3.) Biomarkers of Real
Illness Discovered and Described by Yale and IDSA.
The entire Lyme scam, as you know by now, was performed
by CDC officers (Allen Steere, Alan Barbour, Barbara Johnson, Mark Klempner)
with the assistance of self-alleged smart people like Edward McSweegan and
Durland Fish. The latter 2 see themselves as Double-Oh Secret Bioweaponeers.
The CDC officers admire themselves as clever business people, beating
everyone else to the patent office. They claimed that vector borne diseases
were a "rich vein of gold" from which to mine patent royalties.
However, in addition to attempting to profiteer off the
calamity, the Lyme scam was performed for 2 reasons. The first reason has to
do with the Autism pandemic. The association between Lyme and Autism is
OspA, not necessarily spirochetes. OspA causes imunosuppression and the
reactivation of latent herpes viruses and also tolerance-spreading from
TLR2/1-agonist tolerance to viral and bacterial tolerance (other
TLR2-agonists, like TLR4 and TLR7 and TLR9 - See Medvedev and Harding). Now
it appears that the NIH has endorsed the description by Washington
University St Louis this summer of 2014 and we are calling this post-sepsis.
It implies ongoing active infections, and not just post-septic shock damage.
They (wustl.edu and the NIH) refer to the herpes viruses, especially
Epstein-Barr. This is in parallel with what happens when a child is
immunosuppressed, has a concurrent active bacterial infection and is
vaccinated anyway, or the vaccine vial has been contaminated with
mycoplasma, which is myco, which is fungal, which is like OspA: causes
immunosuppression and the lack of antibody production. The child will get
the virus instead of the protection. Congenital Rubella causes Autism - that
was the reason they decided to vaccinate against it in the first place. The
Occam’s Razor and SASH policy paper on Autism Vaccines and ME/CFS contains
more on this.
The second reason the CDC does not want anyone to know about the mechanisms
of illness from spirochetes constantly shedding outer surface proteins in a
process called blebbing-plus-antigenic variation ("multi-clonal populations
overwhelm the immune system," (Barbour), "even if infected with just one
spirochete" (Barbour, et al), is that the description of a bioweapon happens
to match Alan Barbour’s "multiclonal populations... overwhelm the immune
system." And have no antibodies that identify the original detonator
infection. See the Primers Shell Game report for that data.
However, others are leaking this information. And Russia knows the NYMC
associated Russians were HLA-datapharming (this means they were looking at
HLAs all over the world); one does not design a bioweapon against a
population that will make strong, robust, healthy antibodies. No. You go for
the reverse - populations where there is NO association to HLA
groups that will produce many antibodies and identify the original
infections. See Ethnic Bioweapons in Wikipedia where the Russian Duma kicked
all Americans out in 2007 for this reason.
On Biomarkers, let's look at the present view (due to Mark Klempner's
"Re-treatment study" scam) and then work backwards.
In 1997 Mark Klempner took a 4.7 million dollar grant
to perform research fraud and then declare that more treatment does not help
Lyme victims. Here is that report:
N Engl J Med. 2001
Two controlled trials of
antibiotic treatment in patients with persistent symptoms and a history of
Klempner MS1, Hu
“It is controversial whether prolonged antibiotic
treatment is effective for patients in whom symptoms persist after the
recommended antibiotic treatment for acute Lyme disease.
We conducted two randomized trials:
one in 78 patients who were seropositive for IgG antibodies to Borrelia
burgdorferi at the time of enrollment and the other in 51 patients who were
seronegative. The patients received either intravenous ceftriaxone, 2 g
daily for 30 days, followed by oral doxycycline, 200 mg daily for 60 days,
or matching intravenous and oral placebos. Each patient had well-documented,
previously treated Lyme disease but had persistent musculoskeletal pain,
neurocognitive symptoms, or dysesthesia, often associated with fatigue. The
primary outcome measures were improvement on the physical- and
mental-health-component summary scales of the Medical Outcomes Study 36-item
Short-Form General Health Survey (SF-36)--a scale measuring the
health-related quality of life--on day 180 of the study.
