William Gaatjes
Lifer
- May 11, 2008
- 20,040
- 1,287
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Thank you for your response.
I have to do a little gathering and collecting before i can show my view.
I have to do a little gathering and collecting before i can show my view.
Getting bacteria to make antibodies isn't that hard. Getting them to change the antibodies they make, on their on, when it's unknown what they'll have to change to? I'd like to hear how that might be done. And don't say "phages," that's not an answer.
Personally I think the money spent for a HIV cure is a waste. And i did study microbiology.
Why is it a waste? Like 99% of the people that really need it, can't pay it anyway.
Then the cheapest way "cure" is not to get infected at all. If the research money would be spent on suitable "prevention campaigns", the effect would probably be a lot bigger.
I see it coming, "yeah we finally have a cure/vaccination" after 30 years of effort just to find out 3 years later that the virus is getting resistant.
They actually get resistant within 1 Person against the current medicines.
Here is one possible solution but i do not know if it would work :
A short side step, to explain how (assuming the possibility):
Intel had not so long ago the idea that instead of letting the cpu do the work of finding the optimal stream of data to execute, the compiler should do the work.
Even before that time frame, people had to use mcu and cpu models that just where not fast enough to calculate a desired result within the desired time frame. What did these people do ? They calculated in advance and stored the results as a lookup table. Then no calculation is needed only looking up in memory depending on input.
Translating to this idea :
Thus not letting the bacteria do the work real time. The issue here is location or spatiality while also having to accept temporal effects or the amount of time. The HIV virus itself is not different in it's ability to infect the (for simplicity) immune cells while mutating no ? Well, there should be a limitation in the amount of different version HIV can make before it loses its ability to infect.
I don't think that's possible at this point, or the near future. It's been something of a holy grail problem for structural people going back to the 50s. It seems there are more than a few non-linear processes that determine the overall 3d structure of a protein.With modern technology, this can be predicted how many different versions are possible before it lost it's ability to do what it does.
At the risk of being flip, "where they can." Which in HIV's case, usually means GP 120.When the immune system creates antibodies, where do these antibodies normally suppose to lock on to ?
Not really, no. I mean that's part of it, but it's sort of a given. Antibodies can only bind structures on the outside of the virus. If you want to make something that can bind to the envelope, that would likely be fatal, near 100%.IIRC, parts of the virus that are unique and are not to be recognized as human tissue.
This makes no sense. So they're free to bind or attack human tissue, and that's an advantage? Or they can make autoreactive antibodies? That doesn't help anything. That kills or debilitates people.If this is always the case, then there is the weakness of the immune system. Bacteria or any other pathogen do not have this limitation.
I see no relevance to the problem at hand. The antibody response to HIV isn't really limited by any mimicry on the part of HIV. Unless you want to count the envelope itself, which isn't really mimicry, but real actual self.In the virus thread we discussed long ago about mimicry and the possible link to acquired auto immune deficiency. Do you see ?
The immune system does this pretty well, and in parallel. See the above note about how many different antibodies are possible. It finds a solution from perhaps 10^11 possibilities in a matter of a few days. It starts off in parallel, then works sort of sequentially and in parallel from there.When you know in advance, what possibilities may arise, you know longer have to do it real time. You calculate and produce (in the virtual and the physical realm afterwards) massively parallel what you need. This is one of the true strengths of bacteria and phages. Massively parallel.
To put this in terms you're more familiar with - it would be ideal to produce CPU like RAM keyboards. i.e. it doesn't make sense.It would be ideal to be able to produce phage like antibodies that can only latch on to hiv proteins.
But the immune system isn't "behind" in any sense of the word.Thus giving the immune system a chance to catch up.
... wat.It would be even more fun if the part of the antibody that is used as recognition for the immune system would be recognized as something the immune system already encountered but was less dangers. Think of common flu's, measles, anything that that the immune system is already aware of.
IF I understand what you're trying to say, and I'm not at all sure you understand in the first place - it's a near certainty this would make things much worse, and an absolute certainty it wouldn't cure an HIV infection.This way the "calculation" and production of antibodies is done outside the human body. Only the results (the antibodies) are inserted into the body.
What would be even more better, is that this would even conflict with the infection cycle of HIV itself. For example a CCR5-delta 32 lock.
HIV doesn't "lock on to" delta 32. It can lock on to normal CCR5. Most people have the normal version. If you want to "lock on" to any part of it with a protein, there are some issues to deal with. If you're proposing something like rituxamab, that's a very expensive approach, much moreso that current haart therapy.No, i do not want to lock onto the CCR5-32 delta itself. Only to that which HIV uses. It cannot be exactly the same. It has to be different. Nor do i want foreign pathogens to attack the body.
The immune system, in its normal state, is perfectly capable of responding to multiple challenges simultaneously.The whole problem is that the human immune system must fight multiple pathogens at the same time while also being undermined.
It's as fast as I think it is.And it is not as fast as you think because it has to check if the antibodies will attack friendly tissue.
I do not have enough information at the moment to accurately visualize what an antibody does. How it latches on i can imagine, but i do not know how it is a marker for the immune system.
That's how some autoimmune diseases work. Others don't involve antibodies at all.Why i mentioned mimicry is obvious. Antibodies that are supposed to be safe turn out not to be safe. That is what i believe about acquired auto immune diseases. Auto immune diseases through inherited genetics of course also exists. There is always more then one way to Rome, as they say.
