Protective Antibodies

Rachel Teitelbaum teitelba at aecom.yu.edu
Tue Nov 29 21:02:08 EST 1994


Nah, antibodies don't work, it's the CMI that is essential, that's why
when the CD4 count plummets the patients become sicker.

Just 2 cents from little me.


On Tue, 29 Nov 1994, John Cherwonogrodzky wrote:

> 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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