After a planned interim analysis, the data and safety
monitoring board recommended that the studies be discontinued because data
from the first 107 patients indicated that it was highly unlikely that a
significant difference in treatment efficacy between the groups would be
observed with the planned full enrollment of 260 patients. Base-line
assessments documented severe impairment in the patients' health-related
quality of life. In intention-to-treat analyses, there were no significant
differences in the outcomes with prolonged antibiotic treatment as compared
with placebo. Among the seropositive patients who were treated with
antibiotics, there was improvement in the score on the physical-component
summary scale of the SF-36, the mental-component summary scale, or both in
37 percent, no change in 29 percent, and worsening in 34 percent; among
seropositive patients receiving placebo, there was improvement in 40
percent, no change in 26 percent, and worsening in 34 percent (P=0.96 for
the comparison between treatment groups). The results were similar for the
There is considerable impairment of health-related
quality of life among patients with persistent symptoms despite previous
antibiotic treatment for acute Lyme disease. However, in these two trials,
treatment with intravenous and oral antibiotics for 90 days did not improve
symptoms more than placebo.”
He reported his "results" in the July 13, 2001 NEJM.
There were numerous aspects of fraud committed in the protocol including
using the falsified Dearborn case definition, and that 2/3 of his victims
never had ceftriaxone before, yet he claimed he was retreating with the
standard of care at the time, which was 30 days of ceftriaxone. So, those
patents, the 2/3ds, were not "re-treated." He also did not report which
primers he used to detect NO LYME in the spinal fluid of his victims (this
is written up in the new Primers Shell Game report), when in fact, whenever
he did find such people, he rejected them from the study. Not only did he
say this in the write up of the report protocol - if they were positive for
Bb DNA in the spinal fluid, they would be rejected from the study -, this
actually happened. We know of at least one person who had Bb DNA in her
spinal fluid that Klempner rejected from the study, yet he did not report
In 2005 Klempner wrote 2 important reports; one with a man named Kaplan at
UConn and another with Gary Wormser. The one with Wormser we already talked
about. It was the one where he revealed there were 2 kinds of Lyme: The
Dearborn, HLA-linked arthritis in a knee kind,... and the other, the 85%,
the neurological, seronegative kind, which we learned about in the new
report called "The Lyme Vaccine Scam": The patients with arthritis feel fine
except for their arthritis signs. The report with Kaplan, Klempner reported
that these people had no neurological compromise and therefore their
symptoms were psychiatric:
Cognitive function in post-treatment Lyme disease:
do additional antibiotics help?
Kaplan RF1, Trevino
CH, Klempner MS.
"Patients with post-treatment chronic Lyme disease who
have symptoms but show no evidence of persisting Borrelia infection do not
show objective evidence of cognitive impairment. Additional antibiotic
therapy was not more beneficial than administering placebo."
Everyone knows that's false. Cognitive impairment and
biomarkers of the central nervous system degradation even Mark Klempner
wrote about and reported extensively. Klempner in addition to finding the
Lyme was not curable with IV ceftriaxone - that is, it does not kill all the
spirochetes, even without cells to hide within -, he found that the majority
(79%) of Lyme victims have a unique sign or biomarker of a nerve and
brain-degrading enzyme called matrix-metalloproteinase-130.
Here are those 2 reports:
J Infect Dis. 1998
Matrix metalloproteinases in the cerebrospinal
fluid of patients with Lyme neuroborreliosis.
Perides G1, Charness
AC, Klempner MS.
"Neurologic manifestations of Lyme disease include
meningitis, encephalopathy, and cranial and peripheral neuropathy. There are
no sensitive markers for neuroborreliosis, and diagnosis is often based on
clinical presentation and cerebrospinal fluid (CSF) abnormalities, including
intrathecal antibody production. Matrix metalloproteinase (MMP) activity in
CSF was compared in patients with neuroborreliosis, patients with diverse
neurologic disorders, and healthy controls. The CSF of 17 of 18 healthy
subjects and 33 of 37 patients with neurologic symptoms and normal CSF and
imaging studies contained only MMP2. The CSF of several patients with
neurologic disorders contained MMP2, MMP9, and gelatinolytic activity at 130
and 250 kDa. The 130-kDa MMP was found without the 92-kDa MMP9 in the CSF of
11 (79%) of 14 patients with neuroborreliosis and only 7 (6%) of 118 control
patients (P < .001). This pattern of CSF gelatinase activity may be a useful
marker for neuroborreliosis.”