Google/wiki terms for youThere are other temporary ways to boost the immune system, adrenaline and glucocorticoid suppression. This will boost the immune system but caution must be taken. The human body is evolved and not designed. Everything is connected somehow and will cause serious side effects.
I do not know if it is enough, but i vaguely remember the machines used for automation of biological tests. I wonder about how EMI and EMC shielded these devices are. I mean high powered stepping motors need high power switching devices and perhaps long cables. This in itself will always create EMC and EMI when care is not taken. Perhaps this can have an effect too. It is assumed wrongly that all biological processes are not electric and do not experience interference. This is not always the case, i think. Thus without knowing, some biological experiments may have been tainted.
http://www.youtube.com/watch?v=NItwaz0nLJA
HIV doesn't "lock on to" delta 32. It can lock on to normal CCR5. Most people have the normal version. If you want to "lock on" to any part of it with a protein, there are some issues to deal with. If you're proposing something like rituxamab, that's a very expensive approach, much moreso that current haart therapy.
The immune system, in its normal state, is perfectly capable of responding to multiple challenges simultaneously.
An antibody is a modular protein. It has one part that sticks to the antigen or pathogen (variable region or antigen binding domain), and another part that serves as a "flag" (correct term is constant region or effector region) of sorts, serving as a binding site for cells or other molecules. Think about that old desk that sits in the hallway for a few weeks. One day, someone finally puts a sticker on it that either says "trash" or "for storage." And then it's gone. In humans there are nine different 'flags,' all serving to cause different effects. In some cases the different effects are miniscule.
In the case of viruses and some other things, the 'flag' portion of the antibody isn't always necessary (but it can be helpful). Just covering the binding sites on the virus prevents the virus from entering the next cell. HIV is different though - you can bind it up with antibodies, and it still gets to the next cell.
interferon alpha
interferon gamma
TLR agonists
Isoprinosine
Ribavirin
pegfilgrastim
CCR5 is the full length gene. It has functions in the immune system. Afaik there's very little or no difference in it between most people. The big exception being people with a version called delta 32. This is a much smaller "truncated" version. It's also non-functional. So while people who are homozygous for delta 32 are resistant to HIV, they are more susceptible to some other pathogens. I forget which ones.CCR5 delta 32 is indeed the mutated version that for some people provides protection to for as far as i know HIV-1. Are there not different versions where CCR5 delta 32 is not a protection ?
I got it mixed up. I will read up on it. It is fascinating.
That flag or marker what i called it, that is interesting.
Covering up the binding sites, this is what is interesting. But why does it not work for HIV, assuming for a moment only a single version that is not mutated ?
If you can find data on magnetic field strengths, compare the protein NMR machines to the ones they use in hospitals. They use similar principles, but it's kind of like comparing an atom smasher to a rifle.The NMR scanner you linked to is interesting. Thank you. I have to read up on that as well.
Personally I think the money spent for a HIV cure is a waste. And i did study microbiology.
Why is it a waste? Like 99% of the people that really need it, can't pay it anyway.
Then the cheapest way "cure" is not to get infected at all. If the research money would be spent on suitable "prevention campaigns", the effect would probably be a lot bigger.
I see it coming, "yeah we finally have a cure/vaccination" after 30 years of effort just to find out 3 years later that the virus is getting resistant.
They actually get resistant within 1 Person against the current medicines.
What approach, that might lead to a cure, is not being pursued?20% of gay men in America have HIV, and they can pay. But a cure is probably still not as profitable for drug companies as a lifetime of treatment.
I have a prescription bottle of Zovirax on hand to take internally for cold sores. This medicine has been around a along time plus there is now the vaccination available for HERPES types which cause cancer (highly urged for women by Dr Drew Pinsky).
In effect, these are viral antibiotics.
http://www.medicinenet.com/acyclovir/article.htm
http://www.cdc.gov/vaccines/vpd-vac/shingles/default.htm
http://www.herpes.org/herpesinfo/vaccines.shtml
I have a prescription bottle of Zovirax on hand to take internally for cold sores. This medicine has been around a along time plus there is now the vaccination available for HERPES types which cause cancer (highly urged for women by Dr Drew Pinsky).
In effect, these are viral antibiotics.
http://www.medicinenet.com/acyclovir/article.htm
http://www.cdc.gov/vaccines/vpd-vac/shingles/default.htm
http://www.herpes.org/herpesinfo/vaccines.shtml
Acyclovir is an antiviral drug, a synthetic nucleoside analogue, that is active against the herpes viruses, including herpes simplex 1 and 2 (cold sores and genital herpes), varicella-zoster (shingles and chickenpox), and Epstein-Barr virus (mononucleosis). Viruses take over living cells and reproduce themselves, often at the expense of the host cell. The acyclovir is converted to an active form by the virus itself, and the virus then uses the active form of acyclovir rather than the nucleoside it normally uses to manufacture DNA, a critical component of viral replication. Incorporation of active acyclovir into new viral DNA stops the production of the DNA. Virally infected cells absorb more acyclovir than normal cells and convert more of it to the active form, which prolongs its antiviral activity. The FDA approved acyclovir in March 198
Man, that third link is ... odd. Anyway.
There are about 8 known human herpesviruses, and all seem to be able to contribute to cancer (maybe), but the association/risk isn't that strong, if you exclude AIDS contributions.