Re: More on toll-like receptors in Lyme, per NIH researchers

Imagine a pyramid:


C
CC
CCC
CCCC
*********
NNNNNNN
NNNNNNNNN
NNNNNNNNNNN
NNNNNNNNNNNNN
NNNNNNNNNNNNNNN
NNNNNNNNNNNNNNNNN
NNNNNNNNNNNNNNNNNNN
NNNNNNNNNNNNNNNNNNNNN
NNNNNNNNNNNNNNNNNNNNNNN
NNNNNNNNNNNNNNNNNNNNNNNNN

This pyramid reflects antibody response to Bb exposure among the
population of exposed.
At the top "C" reflects humans with CDC positive serology {a completely
human construct}

The 'N''s reflect humans with serology which is not CDC positive, yet
demonstrate a lesser pattern of antibody binding on western blot. The
cornerstone of all of these serologies is the 41KdA flagellin antibody,
seen in the vast majority if not almost all cases.

As Bb disseminates in the human host, it alters its protein expression
patterns - at first, it expresses ~150 proteins, but later in the
infection this number decreases to around 30 as it settles into its
niches in the brain and other protective nutrient rich environments.

What steere etc. studied was lyme arthritis, which can basically be
regarded as an early inflammatory manifestation of disease. These are
the "C"'s, as all of the clinicians data is heavily biased toward
arthritic presentations. They implicitly admit to this much, what they
don't admit to but what can be demonstrated is a massive scheme to
commit statistical and scientific fraud with respect to certain
antigens especially 41 kDa.

In american DOGS, and in europe, 2 or 3 immunodominant IgG antibodies
are enough to diagnose borreliosis. these criteria are less
politicized, and in the case of europeans more inclusive of other
manifestations of the disease. for instance in the absence of syphilis
39 kDa is diagnostic of exposure. really the same is true for 41 kDa.

Why would they need to define lyme disease serologically in this
manner?

The answer is that the market for a vaccine would basically be focused
on a hyperendemic area. Since probably >25% of the population of this
area is already manifesting serological evidence of baseline exposure
{and possibly nonarthritic manifestations of borreliosis}, this means
that in a considerable portion of potential vaccine consumers AND
clinical trial participants, it would be impossible to tell if the
vaccine was effective based on a truthful serologic criteria for the
disease, since large numbers of vaccinnees ALREADY HAVE THE DISEASE.
{and the vaccine doesn't eliminate latent infections - in fact it
probably is harmful in this regard} In some of them, due to
combinations of genotype and borrelia strain, this is likely a harmless
exposure. However in large numbers for the exact same reason, this is
not the case, and these individuals will go on to develop various late
manifestations of this disabling and life-altering disease. Their lives
sacrificed so that a few avaricious traitorous pigs could profit off of
a vaccine, and insurance consultations for denying treatment to and
otherwise ridiculing the vast numbers of non-steere serological
exposures.

You might be interested to know that a subpopulation of asymptomatic or
latent non-arthritic exposures are actually seropositive by CDC
standards. This is reflective of the meaningless nature of the steere
criteria. It cannot distinguish between asymptomatic and symptomatic
infection either; it was simply a method of qualifying a vaccine, which
by the way is only 70% effective anyway.

The steere criteria misses far more borreliosis cases than it catches.

Eliminating the deer in the early 90's would have meant that by now
there was no lyme problem in the United States.

.

Relevant Pages