up with an Aztec-Nazi-Russian (or a HIV virus with multiple surface markers) so you then know to attack all of them.
You're somewhat right, with this kind of drug it's likely only going to benefit us that we're cautious to make sure it doesn't create a new virus. Hopefully the virus will cause the HIV to present multiple surface markers and by this help the body target the virus more efficiently.
I find a good benchmark is to look and see if there's outcry from within the scientific community. These days if something really is off-the-wall-crazy somebody from that field is going to be ranting about it and it won't be too hard to find.
If that quick little test fails, then what you're worrying about is that if you sail too far west that you'll fall of the edge of the world.
Remember that perhaps the most insidious things about HIV has been not its deadliness (which has been ameliorated by 20 years of research) but the fact that it can be contagious for a long time before it makes itself obvious: i.e., not its deadliness alone, but its delayed deadliness, giving it time to spread to other victims.
Agreed, there's like two stages to the virus. The first infects you (and almost everyone you have unprotected sex with) and only presents flu-like symptoms, then months or years later you'll prevent full blown HIV symptoms and this is when the virus is fighting you and mutating like crazy.
Yea, I am normally extremely pro science, but this just seems like a REALLY bad idea. Setting aside the idea that it would become more deadly, IMO the odds of destroying enough HIV DNA to make a difference without altering human cells seems unlikely.
PS: There are 10's of million's of people with HIV, so randomly mutating trillions strands of viral HIV inside people as they are reproducing and not creating a worse strain seems unlikely.
In genetics, introducing random changes is one of the worst ways to find useful results. Admittedly, across such a large population, the virus might get worse, but if by worse you mean more deadly, then like ebola, it will restrict its growth by not transferring to as many people. If by worse you mean find another receptor that is hard to attack, then I'm not really sure what to do...
In scientific circles the idea is called "crash error". RNA viruses, like HIV and influeza (the flu), mutate very fast, because they use polimerases for their replication that lack sequence proofreading and error correction. Theoreticians have estimated that was the virus to mutate a bit faster, its complement of encoded proteins would stop being able to interact with each other, and the virus would lose the ability to recompose itself and spread. Pushing the viral populations to such "crash error" estate is what these drugs are all about. There are already comercial drugs aiming at this effect, and its effects have been thoroughly tested in vitro.
Realize also that a normal population of millions of HIV virions have a huge percentage of those virions inactive. This is caused by the crash error effect: too many bad copies. With this strategy, the virus accomplishes two things: it explores the maximum possible range of mutations, so that it looks forever different to the immune system, and it saturates the immune system with defective virions and viral antigens, diverging resources and allowing for a very tiny subset (don't recall numbers, but was well under 0.01%) to escape detection.
Another key concept is the synergy of viral particles. Many of those non-crashed virions are actually only partially crashed. When they coinfect a cell, betwen both virions they have enough good proteins that they can survive; i.e. reproduce and spread. Considering the cell infection rate is extremely low compared to the viral load in blood, and the even more extremely low probability of coinfection of two complementary virions, realize that was the number of ineffective virions be increased by a tiny amount, the virus would not be able to spread any further. By all means these drugs that push RNA viruses to the crash-error zone are a very good idea.
