Steere's "Seronegative Lyme" Hysteria about OspA-induced Antibody Inhibition
Read about it also in the 1998 FDA LYMErix meeting transcript:
1990; Steere using Dattwyler and
Volkman's Seronegative Lyme Assay (developed
because Dattwyler knew fungal antigens produced immunosuppression) to
evaluate "Chronic Neurologic Lyme" cases:
See Also, CRYMEDISEASE_CHP3_B.htm
where we show Steere in 1991 actually used this seronegative Lyme assay on
his own lab
workers, 101016.htm (http://www.ncbi.nlm.nih.gov/pubmed/1883122) where
we see Steere knowingly falsely advising the Academy
of Insurance Medicine a year later (1992), and the Plum
Island Chapter of Cryme Disease where Justin Radolf demonstrates in 2001
that OspA vaccination (or
autovaccination via blebbing), results in inhibition of antibody
production via downregulation of HLA.
Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte
responses to Borrelia burgdorferi.
Department of Medicine, State
University of New York, School of
Medicine, Stony Brook 11794-8161.
The diagnosis of Lyme disease often
depends on the measurement of serum
antibodies to Borrelia burgdorferi,
the spirochete that causes this
disorder. Although prompt treatment
with antibiotics may abrogate the
antibody response to the infection,
symptoms persist in some patients.
We studied 17 patients who had
presented with acute Lyme disease
and received prompt treatment with
oral antibiotics, but in whom
chronic Lyme disease subsequently
developed. Although these patients
had clinically active disease, none
had diagnostic levels of antibodies
to B. burgdorferi on either a
standard enzyme-linked immunosorbent
assay or immunofluorescence assay.
On Western blot analysis, the level
of immunoglobulin reactivity against
B. burgdorferi in serum from these
patients was no greater than that in
serum from normal controls. The
patients had a vigorous T-cell
proliferative response to whole B.
burgdorferi, with a mean ( +/- SEM)
stimulation index of 17.8 +/- 3.3,
similar to that (15.8 +/- 3.2) in 18
patients with chronic Lyme disease
who had detectable antibodies. The
T-cell response of both groups was
greater than that of a control group
of healthy subjects (3.1 +/- 0.5; P
less than 0.001). We conclude
that the presence of chronic Lyme
disease cannot be excluded by the
absence of antibodies against B.
burgdorferi and that a specific
T-cell blastogenic response to B.
burgdorferi is evidence of infection
in seronegative patients with
clinical indications of chronic Lyme