Dx: “We Don’t Know What You Have (the science escapes
us)”
Rx: “Put da Lyme in da coconut, den you
feel betta”
Thanks and Have a Nice Day ☺
-- Yale,
CDC &
Big KP
"Anecdotal reports of inadequately documented
clinical or laboratory associations with B. burgdorferi infection ill serve the medical
community and the public. Convincing and compelling evidence
(e.g., like not playing the RNA/DNA
PrimerShellGame with human specimens) should be required to support
extraordinary associations."
http://www.journals.uchicago.edu/doi/pdf/10.1086/313541
Now that it has been proven
(1
,
2,
3), re-proven (4,,
5)
and re-re-proven (6,,
7) once again and in recent history, that indeed “Lyme
Disease (8,
9)” is a chronic, un-eradicable infection primarily of the
central nervous system, formerly, formally serologically known as
Relapsing Fever (10,
11,
12), and that long term intravenous
antibiotic treatment generally results in relief-but-then-relapse (3,
5), one wonders, “Where do we go from here?”
The first order of business is the clarification of falsified
antibody
testing for “Lyme Disease.”
In 1992
Allen Steere went to Germany, with, as he claimed,
“The group 1 strain of B. burgdorferi, G39/40, used in this study and
in the previous study of US patients was isolated from an Ixodes
damini tick in Guilford, Connecticut [21]. The group 2 strain, FRG
[Federal Republic of Germany], was isolated from Ixodes ricinus near
Cologne [22]. The group 3 strain, IP3, was isolated from Ixodes
persulcatus near Leningrad [23]. All three strains used in this study
were high passage isolates, which were classified by Richard Marconi
(Rocky Mountain Laboratory, Hamilton, MT) using 16S ribosomal RNA
sequence determination as described [11, 24]. The recombinant
preparations of OspA and OspB used in this study were purified maltose-
binding protein-Osp fusion proteins derived from group 1 strain B31 [25]. The fusion proteins contained the full-length OspA or OspB
sequence without the lipid moiety or the signal sequence -"
--
illegal,
plasmid-dropping, antigen-and-antibody dropping, “high passage
strains” and OspA and B with no lipids attached (not likely to produce
antibodies), resulting in the new, 1994, Centers for Disease Control
(CDC), “case definition” of “Lyme Disease
(8,
9)."
At the Dearborn, MI, Consensus Conference regarding the
“standardization” of Western Blotting for “Lyme Disease,” the invited
labs assessed Steere’s scientifically fraudulent proposal for a new
diagnostic standard for Lyme from 8% to 28% accurate (detected % of
known cases).
As part of their Dearborn submission, New York Medical College (NYMC)
assessed the Steere proposal in 1993 as:
“Overall, 51 of 59 (86%)
convalescent-phase serum specimens were reactive by IB, 35 of which
were interpreted as positive: 26 based on IgM criteria, 8 based on
both IgG and IgM criteria, and 1 based on IgG criteria,”
or 9 out of
59 patients were positive for Steere’s Dearborn proposal in IgG. Or,
15% accurate (13).
With this Steere/Germany standard the two OspA vaccines (ImmuLyme and
LYMErix) were allegedly assessed for safety and efficacy (14,
15),
which meant 85% of known cases would be thrown out of consideration,
which, hypothetically, was the game plan all along. Later we found
out that the Western Blots in OspA vaccinated people were not readable
due to multiple reactive species or generalized darkening of the
Western Blot strips, rendering any potential bands that would
demonstrate illness/Lyme breakthrough in vaccinated persons,
undecipherable (16,
17).
That leaves us with the years 1992 to the present, almost 2011,
completely wasted.
In terms of research dollar-years and lives we’re now back at Square
One, wondering what is to be done with the testing for “Lyme Disease,”
and even more importantly, what do we call a “case” of “Lyme Disease”
once the millions of people who were misdiagnosed in the Lyme-OspA
scam process have gone on to chronic illness?
We know from scientifically valid
biomarkers of illness
(scientifically valid in the sense that valid methods were used to
assess the markers or signs that a person suffered real illness or
health irregularities), the true and correct DNA and RNA methods to
determine chronic infections status, and especially of the prominent
question of “seronegativity” being associated with the greatest
apparent suffering. In 1994 at the meeting of the Food and Drug
Administration regarding potential Lyme vaccines, Raymond Dattwyler
(SUNY-Stony Brook) noted that “the ones that failed to mount a
vigorous immune response tended to do worse, clinically. So, there was
an inverse correlation between the degree of serologic response and
the outcome.”
In 2005, Mark Klempner (Boston University) and Gary Wormser (NYMC)
reported that the arthritis cases and seroposivity tended to be
associated with Allen Steere’s alleged haplotypes over which
SmithKline was sued in a class action after the Yale-owned LYMErix
trial (18): “Patients generally feel well aside from their arthritis
symptoms.”
In 1988, Raymond Dattwyler published that he wondered about
seronegative “Lyme” and the suppression of NK cells (19), and he
wondered enough to come up with a new assay to determine if exposure
to Lyme and a lowered immunological response (20). His new assay was
called “Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi.” Later, Allen Steere
used this same seronegative “Lyme” assay and determined that 4/9 of
his lab workers had been exposed to Borrelia (21).
The question was why.
We know from the previous history of Relapsing Fever (before the era
of Allen Steere, et al), that antigenic variation was the nature of
the relapse, and that spirochetes become host- and tissue- adapted.
