Why not i asked myself ? HIV destroys the what i understand of it, the more advanced form of immunity we have. The mediated cell response against more dangerous forms of pathogens. A complex communication system from what i understand of it. And a complex system in nature is with a high probability slow because of evolution. It works, but it is not optimized. What makes hiv so dangerous is that it is not hiv that is killing humans. It is the lack of an immunesystem that kills. At least that is what i understand of it.
I am doing this all from memory so i could be a bit wrong.
Why you think it will not work :
#1
We could let a designed bacteria with accompanying phages be a decoy for the hiv and as a host to infect. Creating an auxiliary system that can match the speed at which hiv is mutating into new forms. If i am not mistaken, it is the antibodies production that cannot match the speed of hiv producing new disguises. Thus we need to help the immune system by mimicking the function of the immune system. By use of bacteria and phages. I would not be surprised if the immunesystem started out that way long ago. As humbled down bacteria and phages.
We know how hiv enters cells. Some people have immunity from it. The combination bacteria and phages , both together are able to come up with immunity faster than our immune system cells can mediate. Let the bacteria and phages do the adaptive work i would say. But when i think about, it would only work in a petri dish because the bacteria has to be present throughout the entire body and the entire bloodstream. That would cause problems of it's own, namely bacteremia. And then the immune system would create havoc on it's own causing sepsis. However, some possibilities may arise from the fact that some pathogens (parasites and bacteria) have the ability to be invisible inside the human body. Which is what i mentioned in my other post. Bacteria A warning the immune system about bacteria B from which the immune system cannot detect some very dangerous family members until it is to late for the whole organism, meaning for sure sepsis.
I take the work of Bonnie Bassler quite seriously.
Evolutionary wise, it makes sense we benefit from pathogens we live in symbiosis with who warn about other more dangerous pathogens where an encounter could severely decrease our chances of survival.
Why you think it will not work :
#2
The problem here is that hiv is not a localized infection. However, if there is a part of the body where hiv prefers to accumulate, this might actually work but it will take far more then just syringe shots. This is a multiple strategy system. Not something that can be done as easy as a rigid 3 months long antibiotics course.
It is not impossible. But for cheap to produce medicines, large sums of money are asked. Imagine what this would cost...
1. While it can mutate around an antibody response, that's not really the big problem. The antibodies can apparently be working but HIV still replicates and infects new cells. That is, even the unmutated HIV, that antibodies are recognizing and binding, can still replicate. There's a shit ton going on, stuff that doesn't involve antibodies at all.
2. Why would bacteria be faster than the immune system? They don't have a targeted mutation system (like the immune system does) or a means of selectively propagating the most effective fighters against the pathogen (like the immune system does).
3. Bacteria A "warning the immune system" about Bacteria B is akin to the crack dealer warning the SWAT team about the terrorist hit squad down the street. Or the innocent family of five down the street. He's still a crack dealer, he isn't your friend. Some highly pathogenic bacteria use similar strategies to avoid or deflect the immune response.
4. In any case it's a very bad idea to let bacteria loose inside human tissue.
5. I take her work seriously too, but if you want to understand immunity and disease, it's probably better to learn basic micro and immunology first.
6. Yes, the infection is systemic. It's transported through and found in blood. Here's a start on some of the main places HIV will be found
but you can find it in some amount at almost any other place too. And you need to 'kill' every single one of them.
7. I'm not sure what you mean about a "multiple strategy system" when none of your ideas are at the level of a strategy. None of them state specifically how they'll stop an HIV infection. "Warn the immune system?" The immune system
already knows. "Use bacteria and phages to fight the virus?" How? What are the bacteria and phages going to
do? You simply can't put bacteria into a human anyway. You can kill someone just by doing that with dead bacteria.
7. "Cheap to produce medicines" can be very expensive to develop.
If you want to try to figure out something about HIV, stop thinking about symbiotic bacteria and phages. Just stop.
Look first into the work on recombinant viruses as a vaccine, it's the only approach that's provided some protection vs. infection. And thus far, that protection is marginal at best.
Then look into some things about how HIV replicates inside a cell. If we can effectively and safely manipulate host cells, there's likely a cure there. (Yes, that's a very big if.) Some ideas include -
knocking out some host genes that are essential for HIV replication. We've seen a natural version of this with delta 32 mutation, but there are other host genes that HIV requires. Knocking them out in the main target of the virus (CD4 T cells, maybe macrophages too, why not if we're speculating) might be enough. You would need to find a gene not necessary for the function of those cells though.
RNA based approaches. One problem here is that the virus can find escape mutations, but we do know of a few regions in its genome that are intolerant of mutations.
Novel protein approaches. This is a long way off, we really don't know how to do this so well right now. But a highly specific endonuclease would be pretty neat, or an intracellular protease that targets the right place on the right viral protein, or a really well-designed transcription inhibitor.