FULL TEXT: http://www.actionlyme.org/Retro_Klempnerization.htm
J Infect Dis. 1992 Aug;166(2):440-4.
Fibroblasts protect the Lyme disease spirochete,
Borrelia burgdorferi, from ceftriaxone in
Georgilis K1, Peacocke
M, Klempner MS.
"The Lyme disease spirochete, Borrelia
burgdorferi, can be recovered long after initial infection, even from
antibiotic-treated patients, indicating that it resists eradication by host
defense mechanisms and antibiotics. Since B. burgdorferi first infects skin,
the possible protective effect of skin fibroblasts from an antibiotic
commonly used to treat Lyme disease, ceftriaxone, was examined. Human
foreskin fibroblasts protected B. burgdorferi from the lethal action of a
2-day exposure to ceftriaxone at 1 microgram/mL, 10-20 x MBC. In the absence
of fibroblasts, organisms did not survive. Spirochetes were not protected
from ceftriaxone by glutaraldehyde-fixed fibroblasts or fibroblast lysate,
suggesting that a living cell was required. The ability of the organism to
survive in the presence of fibroblasts was not related to its infectivity.
Fibroblasts protected B. burgdorferi for at least 14 days of exposure to
ceftriaxone. Mouse keratinocytes, HEp-2 cells, and Vero cells but not Caco-2
cells showed the same protective effect. Thus, several eukaryotic cell types
provide the Lyme disease spirochete with a protective environment
contributing to its long-term survival."
REPEAT: Mark Klempner also wrote in 1998 that anti-OspA antibodies might be
the cause of anti-myelin antibodies or probably contributed to the MS form
of Lyme. I think he may have meant OspC, since that was my reading of Roland
Martin's 1988 "Lyme causes Multiple Sclerosis" report, but regardless, MS is
not a personality or anxiety disorder:
So, obviously that guy Klempner is lying about
everything. Lyme is incurable and causes nerve and brain degrading enzymes
as a marker of this terrible disease... that is not a disease and people are
inventing their symptoms?
Next, what are the other biomarkers discovered by the
Same-Crooks-Who-Now-Call-Us-Psychiatric or Poisoners-of-Our-Children
(Munchausen's, yes, straight up Munchausen's accusations; this was meant for
what happened after the fake vaccines were on the market- they intended to
blame the parents for poisoning their children should they become sick from
the OspA vaccines)??
A) MMP-130 -
Klempner as shown above.
B) GFAp, or glial-fibrillary acidic protein - ROBERT SCHOEN, - and
this one you are really going to love perhaps even more than Klempner, as
you will later see, re what Schoen says to the press about us - found in the
CNS as a biomarker of glial cell degradation. Now what is a glial cell?
To surround neurons and hold them in place
To supply nutrients and oxygen to neurons
To insulate one neuron from another
To destroy pathogens and remove dead neurons.
When trying to push the Yale LYMErix vaccine, Schoen mentions this
biomarker, when trying to show how devastating Lyme is, and that you'd
better get that vaccine (2000, while LYMErix was still on the market),
mentioning the destruction of these cells, the sign of which is GFAp in the
Ann Intern Med. 2000
The Lyme disease vaccine: conception, development,
Thanassi WT1, Schoen
"Other peripheral neuropathies and Lyme meningitis are also seen at this
stage. In late-stage disease, the central nervous system may be involved. A
new diagnostic test measuring glial fibrillary acidic protein in
cerebrospinal fluid may prove to be a useful tool for measuring such
C) Anti-heat-shock antibodies (Sigal
and Barbour, re anti-flagellar antibodies crossreacting):
Cell Mol Neurobiol. 2001
H9724, a monoclonal antibody to Borrelia
burgdorferi's flagellin, binds to heat shock protein 60 (HSP60) within live
neuroblastoma cells: a potential role for HSP60 in peptide hormone signaling
and in an autoimmune pathogenesis of the neuropathy of Lyme disease.