This meant that persons who had missed the opportunity for early
diagnosis and treatment would not have the Dearborn “case definition”
of “late, OspA-hypersensitivity, specific HLA-linked, Lyme Arthritis”
in “early Lyme,” would be left to his/her peril in finding a competent
MD who had been exposed in pre-medicine undergraduate study to a
course in genetics. These organisms are taxonomically classified by
differences in flagellin. The best way to detect Lyme with antibody
testing is via all-borrelial-specific anti-flagellin antibody
detection, because flagellin is not a variable antigen. The group
who perfected and patented the anti-Borrelia- burgdorferi specific
flagellin method was Yale’s Erol Fikrig and Richard Flavell in 1991
(22,
23).
Why this test was not used to assess Fikrig and Flavell’s
OspA vaccine patent, LYMErix, is anyone’s guess.
Regardless of this State of Nonsense (Connecticut), …
People wonder what to make of the serious illness they suffer as a
result of “Lyme” and LYMErix vaccination, which appeared to be similar
(24). In 1995, David Persing and Yale’s Robert Schoen patented a
method wherein they, the winners, would be in receipt of all the
government funding and also a national monopoly on the - as they hoped
and intended - post-OspA-vaccinated United States:
“Additional uncertainty may arise if the-vaccines are not completely
protective; vaccinated patients with multisystem complaints
characteristic of later presentations of Lyme disease may be difficult
to distinguish from patients with vaccine…. ” (25,
26).
And they,
most of all, would have access to all the potentially patentable
goodies in the national blood with this monopoly on testing.
Further investigations into the outcomes of other lipoprotein/fungal
vaccines revealed a similar outcome to that observed in the un-reported LYMErix adverse events patients, resulting in the January
2001 FDA hearing on the matter and the class action lawsuits. Adverse
events were only reported to the FDA by the vaccines trials'
administrators if they were of the arthritis kind, since “arthritis
only” had become the new “case definition” at the 1994 Dearborn
”conference.” When Dennis Parenti of SmithKline reported that there
were only two neurological adverse events to LYMErix at the 2000 Lyme
Disease Foundation Conference in Hartford, CT, several physicians and
attendees immediately got up and walked out of the conference room,
while the rest groaned.
The functional results of OspA vaccination were, we hypothesize, not
dissimilar from the results of structurally similar vaccine antigens
that are managed by TLR2:
“These results are consistent with a model in which the presence of
the 19-kD protein [of Mycobacteria tuberculosis] has a detrimental
effect on the efficacy of vaccination with live mycobacteria.” (27)
“Synthetic analogs of lipopeptides from Treponema pallidum also
inhibited Ag [antigen] processing.”
(28)
“the immunosuppressive effect is dependent on glycosylated and
acylated 19-kDa lipoprotein [of Mycoplasma tuberculosis] present in
the phagosome containing the mycobacterium. These results suggest that
the diminished protection against challenge with M. tuberculosis seen
in mice vaccinated with M. smegmatis expressing the 19-kDa lipoprotein
is the result of reduced TNF-alpha and IL-12 production, possibly
leading to reduced induction of T-cell activation. (29)
“Thus, tolerance to LPS and mycobacterial components cannot be
attributed solely to a decrease in TLR/MD-2 expression levels,
suggesting inhibition of expression or function of other signaling
intermediates 2002, Induction of bacterial lipoprotein tolerance is
associated with suppression of toll-like receptor 2 expression.”(30)
"Surprisingly, in 27-kDa-vaccinated mice (protein or DNA vaccines)
challenged by M. tuberculosis H37Rv or BCG strains, there was a
significant increase in the numbers of CFU in the spleen compared to
that for control groups. Furthermore, the protection provided by BCG
or other mycobacterial antigens was completely abolished once the 27-kDa antigen was added to the vaccine preparations. This study
indicates that the 27-kDa antigen has an adverse effect on the
protection afforded by recognized vaccines." (31)
And, we know that:
[((2003) Borrelia burgdorferi-induced tolerance as a model of
persistence via immunosuppression.]
“If left untreated, infection with Borrelia burgdorferi sensu lato may
lead to chronic Lyme borreliosis. It is still unknown how this
pathogen manages to persist in the host in the presence of competent
immune cells. It was recently reported that Borrelia suppresses the
host's immune response, thus perhaps preventing the elimination of the
pathogen (I. Diterich, L. Härter, D. Hassler, A. Wendel, and T.
Hartung, Infect. Immun. 69:687-694, 2001). Here, we further
characterize Borrelia-induced immunomodulation in order to develop a
model of this anergy. We observed that the different Borrelia
preparations that we tested, i.e., live, heat-inactivated, and
sonicated Borrelia, could desensitize human blood monocytes, as shown
by attenuated cytokine release upon restimulation with any of the
different preparations. Next, we investigated whether these Borrelia-specific stimuli render monocytes tolerant, i.e. hyporesponsive,
towards another Toll-like receptor 2 (TLR2) agonist, such as
lipoteichoic acid from gram-positive bacteria, or towards the TLR4
agonist lipopolysaccharide. Cross-tolerance towards all tested stimuli
was induced. Furthermore, using primary bone marrow cells from TLR2-
deficient mice and from mice with a nonfunctional TLR4 (strain C3H/
HeJ), we demonstrated that the TLR2 was required for tolerance
induction by Borrelia, and using neutralizing antibodies, we
identified interleukin-10 as the key mediator involved. Although
peripheral blood mononuclear cells tolerized by Borrelia exhibited
reduced TLR2 and TLR4 mRNA levels, the expression of the respective
proteins on monocytes was not decreased, ruling out the possibility
that tolerance to Borrelia is attributed to a reduced TLR2 expression.
