Protective Antibodies

John Cherwonogrodzky jcherwon at dres.dnd.ca
Tue Nov 29 23:58:32 EST 1994


Dear Immunologists:
     I'm not an immunologist, not a virologist, and only, hopefully, a fair 
bacteriologist. However, a few things appear to be falling into place, and I'd 
like to have your opinions and insight.
     Years ago, I was lucky enough to work for Agriculture Canada and to 
collaborate with the National Research Council of Canada on the antigens of 
Brucella (a facultative parasitic bacterium). Our group was the first to 
differentiate and characterize antibodies of vaccinated cattle (having 
affinity to the O-polysaccharide or OPS, these only precipitated 
smooth-lipopolysaccharide or LPS) from infected cattle (also having affinity 
to OPS, these antibodies precipitated OPS and LPS). Although the current view 
is that protection stems from the immuno-globulin class, our work with 
monoclonal antibodies showed this was not the case. It was likely that the 
antibodies raised were to the "tip" epitopes for the former, and "length" 
epitopes for the latter. Competitive ELISAs have been developed which take 
advantage of the specificities.
     Current work in Mexico is looking at the specificity of antibodies from 
different groups of people. These include negative controls, positive acute 
infected, positive chronic infected, vaccinates (those receiving the French 
vaccine with most of the LPS removed) and co-vivants (those living with 
patients, that were exposed to the disease, but never produced symptoms). they 
found a general trend. Vaccinates which were exposed to the bacterium only 
briefly developed antibodies to outer antigens, infecgted patients exposed to 
the bacterium for some time developed antibodies to inner antigens, co-vivants 
were somewhere in between.
     On a radio show called Quirks and Quarks, they interviewed Dr. karpo 
(spelling?), Department of Haematology, Cambridge, England. He found that if 
serum is transferred from HIVpositive/AIDSneagative people to AIDS patients, 2 
effects happened. The symptoms of the latter were alleviated, and the 
appearance of symptoms for the former were delayed.
    Years ago, Dr. Mychuk (spelling?) at Queen's University in Knigston had a 
possible explanation for why some cases of brucellosis are delayed for years. 
His view was that initially protective antibodies are made, holding any 
outbreak of Brucella from parasitized cells in check. After several years, the 
body senses that it is wasting its resources, produces anti-idiotype 
antibodies to "clear the slate", and without circulating protective antibodies 
any outbreak of Brucella has a free reign to develop disease (new antibodies 
are not protective.

     Combining the above concepts, is it possible that when a preson is 
infected with an HIV virus (and such infection may need immuno-suppression to 
begin with, such as drug use, haemophilia, immuno-suppressive proteins in 
semen), initially they are symptom-free because protective antibodies, which 
recognize outer epitopes, are being produced. As the disease progresses, there 
is a transition to the production of non-protective antibodies to inner 
epitopes and possibly anti-idiotypic antibodies to the former.    Are we 
pouring  a potential therapy down the drain each time an HIVpositive blood 
unit from a volunteer is discarded, and given that the key antibody may be "a 
needle in the haystack" due to polyvalent populations of antibody, would 
monoclonal antibodies be the key to protection?
     Thanks for listening. Comments?....John Cherwonogrodzky



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