Sigal LH1, Williams
"Although Borrelia burgdorferi, the causative agent of
Lyme disease, is found at the site of many disease manifestations, local
infection may not explain all its features. B. burgdorferi's flagellin
cross-reacts with a component of human peripheral nerve axon, previously
identified as heat shock protein 60 (HSP60). The cross-reacting epitopes are
bound by a monoclonal antibody to B. burgdorferi's flagellin, H9724.
Addition of H9724 to neuroblastoma cell cultures blocks in vitro spontaneous
and peptide growth-factor-stimulated neuritogenesis. Withdrawal of H9724
allows return to normal growth and differentiation. Using electron
microscopy, immunoprecipitation and immunoblotting, and FACS analysis we
sought to identify the site of binding of H9724, with the starting
hypotheses that the binding was intracellular and not identical to the
binding site of II-13, a monoclonal anti-HSP60 antibody. The current studies
show that H9724 binds to an intracellular target in cultured cells with
negligible, if any, surface binding. We previously showed that sera from
patients with neurological manifestations of Lyme disease bound to human
axons in a pattern identical to H9724's binding; these same sera also bind
to an intracellular neuroblastoma cell target. II-13 binds to a different
HSP60 epitope than H9724: II-13 does not modify cellular function in vitro.
As predicted, II-13 bound to mitochondria, in a pattern of cellular binding
very different from H9724, which bound in a scattered cytoplasmic,
nonorganelle-related pattern. H9724's effect is the first evidence that
HSP60 may play a role in peptide-hormone-receptor function and demonstrates
the modulatory potential of a monoclonal antibody on living cells."
So they're saying antibodies against flagellin causes some pathology, while
at the same time saying band 41 means nothing and you have a non-disease. It
happens to be for the very reason - says Barbour - that antibodies against
flagellin cause cross-reactive antibodies against human heat shock
protein-60 that there is no flagellin vaccine. So, because the
anti-flagellar antibody causes harm and damage, the crooks say of you HAVE
that antibody, if means you're psychiatric and don't have a real disease :)
D) QEEG or electroencephalograms (Sigal,
primary Munchausen's accuser)
Clin Electroencephalogr. 1995
evoked potentials in central nervous system Lyme disease.
Chabot RJ1, Sigal LH.
"Quantitative EEG, flash visual evoked potentials,
auditory evoked potentials to common and rare tones, and median nerve
somatosensory evoked potentials were obtained from 12 patients with active
CNS Lyme disease and from 11 patients previously treated for active CNS Lyme
disease. Abnormal QEEG and/or EPs were found in 75% of the active Lyme
disease patients and in 54% of the post CNS Lyme disease patients. Three
different types of neurophysiological abnormality were observed in these
patients including QEEG slowing, possible signs of cortical
hyperexcitability, and focal patterns indicating disturbed interhemispheric
relationships. In patients tested before and after treatment QEEG and EP
normalization was associated with clinical improvement.”
E) SPECT or brain perfusion scanning (Steere)
Reversible cerebral hypoperfusion in Lyme
Logigian EL1, Johnson
"Lyme encephalopathy (LE) presents with subtle
neuropsychiatric symptoms months to years after onset of infection with
Borrelia burgdorferi. Brain magnetic resonance images are usually normal. We
asked whether quantitative single photon emission computed tomography
(SPECT) is a useful method to diagnose LE, to measure the response to
antibiotic therapy, and to determine its neuroanatomic basis. In 13 patients
with objective evidence of LE, SPECT demonstrated reduced cerebral perfusion
(mean perfusion defect index [PDI] = 255), particularly in frontal
subcortical and cortical regions. Six months after treatment with 1 month of
intravenous ceftriaxone, perfusion significantly improved in all 13 patients
(mean PDI = 188). In nine patients with neuropsychiatric symptoms following
Lyme disease, but without objective abnormalities (e.g., possible LE),
perfusion was similar to that of the treated LE group (mean PDI = 198); six
possible LE patients (67%) had already received ceftriaxone prior to our
evaluation. Perfusion was significantly lower in patients with LE and
possible LE than in 26 normal subjects (mean PDI = 136), but 4 normal
subjects (15%) had low perfusion in the LE range. We conclude that LE
patients have hypoperfusion of frontal subcortical and cortical structures
that is partially reversed after ceftriaxone therapy. However, SPECT cannot
be used alone to diagnose LE or determine the presence of active CNS
Keep in mind that Allen Steere’s official position is
that Lyme only causes a bad knee and no other symptoms.
