From: Billi Goldberg <bigoldberg@igc.apc.org>
Subject: Re: AZT and the Immune System: Revisite
Note: non-commercial reproduction.
Archive-Number: 5793
Organization: UCLA, Computer Science Department
Date: Mon, 27 Jul 92 20:59:59 PDT

In post <12:28 am  Jul 26, 1992 by lfoard@Turing.ORG in 
cdp:sci.med.aids>, it was written:
 ** 
>I assume what your theory is saying is that there would be in effect an 
>allergic response to AZT? The data to partially confirm (or unconfirm) 
>the theory is probably already out there. If the theory was correct 
>then an HIV+ person who is taking allergy shots, or is exposed to 
>something they are allergic to would receive the same benefits.   
>If this was actually the case I assume someone could switch from one  
>allergy causing substance to another as they got tolerances for each 
>one? 

No, that would not be so.  Allergy is DTH Type I also known as immediate 
hypersensitivity.  The primary pathologic immune mechanism is the IgE 
antibody and the effector mechanisms are mast cells and their mediators. 
DTH Type II involves IgM and IgG antibodies against tissue or cell 
surface antigen.  DTH Type III involves immune complexes of circulating 
antigens and IgM or IgG antibodies.

An HIV+ individual would only benefit from the cell mediated immune 
response (DTH Type IV) without involvement of the antibody system.  This 
response depends on antigen presentation of Langerhans/dendritic cells 
or macrophages and activation of helper T cells and cytotoxic T cells.  
B cells are not involved in this response.  A later post will explain in 
more detail on the various microbial parasites that macrophages are 
effective against.

>How would this differ from DNCB? 

DNCB is a hapten that combines with a protein when the Langerhans cell 
migrates from the topical application site.  The LC then differentiates 
into a veiled dendritic cell on its pathway to the lymph node where it 
presents the DNCB hapten to a memory T4 cell.  If the DNCB is not 
applied according to treatment instructions (on a weekly basis), jamming 
could occur and effectiveness could be lost.  If DNCB is used orally 
and then on the skin, there would be tolerance to DNCB.  Also, if an 
individual had been environmentally sensitized to DNCB previously, that 
person would probably be tolerant to DNCB, and DNCB would not be 
effective.  DNCB is used for contact sensitization because over 95% of 
the population has never been in contact with DNCB.  There have been 
studies on DNCB for over thirty years which are part of the scientific 
literature.

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To make the whole AZT picture even more confusing is the quote below 
from "Clinical Immunology" by Brostoff, Scadding, Male, and Roitt 
published in 1992 by Gower Medical Publishing:

"Drug-induced antibodies may cause selective haemolytic anaemia, 
thrombocytopenia, neutropenia or a combination of these in the same 
patient.  Drugs act as haptens and become immunogenic after binding to a 
macromolecular carrier, usually protein.  They may bind weakly or 
strongly to the cell surface, the strength of the bond determining to a 
large extent the mechanism of subsequent immune destruction of the cell 
by the drug-induced antibody."

Is it possible that the cytopenia seen in AZT users is not cause by DNA 
chain termination but by a drug-induced antibody?
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