In summary, we characterized tolerance induced by B. burgdorferi,
describing a model of desensitization which might mirror the
immunosuppression recently attributed to the persistence of Borrelia
in immunocompetent hosts”. (32)
AGAIN: “Next, we investigated whether these Borrelia-specific stimuli render
monocytes tolerant, i.e. hyporesponsive, towards another Toll-like
receptor 2 (TLR2) agonist, such as lipoteichoic acid from gram-positive bacteria, or towards the TLR4 agonist lipopolysaccharide.
Cross-tolerance towards all tested stimuli was induced.”
Epstein-Barr’s activity regarding TLR2:
(2007) Epstein-Barr virus induces MCP-1 secretion by human monocytes
via TLR2.
“Epstein-Barr virus (EBV) is a gammaherpesvirus infecting the
majority
of the human adult population in the world. TLR2, a member of the Toll-like receptor (TLR) family, has been implicated in the immune
responses to different viruses including members of the herpesvirus
family, such as human cytomegalovirus, herpes simplex virus type 1,
and varicella-zoster virus. In this report, we demonstrate that
infectious and UV-inactivated EBV virions lead to the activation of NF-kappaB through TLR2 using HEK293 cells cotransfected with TLR2-expressing vector along with NF-kappaB-Luc reporter plasmid. NF-kappaB
activation in HEK293-TLR2 cells (HEK293 cells transfected with TLR2)
by EBV was not enhanced by the presence of CD14. The effect of EBV was
abrogated by pretreating HEK293-TLR2 cells with blocking anti-TLR2
antibodies or by preincubating viral particles with neutralizing anti-EBV antibodies 72A1. In addition, EBV infection of primary human
monocytes induced the release of MCP-1 (monocyte chemotactic protein
1), and the use of small interfering RNA targeting TLR2 significantly
reduced such a chemokine response to EBV. Taken together, these
results indicate that TLR2 may be an important pattern recognition
receptor in the immune response directed against EBV infection.” (33)
And we know that:
“Yale researcher Stephen Barthold, a veterinarian and professor of
comparative medicine who developed the first mouse model of Lyme
disease, studies the expression of B. burgdorferi surface proteins
throughout various stages of the spirochete’s life cycle. He finds
that during the early stages of infection, B. burgdorferi avoids
immune detection by decreasing its expression of surface proteins or
cloaking its expressed surface proteins under a layer of slime. "It's
using some sort of stealth-bomber-type mechanism," he says. Or, using
another diversionary tactic called blebbing, the spirochete can pinch
off bits of its membrane in order to release its surface proteins
Explains Barbour: "It’s like a bacterial Star Wars defense program,"
in which released surface proteins might intercept incoming host
antibodies keeping the spirochete safe from immunological
attack.” (34)
which is what we call the auto-vaccination with OspA - the immune-suppressing fungal antigen
amd TLR2-agomist known also, structurally, as Pam3Cys
(35).
In short, “Lyme Disease” is chronic and seronegative because it is
chronic, or chronically shedding variable (Relapsing Fever-esque)
outer surface lipoproteins like OspA, or, as Alan Barbour states in
his US Patent #6,719,983:
“2.1 Methods of Treatment
”An important aspect of the invention is the recognition that
Borrelia
VMP-like sequences recombine at the vls site, with the result that
antigenic variation is virtually limitless. Multiclonal populations
therefore can exist in an infected patient so that immunological
defenses are severely tested if not totally overwhelmed. Thus there is
now the opportunity to develop more effective combinations of
immunogens for protection against Borrelia infections or as preventive
inoculations such as in the form of cocktails of multiple antigenic
variants based on a base series of combinatorial VMP-like antigens.”
“antigenic variation is virtually limitless. Multiclonal populations
therefore can exist in an infected patient so that immunological
defenses are severely tested if not totally overwhelmed.”
What are the other functional outcomes of the chronic agonism of TLR2
– the one that manages triacyl lipopeptides like OspA or Pam3Cys that
render the immune system overwhelmed, not to mention the persons who late in
the disease who do not serologically (antibodies) react to antigen
from spirochetes fresh out of a tick due to antigen variation,… not to
mention the diminution of antibody production due to chronic TLR2
agonism?
Says Paul Duray of the National Cancer Institute and Ft. Detrick
(hint, hint):
"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 suibsets 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 infections. Does 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." (36)
The lymphocytes of these chronic “Lyme” victims look like
Epstein-Barr
transformed cells.
In 2003, Hulinska et al report in
“Interaction of Borrelia
burgdorferi
sensu lato with Epstein-Barr virus in lymphoblastoid cells:
“Since the possibility of interruption of latent EBV infection has
been suggested by the induction of the lytic virus cycle with chemical
substances, other viruses, and by immunosuppression, we hypothesized
that the same effect might happen in B. burgdorferi sensu lato
infection as happens in Lyme disease patients with positive serology or both agents. We have observed EBV replication in lymphoblastoid
cells after superinfection with B. garinii and B. afzelii strains
after 1 and 4 h of their interaction. We found that viral and
borrelial antigens persisted in the lymphoblasts for 3 and 4 days.