F) Antiphospholipid antibodies (Steere and Yale claiming
Lyme caused Lupus - probably more likely to be due to the reactivated EBV,
but we will look more closely later)
"Reactivity of neuroborreliosis patients (Lyme
disease) to cardiolipin and gangliosides."
"A subset of patients (50%) with neuroborreliosis (Lyme
disease) showed IgG reactivity to cardiolipin in solid phase ELISA. In
addition, a subset of patients with neuroborreliosis (29%) and syphilis
(59%) had IgM reactivity to gangliosides with a Gal(beta 1-3) GalNac
terminal sequence (GM1, GD1b, and asialo GM1). Anti-ganglioside IgM
antibodies were significantly more frequent in these two groups of patients
compared to patients with cutaneous and articular Lyme disease, primary
antiphospholipid syndrome, systemic lupus erythematosus and normal controls.
Correlative evidence and adsorption experiments indicated that antibodies to
cardiolipin had separate specificities from those directed against the
gangliosides. IgM antibodies to Gal(beta 1-3) GalNac gangliosides appeared
to have similar specificities since these were positively correlated and
inhibitable by cross adsorption assays. Given the clinical associations of
patients with neuroborreliosis and syphilis with IgM reactivity to
gangliosides sharing the Gal(beta 1-3) GalNac terminus, we suggest that
these antibodies could represent a response to injury in neurological
disease or a cross reactive event caused by spirochetes."
G) Quin or quinolinic acid found in the central
nervous system, which is a produce of the immune response against a
bacterial infection (JJ Halperin)
Now all of these fellows, remember, say Lyme disease
does not cause a disease at all. but is a mental illness similar to a
somatoform illness, the definition of which is that you can have valid,
scientifically detectable outlier markers signs of a real illness, but that
you don't have a real illness. Somatoform means "magic" or done with your
brain like a paranormal event. That is the technical definition; Magic.
Neuroactive kynurenines in Lyme borreliosis.
Halperin JJ1, Heyes
"In patients with encephalopathy, serum QUIN was
elevated with corresponding increments in CSF QUIN. Lymphokine
concentrations were not consistently elevated. We conclude that CSF QUIN is
significantly elevated in B burgdorferi infection--dramatically in patients
with CNS inflammation, less in encephalopathy. The presence of this known
agonist of NMDA synaptic function--a receptor involved in learning, memory,
and synaptic plasticity--may contribute to the neurologic and cognitive
deficits seen in many Lyme disease patients...."
H) Lyme Is associated with ALS (Halperin,
Arch Neurol. 1990
Immunologic reactivity against Borrelia burgdorferi
in patients with motor neuron disease.
Halperin JJ1, Kaplan
RH, et al.
"Of 19 unselected patients with the diagnosis of
amyotrophic lateral sclerosis (ALS) living in Suffolk County, New York (an
area of high Lyme disease prevalence), 9 had serologic evidence of exposure
to Borrelia burgdorferi; 4 of 38 matched controls were seropositive. Eight
of 9 seropositive patients were male (8 of 12 male patients vs 2 of 24
controls). Rates of seropositivity were lower among patients with ALS from
nonendemic areas. All patients had typical ALS; none had typical Lyme
disease. Cerebrospinal fluid was examined in 24ALS patients--3 (all with
severe bulbar involvement) appeared to have intrathecal synthesis of anti-B
burgdorferi antibody. Following therapy with antibiotics, 3 patients with
predominantly lower motor neuron abnormalities appeared to improve, 3 with
severe bulbar dysfunction deteriorated rapidly, and all others appeared
unaffected. There appears to be a statistically significant association
between ALS and immunoreactivity to B burgdorferi, at least among men living
in hyperendemic areas."
Keep in mind that if it is not Borrelia causing all
these signs, it would be due to all the secondary opportunistics that take
over in post-sepsis syndrome. Meanwhile, the Cabal says all sorts of
slanderous and libelous things about neurologic Lyme victims, which is a
I) NO in the brain (Steere):
J Infect Dis. 1994
and Escherichia coli lipopolysaccharides induce nitric oxide and
interleukin-6 production in cultured rat brain cells.
