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