Morphological and functional transformation of both agents facilitate
their transfer to daughter cells. Association with lymphoblasts and
internalization of B. garinii by tube phagocytosis increased
replication of viruses more successfully than B. afzelii and chemical
inductors. Demonstration of such findings must be interpreted
cautiously, but may prove a mixed borrelial and viral cause of severe
neurological disease.” (37)
One of the characteristics of chronic neurologic “Lyme” is that it is
called an “aseptic meningitis” (38,
39,
40).
This is, of course, while the German Multiple Sclerosis expert Roland
Martin had been recruited by the National Institute of Health to
research the association between “Lyme” and Multiple Sclerosis.(41,
42). Martin went home once he found out that OspA-induced
immunosuppression was the likelier reason “Lyme” was mistaken for
Multiple Sclerosis or vice versa.
DISCLAIMER: We Lyme victims did not dream up this nonsense. We only
report it.
Could the co-TLR2 agonists (inducing tolerance and a lack of
antibodies) Epstein-Barr and Borreliosis
be simply responsible for: “These immunoblastoid cells in Bb infections
at times resemble those found in Epstein-Barr virus infections. Does 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?”(36) ?
It is common knowledge that 95% of the adult population in Western
cultures has been exposed to Epstein-Barr and its common similar
herpes viruses. Hypothetically, there is a mouse herpesvirus
(gamma2herpes) that to our knowledge has not been investigated
regarding transmission to other hosts via ticks. We’re not privileged
to know much about what happens on Plum Island. We only know there is
a “Plum Island” strain of mycoplasma, and that Yale’s Durland Fish
experimented with trying to get African Swine Fever virus to “take” to
local hard-bodied ticks at that Not-Bioweapons/Just-Helpin laboratory
(43,
44).
However, it's something that might have been discovered 10 or 15 years
sooner had not certain persons associated with Yale and New York
Medical College made an agreement with Kaiser-Permanente (45) to sell
a vaccine against a disease they suddenly decided doesn’t actually
cause any illness (and the world is flat, the moon made of green
cheese, and all hospitals are going to become brothels because it’s
cheaper and therefore cost-effective to deploy self-alleged MDs who
never perform any scientifically valid rule-outs before making
theoretical diagnostic assumptions based on “projection,” rather than
bog down the likes of the actual laboratories with the fancy machinery
that serves no purpose other than to take up space and look shiny,
just like the misguided folks at Silly NASA…).
“Epstein-Barr virus (EBV) efficiently drives proliferation of human
primary B cells in vitro, a process relevant for human diseases such
as infectious mononucleosis and posttransplant lymphoproliferative
disease. Human B-cell proliferation is also driven by ligands of Toll-like receptors (TLRs), notably viral or bacterial DNA containing
unmethylated CpG dinucleotides, which triggers TLR9. Here we
quantitatively investigated how TLR stimuli influence EBV-driven B-cell proliferation and expression of effector molecules. CpG DNA
synergistically increased EBV-driven proliferation and transformation,
T-cell costimulatory molecules, and early production of interleukin-6.
CpG DNA alone activated only memory B cells, but CpG DNA enhanced EBV-mediated transformation of both memory and naive B cells. Ligands for
TLR2 or TLR7/8 or whole bacteria had a weaker but still superadditive
effect on B-cell transformation. Additionally, CpG DNA facilitated the
release of transforming virus by established EBV-infected
lymphoblastoid cell lines. These results suggest that the
proliferation of EBV-infected B cells and their capability to interact
with immune effector cells may be directly influenced by components of
bacteria or other microbes present at the site of infection.--
Toll-like receptor agonists synergistically increase proliferation and
activation of B cells by epstein-barr virus. (46)
We know that “Lyme” is associated with the production of Amyotrophic
Lateral Sclerosis (in 47% of the ALS cases in Lyme-endemic areas) (47)
and Multiple Sclerosis. And we know that ALS is associated with
mycoplasmal infection (tolerance to TLR2 agonists), and, MS, and
apparently “Lyme” is associated with Epstein-Barr virus or something
like it (36,
48).
We know that 90% of Chronic Fatigue patients found out they had “Lyme
Disease” when finally assessed by a reputable laboratory – one not
like Quest Diagnostics, which uses strain B31, the non-neurotropic,
non-OspC- bearing, non-band-23-producing strain (49). We hypothesize
that since it is known that mycoplasmal infections in the blood
disrupt the osmotic potential in erythrocytes (disrupt the transfer of
oxygen), and metabolism (these things need to be fed, after all) (50,
51), and since there has been reported a high association to
mycoplasmal infections in Chronic Fatigue and Gulf War Illness victims
(52,
53), that the tolerance to TLR2 agonists Lyme/LYMErix results in
tolerance to mycoplasma in the blood (Chronic Fatigue) with no
relative antibody production (28).
“Lyme” also produces a Lupus-like syndrome (54), and recently (and
formerly, formally associated with Allen Steere) was linked by the
Allen-Steere-Lupus-Lyme group (now known as the biotech spin-off, “L2-Diagnostics”) with Epstein-Barr (55).