Tatro JB1, Romero
"Lyme Disease" refers to "only the bad knee or arthritis," so brains are not
knees unless Steere has finally made that fantastic discovery for which he's
Nitric Oxide is a free-radical, neurotoxin.
J) Anti-ganglioside antibodies (Benach)
Infect Immun. 1995
Experimental immunization with Borrelia burgdorferi induces development of antibodies to gangliosides.
Garcia-Monco JC1, Seidman
"Patients with neuroborreliosis produce antibodies,
mostly of the immunoglobulin M (IgM) class, to gangliosides, particularly to
those with Gal(beta 1-3)GalNac terminal sequences. Lewis rats were immunized
with a nonpathogenic strain of Borrelia burgdorferi and with a
chloroform-methanol extract (nonprotein) of this organism (CM) to determine
whether antibodies to B. burgdorferi also recognized gangliosides. Rats were
also immunized with asialo-GM1 to determine whether the elicited antibodies
recognized antigens in B. burgdorferi. Rats immunized with B. burgdorferi
produced low levels of IgM antibodies that cross-reacted with asialo-GM1 and
GM1. Rats immunized with CM had marked IgM reactivity to asialo-GM1 and GM1.
Immunization with asialo-GM1 resulted in antibodies that cross-reacted with
B. burgdorferi antigens. Although antibodies to B. burgdorferi were of both
the IgM and IgG classes, those to CM and to asialo-GM1 and GM1 were
predominantly in the IgM fraction. Reactivity of the IgM antibodies
decreased after adsorption with the heterologous and the homologous
antigens, indicating bidirectional cross-reactivity between CM, asialo-GM1,
and GM1 and that immunization with one produces antibodies to the other.
There was no in vivo deposition of Ig in peripheral nerves, nor was there
nerve pathology as a result of immunizations, but IgM antibodies to
asialo-GM1 and CM recognized homologous antigens in the nodes of Ranvier of
peripheral nerves from nonimmunized rats. This immunization model suggests
that antibodies to gangliosides in Lyme disease have a microbial origin and
are potentially relevant in pathogenesis."
So, follow. “Experimental infection with Borrelia by
immunization causes cross reacting antibodies to nerve and brain, but Lyme
is just a bad knee.” (Benach is not part of the cabal, but one could look
to see who cited that report, and do that routinely with these reports.)
K) And Last but Not Least, Paul Duray in
IDSA's own journal with the most important biomarker of all !!!! (How
can they deny this?)...
1989 (this is in IDSA's own journal):NCI and US Army Ft
Detrick Pathologist Paul Duray on the CSF cells looking like
"Epstein-Barr-like transformed cells" in IDSA's 1989 Reviews Supplement on
Spirochetal Diseases:Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Rev Infect Dis. 1989
Sep-Oct;11 Suppl 6:S1487-93.
Clinical pathologic correlations of Lyme disease.
"Immature B cells can also be seen in the spinal fluid.
These cells can appear quite atypical- not unlike those of transformed or
Full Text: http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm
Epstein-Barr like transformed or neoplastic
(pre-cancerous) B cells found in the spinal fluid of persons who just have
bad knees and no other symptoms. Hmmm.
Duray again in 1992, in Steve Schutzer's review of the
1992 Cold Spring Harbor Conference on Lyme:
"On occasion, these atypical-appearing large lymphocytes have been
misinterpreted in biopsy by several laboratories as cells of a malignant
lymphoma or leukemia. Bb antigens, then, may stimulate growth of immature
lymphocytic subsets in some target organs, as well as in the cerebrospinal
fluid (Szyfelbein and Ross 1988). Usual bacterial infections do not produce
such lymphocytic infiltrates in tissue. ****These immunoblastoid cells in Bb
infections at times resemble those found in Epstein-Barr virus
Bb reactivate latent virus infections in tissues? Do some tick inocula
harbor simultaneous infectious agents (ixodid ticks can harbor Rickettsiae,
Babesia microti, and Ehrlichia bacteria, in addition to Bb), producing
multi-agent infections in some hosts? Further studies can clarify these
issues by mans of tissue-based molecular probe analysis." -
Paul Duray, NCI, NIH, Ft. Detrick, at the 1992 Cold Spring Harbor Crooks'
Conference, published in Steve Schutzer's Lyme Disease: Molecular and
Immunologic Approaches. – book:
Publisher, Cold Spring Harbor Press, 1992, ISBN: 087693770, 978087969377
The NIH (NINDS’ MS-Lyme Group) group that discovered
that *** OspA *** was the cause of the MS/New Great Imitator outcome of Lyme
reporting in the New York Times in the summer of 2013 by saying that
Epstein-Barr might be the real culprit. (OspA causes immunosuppression and
the reactivation of latent herpes viruses.)
