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From: denbeste@spdcc.com (Steven Den Beste)
Newsgroups: sci.med.aids
Subject: Re: AIDS
Message-ID: <31599@shemp.CS.UCLA.EDU>
Date: 7 Feb 90 01:09:21 GMT
References: <31500@shemp.CS.UCLA.EDU> <31537@shemp.CS.UCLA.EDU>
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In article <31537@shemp.CS.UCLA.EDU> bob@ozdaltx.UUCP (bob) writes:
>In article <31500@shemp.CS.UCLA.EDU>, Drew.Hamilton@p5.f180.n221.z1.fidonet.org (Drew Hamilton) writes:
>> 
>>  
>>    Also, Can the immune system be taught to battle AIDS (just like chiken pox)  
>> cause we could just develop an immunity shot to give a small dosage of AIDS to  
>> the person.
>>  
>It is worth noting that the chicken pox example and other vaccines
>differ in another critical way from HIV - they don't attack the immune
>system directly.  And in some of these vaccinations we are looking at
>using a less serious disease to provoke immunity which also works
>against a more serious disease which is genetically close.  So far
>there doesn't appear to be anything like that with AIDS. 
>

The only theoretical basis for a perfectly safe AIDS vaccine appears to require
genetic information. The immune system antibody response is not to the genetic
information within HIV, but rather to the shell encasing that genetic
information. If you can reproduce the proteins (?? sugars?) alone, and inject
those into someone, there is no chance that they will get AIDS. Nonetheless,
their immune system would go through a recognition/battle response, and
thenceforth there would be a residual level of anti-HIV antibodies in their
blood. (They'd react as being positive thereafter on the HIV tests available
now, which is ironic if they turn out to be immune! How are the insurance
companies going to tell the difference between HIV-infected (positive test
response) people that they don't want to insure, and HIV-vaccinated (positive
test result) people that they really DO want to insure?)

Hopefully, what would then occur takes advantage of the relatively high
proportion of antibodies within a unit volume of blood as opposed to the number
of T4 cells. The virus has no active propulsion system, but relies solely on
turbulence to bring it into contact with T4 cells, which it then invades. If
there are a million times as many anti-HIV antibodies as T4 cells then the
virus is much more likely to touch one of THEM (and stick, deactivating the
virus) first.

At least, that is the hope. The problem with all this reasoning is that the
initial HIV infection appears to cause a quite reasonable anti-body response,
so after the first invasion the HIV being re-released into the blood from T4
cells should be getting deactivated immediately. In other words, they should be
getting well. They don't, however.

I think that there are two reasons that research in this area is continuing:

1. Possibly if there are already antibodies in place when the initial invasion
occurs it can be controlled. It may sort of be like stopping a forest fire when
it is 1 foot across by throwing a bucket of water on it, instead of waiting
until it consumes half the state of Wyoming before you begin fighting.

2. The other reason is desperation. If this doesn't work, then there doesn't
appear to be any other way to prevent the disease at the current state of the
art. So even though this kind of vaccine doesn't look promising, it's the
only game in town. So work continues.