Macrophage Theory of HIV
Alex Dickman
Sonoma State University
9/21/02
Here is my theory as to why AIDS research has come up with bupkus. Ever since Middle school I've heard nothing but T cell infection, in reference to HIV, a sneaky bastard, little virus. When I got to college, they said that the virus also infects other cells, like macrophages. The impact of this statement was usually "who knows", when asked about it. It is my goal to convince people, that AIDS is a war on two fronts, T cells and Macrophages.
I do understand how we came to such biological dogma. The lack of T cells, well, CD4 bearing helper cells, is what kills you. People take that personally, and want to avenge their death. The problem with that is; T cell infection is a symptom, not the cause of the disease. Here are my cold hard facts, which you can take on faith, if you wish, to push my agenda.
Facts:
1. Macrophages are the first cells to be infected, since they are in the skin, including at ground zero, your genitalia.
2. So, far vaccines for HIV have had complete failure. A.K.A trying to invoke the specific immune response.
3. Cytoxic T cells, CD8 bearing cells, can kill infected CD4 cells, and do.
4. There high and increasing viral loads in patients in the final stages of AIDS, that have barely any T cells.
5. Humans are susceptible to other macrophage infecting viruses, like Leishmania, with or without HIV.
T cells are part of the specific immune response, macrophages are in the non-specific category. CD4 T helper cells help CD8 Cytoxic T cells to punch holes in things. Macrophages are like amoebas, they engulf and dissolve things. So, in theory, we should be able to construct a virus modus operandi (sic).
Classical Model: gp120 protein on HIV virus meets CD4 protein on T cell, fuses membranes with cell. Then the virus uploads its RNA into the cell genome, The cell becomes a factory for HIV, and new virus bud off, weakening and killing the T cell, and infecting other cells. Patient eventually dies because of inability to fight off other diseases.
That's great and all, it sounds nasty and uncontrollable, but it is too simple to not be licked by our immune system.
The Dickman Model: Classical model plus the fact that Cytoxic T cell finds infected T cell. Half the time it catches the T cell before it produces virus particles, battle won for humans, the other half, Cytoxic "kills" the T cell, and helps spread progeny virus, although half naked. See, Cytoxic cells kill living things by poking holes in them, viruses laugh at this because they don't have plasma membranes, or a lot of things for that matter. So the end product is parts of the virus, that can self assemble, or fully functioning HIV viruses without the mask of the T cell plasma membrane.
This is where macrophages come in. If macrophage was present at the battle, and they are, they should come up and eat the free virus particles, end of story. Except you die, so that can't be the end. The virus must take over a small percentage of the macrophages, and this is a very even battle. The virus replicating in some macrophages, macrophages ingesting other infected macrophages, or virus particles and destroying them. I figure there is a lot of give and take, with HIV having a slight upper hand. Therefore the viral growth is exponential but starting with a very small rate. So my conclusion is that macrophages are actually the weak link, and the timer for a virus beneficial, slow progression.
So, I'll go over the facts in detail, and non-scientists can tune out.
1. Mac's are the first to be infected, uh, hello, if you want to prevent spread you don't attack the secondary host, now do you.
2. Vaccines no trabajo. Well, they do but we don't notice the difference, because we already have ability to kill HIV specifically, just not very well.
3. CD8 vs CD4. In the classic model this shouldn't be an auto-immune syndrome, since Cytoxic will eventually kick HIV's ass (Hypothetically)
4. High viral load at end. It's coming from somewhere
5. Leishmania. We already know that our little buddies, the macrophages, are getting their hats handed to them by lesser viruses. Antimonials are used to treat that disease, but I have no idea how that blocks the virus from entering the macrophage. Maybe transferable to HIV, but that's a pope-in-a-bustier, big maybe.
So I would suggest, that the future AIDS research money go towards:
Making macrophages stronger
Designing catalysts to help macrophage chemicals break down the virus
Non-human macrophage injections?
Anti-inflammatory ingredients in the coctail
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