We hypothesize that due to the induction of tolerance to TLR2
agonists
like fungal or mycoplasmal antigens (Pam3Cys or OspA blebbing or
vaccination) interrupting Epstein-Barr latency,
"Chronic infection or colonization by mycoplasma(s) could gradually
and
significantly alter many biologic properties of mammalian host cells
in culture, including induction of malignant transformation. We
examined effects of Mycoplasma fermentans infection on the continuing
survival and immortality of human peripheral blood mononuclear cells
(PBMCs) from healthy blood donors. Without specific supplemental
growth factors, human PBMCs normally die rapidly, with few cells other
than macrophages/monocytes surviving after 2 weeks in cultures. Only
occasional Epstein-Barr virus (EBV)-positive B lymphocytes would
continue to proliferate and undergo spontaneous immortalization. Our
present study revealed that infection of human PBMCs in culture with
the incognitus and PG18 strains of M fermentans, but surprisingly not
with some other strains tested in parallel, markedly enhanced the rate
of EBV-positive B lymphocytes to undergo immortalization (74% vs 17%).
Compared with spontaneously immortalized PBMCs, the PBMCs immortalized
in cultures infected with the mycoplasmas often had prominent
karyotype changes with chromosomal loss, gain, or translocations.
Furthermore, many of these immortalized B lymphocytes were found to be
monoclonal in nature. The in vitro findings would be of relevance to
lymphoproliferative disorders that occurred in patients with immune
suppression. The mycoplasma-mediated promotional effect in cell
immortalization and its potential clinical implications warrant
further study. --2004; Blood; Mycoplasma fermentans infection promotes
immortalization of human peripheral blood mononuclear cells in
culture. (56)
the induction of chronic Lyme results in the un-latency of Epstein-Barr. Says one researcher,
Regulation and dysregulation of Epstein-Barr virus latency:
implications for the development of autoimmune diseases.
"Epstein-Barr virus (EBV) is a human herpesvirus hiding in a latent
form in memory B cells in the majority of the world population.
Although, primary EBV infection is asymptomatic or causes a self-limiting disease, infectious mononucleosis, the virus is associated
with a wide variety of neoplasms developing in immunosuppressed or
immunodeficient individuals, but also in patients with an apparently
intact immune system. In memory B cells, tumor cells, and
lymphoblastoid cell lines (LCLs, transformed by EBV in vitro) the
expression of the viral genes is highly restricted. There is no virus
production (lytic viral replication associated with the expression of
all viral genes) in tight latency. The expression of latent viral
oncogenes and RNAs is under a strict epigenetic control via DNA
methylation and histone modifications that results either in a
complete silencing of the EBV genome in memory B cells, or in a cell-type dependent usage of latent promoters in tumor cells, germinal
center B cells, and LCLs. Both the latent and lytic EBV proteins are
potent immunogens and elicit vigorous B- and T-cell responses. In
immunosuppressed and immunodeficient patients, or in individuals with
a functional defect of EBV-specific T cells, lytic EBV replication is
regularly activated and an increased viral load can be detected in the
blood. Enhanced lytic replication results in new infection events and
EBV-associated transformation events, and seems to be a risk factor
both for malignant transformation and the development of autoimmune
diseases. One may speculate that an increased load or altered
presentation of a limited set of lytic or latent EBV proteins that
cross-react with cellular antigens triggers and perpetuates the
pathogenic processes that result in multiple sclerosis, systemic lupus
erythematosus (SLE), and rheumatoid arthritis. In addition, in SLE
patients EBV may cause defects of B-cell tolerance checkpoints because
latent membrane protein 1, an EBV-encoded viral oncoprotein can induce
BAFF, a B-cell activating factor that rescues self-reactive B cells
and induces a lupus-like autoimmune disease in transgenic mice."(57)
Down-regulation of MHC class II expression
through inhibition of CIITA transcription by lytic transactivator
Zta during Epstein-Barr virus reactivation.
"The presentation of peptides to T
cells by MHC class II molecules is of critical importance in
specific recognition to a pathogen by the immune system. The level
of MHC class II directly influences T lymphocyte activation. The aim
of this study was to identify the possible mechanisms of the
down-regulation of MHC class II expression by Zta during EBV lytic
cycle. The data in the present study demonstrated that ectopic
expression of Zta can strongly inhibit the constitutive expression
of MHC class II and CIITA in Raji cells. The negative effect of Zta
on the CIITA promoter activity was also observed. Scrutiny of the
DNA sequence of CIITA promoter III revealed the presence of two Zta-response
element (ZRE) motifs that have complete homology to ZREs in the DR
and left-hand side duplicated sequence promoters of EBV. By
chromatin immunoprecipitation assays, the binding of Zta to the
ZRE(221) in the CIITA promoter was verified. Site-directed
mutagenesis of three conserved nucleotides of the ZRE(221)
substantially disrupted Zta-mediated inhibition of the CIITA
promoter activity. Oligonucleotide pull-down assay showed that
mutation of the ZRE(221) dramatically abolished Zta binding.
Analysis of the Zta mutant lacking DNA binding domain revealed that
the DNA-binding activity of Zta is required for the trans repression
of CIITA. The expression of HLA-DRalpha and CIITA was restored by
Zta gene silencing. The data indicate that Zta may act as an
inhibitor of the MHC class II pathway, suppressing CIITA
transcription and thus interfering with the expression of MHC class
II molecules." (58)
It could be that it’s actually OspA-induced Epstein-Barr that is the
“New Great Imitator.”
And that the Yale-Plum-Permanentes are the Greatest Great-Imitators.
Of either physicians or scientists.
Still, where do we go from here?