The following journal article says these OspA like antigens constantly shed
by Borreliae cause immunosuppression in the humoral immune system, but
apparently a chronic inflammatory state in the central nervous system:
J Neuropathol Exp Neurol. 2006
Borrelia burgdorferi Induces TLR1
and TLR2 in human microglia and peripheral blood monocytes but
differentially regulates HLA-class II expression.
Cassiani-Ingoni R1, Cabral
that stimulation with B. burgdorferi lysate
increased the expression of Toll-like receptors (TLRs) 1 and 2 in all cell
types except neurons. However, despite similarities in global gene profiles
of monocytes and microglia, only microglial cells responded to the
stimulation with a robust increase in HLA-DR, HLA-DQ, and also coexpressed
CD11-c, a dendritic cell marker. In contrast, a large number of HLA-related
molecules were repressed at both the RNA and the protein levels in
stimulated monocytes, whereas secretion of IL-10 and TNF-alpha was strongly
induced. These results show that signaling through TLR1/2 in response to B. burgdorferi can
elicit opposite immunoregulatory effects in blood and in brain immune cells,
which could play a role in the different susceptibility of these
compartments to infection.”
So, OspA and spirochetes cause
humoral immunosuppression (no antibodies and a result like post-sepsis
syndrome), with chronic brain inflammation, says the NIH. And since they
are talking about TLR2/1 ligands, that means the triacyl Osps, like OspA.
You can’t make this up.
This next report by the same people (NINDS’ Martin and
Marques) means you might not even have anti-flagellar antibodies (flagellin
is a TLR5-agonist) after being exposed to shed fungal OspA like antigens
J Infect Dis. 2006
Mar 15;193(6):849-59. Epub 2006 Feb 8.
Borrelia burgdorferi lipoprotein-mediated
TLR2 stimulation causes the down-regulation of TLR5 in human monocytes.
Cabral ES1, Gelderblom
monocytes stimulated with TLR5 ligands (including p37 or flaA, the minor
protein from B. burgdorferi flagella)
up-regulated TLR5. In addition, TLR2 stimulation rendered cells
hyporesponsive to a TLR5 agonist. These results indicate that diverse
stimuli can cause differential TLR expression, and we hypothesize that these
changes may be useful for either the pathogen and/or the host.”
You’ll see a lot of these same reports again in the
Occam’s Razor report, since that is what happened: We saw these outcomes in
parallel in other instances of fungal vaccine attempts and other
immunosuppresion outcomes, and in the end… All Roads Lead to Epstein-Barr,
et al. That’s a Razor.
One has to remark about how amazing it is that the
State of Connecticut and Yale university wanted to throw away all this
discovery related to how OspA caused an immunosuppression disease and New
Great Imitator outcomes too. They would have been 20 years ahead of the
curve in bioscience and discovery. Instead they chose to terrorize their
victims in every way imaginable.
2013 – The same NIH MS-Lyme Group as above, Martin and
"When Lyme Disease Lasts and Lasts" –
Jane Brody, NYTimes.com
"Complicating the picture is the fact that some people
with PTLDS symptoms apparently never had Lyme disease in the first place,
Dr. Marques said in an interview. There are other infectious organisms —
Epstein-Barr virus, for example — that can produce similar symptoms and may
be the real culprits."
