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
>