“We don’t know.” First, we have to deal with the sugarplum fairy-dancing cocoanut-heads, masquerading as “MDs” and “scientists,” doing
perpetual, eternal lapses and re-lapses between the green cheese moon
and the flat earth on the dot guv dime because they haven’t the plain
old regular nuts to admit that they knew all along - and from the
beginning, 1992, when Allen Steere went to Europe with his “high
passage” plasmid-dropping spirochete strains and “recombinant OspA-B
with the no-lipid attached” to come up with a “diagnostic standard”
for “Lyme” that ended up with none of the two “primary immunodominant
antigens” represented - that OspA was not a vaccine.
-- -- -- -- --
“To be most effective, advances in regulatory
science must be fully integrated into the entire product development
process,” says the new
FDA chief, Margaret Hamburg.
The Biomarkers if Illness, developed
by the ALDF.com or IDSociety.org
And the End of the Almighty Checklist - a sign
of the auto-detonation of the adherents to Psychiatry:
What do the Biomarkers, published by the
same gang who now says "Lyme is a consequence of inadequate sexual
release," say "Chronic Lyme/LYMErix Disease" is?.
1)
Using Dark Field to study the
modified erythrocytes, modified via the tolerance induced from
chronic stimulation of TLR2 by spirochetal blebbing of the likes of TLR2
agonist OspA, and subsequent colonization by mycoplasma [recall that
many sufferers of “Chronic Fatigue Syndrome” have been found to own a
colony of Candida (a fungus)].
Brazil makes fun of US "Lyme" "scientists"
mycoplasma-like and spiroplasma-like organisms in the blood of Lyme-like
illness
See Erythrocytes of RBC in Biomarkers page. Crooks don’t want anyone
using Dark Field to look at the blood. Sweeg went after Lisa Masterson
for making this proposal.
2)
The "We Don't Know What
You Have" Negative Data Rule re the DNA/RNA testing for all the mycoplasma
and activated viral infections that won't be producing antibodies (because some are also TLR2 agonists
like Epstein-Barr, and chronic TLR2 agonism results in no-antibodies (Justin
Radolf: ,” Inhibition of
MHC-II Ag processing by either MTB bacilli or purified MTB
19-kDa lipoprotein was dependent on Toll-like receptor (TLR)
2 and independent of TLR 4. Synthetic analogs of lipopeptides
from Treponema pallidum also inhibited Ag processing. Despite
the ability of MTB 19-kDa lipoprotein to activate
microbicidal and innate immune functions early in infection,
TLR 2-dependent inhibition of MHC-II expression and Ag
processing by MTB 19-kDa lipoprotein during later phases of
macrophage infection may prevent presentation of MTB Ags and
decrease recognition by T cells.”
http://www.jimmunol.org/cgi/content/full/167/2/910 )]
This may be the
main reason the crooks don’t want us treated with antibiotics- we will
create antibiotic resistant Tuberculosis (because we will likely have
seronegative TB oand other primarily TKR2 agonising infections like
Staph aureus), not to mention, changing the RNA of the likes of
mycoplasma as the Chinese did:
J Clin Microbiol. 2010 Sep 22. [Epub ahead of print]
Nested PCR-Linked Capillary Electrophoresis and Single-Strand
Conformation Polymorphisms for Detection of Macrolide-Resistant
Mycoplasma pneumoniae in Beijing.
http://www.ncbi.nlm.nih.gov/pubmed/20861333
3)
QEEG or Fibro-Lenny Sigal’s
(who we’ll now refer to as Lenny Squiggy) findings that persons with
chronic Lyme have changes to electroencephalograms.
http://www.ncbi.nlm.nih.gov/pubmed/7554300 “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.”
4)
modified cytokine profile
suggested by Lenny Sqiggy in the Cold Spring Harbor Conference
book (1992, Schutzer:) mentioned above, to which Paul Duray attended and
re-iterated his “EBV-modified lymphocytes” findings:
page 205:
Says Sigal: “Since cytokines can alter endothelial cell function and
increase the entry of inflammatory cells to the organ whose vasculature
has been modified, the presence of cytokines in the Lyme synovium may
have an important indirect effect on local inflammation [Yednock et al.
1992]. The presences of circulating levels of these cytokines may be
the cause of the certain clinical features of Lyme disease; eg., sleep
disorder due to elevated levels of IL-1 (Opp and Krueger 1991) may be
part f the cause of fibromyalgia seen during and after active Lyme
disease (Sigal 1990)
http://www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770
1991, Steve Schutzer.
5) MMP-130 and
GFAp in the CSF of
Mark Klempner's Neuroborreliosis (which is not "Lyme Disease,"
BTW, because Lyme Disease became "only the HLA-linked knee-presentation"
at Dearborn),
http://www.ncbi.nlm.nih.gov/pubmed/9466528
http://www.actionlyme.org/Retro_Klempnerization.htm
6)
Allen Steere's
Nitric Oxide in the CSF of Lyme victims (we now know that the
exposure to these reactive oxygen species/byproducts are downregulators
of TLR2)
J Infect Dis. 1994
May;169(5):1014-22.
Borrelia burgdorferi and Escherichia coli lipopolysaccharides induce
nitric oxide and interleukin-6 production in cultured rat brain cells.
Tatro JB,
Romero LI,
Beasley D,
Steere AC,
Reichlin S.