Ya think? What causes everything? MS, Lupus, Cancer,
Washington University at St. Louis (wustl.edu)
discovers that sepsis is like Lyme in that the survivors of it are likely to
have survived via the immunosuppression (TLR2-agonist tolerance/Endotoxin
tolerance), but the result is the reactivation of latent viruses:
"Dormant viruses re-emerge in patients with lingering sepsis, signaling
"Patients with lingering sepsis had markedly higher
levels of viruses detectable in the blood, compared with the healthy
controls and critically ill patients without sepsis. Among the sepsis
patients, for example, the researchers found that 53 percent had
Epstein-Barr virus, 24 percent had cytomegalovirus, 14 percent had
herpes-simplex virus, and 10 percent had human herpes simplex virus-7.
"These viruses generally don’t lead to significant
illness in people who are healthy but can cause problems in patients who are
FULL JOURNAL REPORT, snippet…
PLoS One. 2014
Jun 11;9(2):e98819. doi: 10.1371/journal.pone.0098819. eCollection 2014.
Reactivation of multiple viruses in patients with sepsis.
Walton AH1, Muenzer
“Sepsis is the host's non-resolving inflammatory
response to infection that leads to organ dysfunction , . A current
controversial hypothesis postulates that if sepsis pursues a protracted
course, it progresses from an initial primarily hyper-inflammatory phase to
a predominantly immunosuppressive state –. Experimental therapeutic
approaches in sepsis have almost exclusively focused on blocking early
inflammation or host-pathogen interaction and failed –. Recently,
immuno-adjuvant therapies that boost host immunity, e.g., GM-CSF and
interferon-γ, have been successful in small clinical trials thereby
supporting the concept that reversing immunosuppression in sepsis is a
plausible strategy to improve outcome , . However, several issues
have limited this approach including lack of consensus that
immunosuppression is a clinically important phenomenon , , . Also,
difficulty in identifying patients with impaired immunity as well as
determining optimal timing for administration pose significant challenges to
pursuing this approach . While immuno-adjuvant therapies might improve
sepsis survival if administered during the later immunosuppressive phase,
these agents might worsen outcome if given during the early
hyper-inflammatory phase , . Thus, a means to distinguish these two
contrasting phases of sepsis is needed not only to verify the hypothesis
that sepsis progresses to an immunosuppressive state but also to guide use
of potential agents which boost immunity.
“Latent viruses such as cytomegalovirus are normally
held in abeyance by cellular and immune surveillance mechanisms which if
impaired, for example by immunosuppressive medications, often result in
viral reactivation, replication, and virally-mediated tissue injury
–. Sepsis impairs innate and adaptive immunity by multiple
mechanisms including apoptosis-induced depletion of immune effector cells
and induction of T-cell exhaustion thereby possibly predisposing to viral
reactivation and dissemination –. …”
2014, Here the NIH confirms that they agree that post-sepsis, like wustl
above describes, matches their own observations of what happens as a result
of Chronic Lyme (EBV reactivated; i.e., that being generally accepted as the
main driver of MS and Lupus):
”Surviving Sepsis: Detection and Treatment Advances"
By Carolyn Beans for
the National Institutes of Health | August 18, 2014 08:43am ET
"Some people who survive sepsis can develop secondary
infections days or even months later. A research team that included Richard
Hotchkiss, Jonathan Green and Gregory Storch of Washington University School
of Medicine in St. Louis suspected that this is because sepsis might cause
lasting damage to the immune system. To test this hypothesis, the scientists
compared viral activation in people with sepsis, other critically ill people
and healthy individuals. The researchers looked for viruses like
Epstein-Barr and herpes simplex that are often dormant in healthy people but
can reactivate in those with suppressed immune systems. [Sepsis Has
Long-Term Impact for Older Adults, Study Finds]"
Sepsis Has Long-Term Impact for Older Adults, Study Finds
Rettner, Senior Writer | October
percent of sepsis patients experienced worsening cognitive or physical
both, after their infection, the researchers say… Nearly 17 percent showed
signs of moderate to severe cognitive impairment, compared with about 6
percent before the sepsis infection. Patients hospitalized for something
other than sepsis did not show an increase in cognitive problems.”
One is allowed to wonder how IDSA gets off saying Lyme has no illness signs
other than an autoimmune bad knee,… or else is a somatoform disorder.