Division of Endocrinology, New England Medical Center Hospitals, Boston,
MA 02111.
http://www.ncbi.nlm.nih.gov/pubmed/7513330
7)
CORRECT Borrelia (all species) DNA/RNA
primers and not the OspA gene,
because that changes according to
Alan Barbour; we can throw out all "studies" in which the
OspA gene was the determinant for infection with the "Lyme"
spirochete [~10 citations]
8)
Quinolinic acid
and the degradants of monoamines in the CSF of borreliosis victims (JJ
Halperin),
http://www.ncbi.nlm.nih.gov/pubmed/1531156
9)
brain SPECT and PET imaging
(we now know that the metabolism of erythrocytes are hijacked by the
mycoplasma in the blood - infections we can't fight off because they
have OspA or TLR2 agonizing lipoproteins in them),
NOTE: psychiatry likes to suggest that changes
to the brain perfusion seen in chronic Lyme/Fatigue victims is a result
of Bipolar, when not ever once was anyone who was diagnosed with Bipolar
have shown hyper- or hypo- perfusion as a result of any of the “poles”
without other true, real, scientific valid biomarkers of real illness
first performed as a rule out. Secondarily, when studies have been
performed in which there are brain structural changes to the likes of 17
year olds who are determined to be psychopathic or sociopathic, have
these conditions studied a contribution by trauma. As a third
outstanding parameter, why, we wonder, are lawyers undable to view
anything from a scientific standpoint? Why do they score so low on the
visual-spatial scale of cognitive abilities? Why are lawyers so
left-brain dominant and why do they have no understanding of vocabulary
as a simple means to draw a picture in the mind of another.
Most of all, why is this seen in both lawyers and psychiatrists? Why
are the best scientists and engineers known to be visual-spatial or
right-brain dominant? Is this nature or nurture? The victims of their
chronic fraud crime are not entitled to know why self-alleged scholars
as these are clearly unable to think. We are not entitled to see their
own cognitive differentials and potentials.
10)
Allen Steere's
anti-phospholipid antibodies (now known to be caused by activated
Epstein-Barr, as reported by Allen Steere's own Lyme/Lupus
reporting team member, Joe Craft at Yale),
(54)
11)
the auto-reactive
band 41
[specific to borrelia or not; scientists seem to think an antibody
against flagellin cross reacts with nerve and other tissues, such as
skin and intestine (H. pylori and Campylobacter, producing autoimmune
hives, thyroid disease, GERD...)], [Refs,
Barbour patent, Lenny Sigal]
http://patft.uspto.gov/5,585,102
Biochim Biophys Acta. 1993 Mar
24;1181(1):97-100.
Molecular mimicry in Lyme disease: monoclonal antibody H9724 to B.
burgdorferi flagellin specifically detects chaperonin-HSP60.
Dai Z,
Lackland H,
Stein S,
Li Q,
Radziewicz R,
Williams S,
Sigal LH.
Center for Advanced Biotechnology and Medicine, Piscataway, NJ.
http://www.ncbi.nlm.nih.gov/pubmed/8096152
12)
anti-heat shock proteins
(a sign of MS), (others besides Sigal) Bands 60, 74, etc.
13)
anti-gangliosides,
Benach, Steere
http://iai.asm.org/cgi/reprint/63/10/4130?view=long&pmid=7558329
1989; Total, anti-viral,
and anti-myelin IgG subclass
reactivity in inflammatory
diseases of the central nervous
system.
Total IgG
subclass levels, anti-viral,
anti-myelin basic protein (anti-MBP),
and anti-ganglioside 1
(anti-GM1) IgG subclass levels
were measured in 6 patients with
herpes simplex virus
encephalitis (HSVE), 16 with
borreliosis, 8 with other
bacterial infections, 12 with
multiple sclerosis (MS), 13 with
subacute sclerosing
panencephalitis (SSPE), 5 with
glioblastoma and 12 controls.
Total IgG1 levels were elevated
in cerebrospinal fluid (CSF)
from all patient groups (but not
in the controls), IgG2 in
bacterial infections, IgG3 in
HSVE and borreliosis and IgG4 in
some SSPE patients. The
anti-viral (anti-measles,
varicella zoster virus and
rubella) IgG antibodies in MS
were restricted to IgG1,
anti-measles IgG to IgG1 and
sometimes IgG4 in SSPE,
anti-borrelia IgG to IgG1, IgG2
and IgG3. In contrast to
anti-viral antibodies, anti-MBP
and GM1 antibodies belonged to
IgG1, IgG3 or IgG4 in MS. The
nature of the immunological
activation appears to be
reflected in the subclass
patterns elicited in the central
nervous system. Different IgG
subclass patterns in infectious
diseases and MS suggest a
difference between
antigen-specific and
non-specific B-cell activation.
http://www.ncbi.nlm.nih.gov/pubmed/2760636
14)
GFAp or glial fribrillary acidic protein in the CSF - signs of
gliosis mentioned by Yale's Robert Schoen when he mentioned
reasons why we need a Lyme vaccine,
http://www.annals.org/content/132/8/661.full.pdf+html (gliosis would
be a sign of multiple CNS degenerative diseases),
"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
involvement (20)."
-- Yale's Robert Schoen talking
about how serious Lyme is, and
that we need a vaccine for this
disease that goes away and has
no illness signs and is
psychiatric and the result of
not-enough-sex or
self-poisoning.
15)
Gadolinium-Contrast MRI
- performed in monkeys with Lyme but never Lyme-MS Victims which show
Lyme is an active meningitis, and now performed by the Japanese when
deciphering the cause of meningitis in a patient who was mistakenly
diagnosed with MS when they had Large B-cell Lymphoma of the CNS:
Primary central nervous system large B-cell lymphoma with prolific,
mixed T-cell and macrophage infiltrates, mimicking multiple sclerosis.
16)
EMG
Allen Steere:
http://www.ncbi.nlm.nih.gov/pubmed/1310529
I think we should fund an
EMG study where we try to find out
whether or not Lyme victims suffer “hysteria” or the
electrification of our hysters. I think this most of all would be a
fun study: Could we find out via EMG that not-enough-sex really causes
Lyme-ALS, or Lyme-MS or Lyme-Lupus, or Lyme-stroke, or bad knees, or
Guillain-Barre? Who wants to volunteer for that study? And what about
men with Low-T? Can that study be performed? Can we women watch?
We’ll rate their manliness while this EMG study of their genitals to
determine if not-enough sex is “The Reason for Low T or the Inability of
Psychiatrists and Lawyers to Think like Scientists or Engineers” is
performed with our own Checklist.
17) T cell proliferation:
Steere references Dattwyler’s report
here:
None of these biomarkers were applied by Mark Klempner from 1997 to 2001
when he determined that “there is no such thing as Chronic Lyme,”
despite being the author of two of the main signs that it is. The first
was Klempner’s MMP-130 only found in the spinal fluid of chronic Lyme
victims and his other two studies from 1992 where he determined and
published the reasons he believed ceftriaxone failed to eradicate all
spirochetes [REF]
Now, back to Reason:
What we do know about
such emotionalisms over science is that aggression comes from cowardice
or the fear of being less-than another person. We call it jealousy, we
call is envy and we call it pride, hubris and arrogance. Or we fear not
being believed that we suffer a terrible illness – one not detectable by
antibodies, such as those fungal like stealth infections as Relapsing
Fever or Relapsing Fever plus the synthetic antigen Pam3Cys.
Common sense tells us that you can’t see Multiple
Sclerosis or Lupus, but sometimes medical schools attract and even
accept people who have studied only the likes of English literature or
psychology or philosophy in undergraduate study. These are the toughest
nuts to crack. You can’t teach an old dog new tricks.
7"You
hypocrites, rightly did Isaiah prophesy of you:
8'(F)THIS
PEOPLE HONORS ME WITH THEIR LIPS,
BUT THEIR HEART IS FAR AWAY FROM ME.
9'BUT IN VAIN DO THEY WORSHIP ME,
TEACHING AS (G)DOCTRINES
THE PRECEPTS OF MEN.'"
Or, they purport self-flattering, unscientific
concepts as medical doctrine because it is too frightening to see and
accept the reality that they’re truly addicted (repetitious cognitive
loops or mental frameworks) in a medical sense to some philosophical
(psychiatric) Kool Aid, dreamed up by some pervert and drug addict
(Freud).
The biggest of the guns in our arsenal – besides
all of the published applications of the science that says Pam3Cys or
OspA or LYMErix or the HIV antigens gp120 and 41 – are TLR2 agonists and
result in the downregulation of the immune response and the inhibition B
cell apoptosis… is the RNA/DNA Shell Game, we know to be criminal in
anyone’s mind.
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Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi,
from ceftriaxone in vitro.
Georgilis K, Peacocke M, Klempner MS.
Department of Medicine, New England Medical Center, Boston,
Massachusetts.
http://www.ncbi.nlm.nih.gov/pubmed/1634816
2) Ann Intern Med. 1994 Oct 15;121(8):560-7.
The long-term clinical outcomes of Lyme disease. A population-based
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Shadick NA, Phillips CB, Logigian EL, Steere AC, Kaplan RF, Berardi
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Department of Rheumatology-Immunology, Brigham & Women's Hospital,
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Krupp LB, Hyman LG, Grimson R, Coyle PK, Melville P, Ahnn S, Dattwyler
R, Chandler B.
Department of Neurology, Stony Brook University Medical Center, Stony
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http://www.ncbi.nlm.nih.gov/pubmed/12821734
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Livengood JA, Gilmore RD Jr.
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Center for Comparative Medicine, School of Medicine, University of
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swbarth...@ucdavis.edu
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7) Serum-starvation-induced changes in protein synthesis and
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Alban PS, Johnson PW, Nelson DR.
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http://www.ncbi.nlm.nih.gov/pubmed/3531237
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Division of Experimental Pathology, Mayo Clinic, Rochester, Minnesota
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Molloy PJ, Berardi VP, Persing DH, Sigal LH.
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with posttreatment chronic Lyme disease.
Klempner MS, Wormser GH, Wade K, Trevino RP, Tang J, Kaslow RA, Schmid
C.
Boston University School of Medicine and Boston Medical Center,
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Full Text
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22) Flagellin-based polypeptides for the diagnosis of lyme disease
Yale Flagellin Patent US Patent # 5, 618, 533, Inventors, Fikrig and
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Section of Immunobiology, Yale University School of Medicine, New
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http://www.ncbi.nlm.nih.gov/pubmed/1894359
24) Presentation of Kathleen Dickson to the FDA LYMErix hearing,
Bethedsa, MD, Jan 31, 2001:
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
25) Method for detecting B. burgdorferi infection, Persing, US Patent
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34) Researchers Finding Rewarding Careers As Software Entrepreneurs
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