Subject: Amjmed.org made *changes* to "Lyme" claims - the HLA-linked aspect
Date: Jan 31, 2013 6:46 AM
130129-130131 Answering Alpert’s
(American Journal of Medicine) Latest
Changes re “Lyme Disease”
Dear Mr. Alpert,
I can see what your problem is now: you
apparently have no background in this
science. You apparently went back to the
people for whom you are debasing your
profession and your journal in order to
have them tell you how to respond to the
scientific facts, citations and evidence
of this crime we are revealing to you.
Here is the newer version of your video,
which you modified and following that as
far as I am told, here are your
modifications:
http://www.youtube.com/watch?feature=player_detailpage&v=sUqkhhdwyss
ALPERT TRANSCRIPT II (January 28, 2013):
”Hello, I'm Joseph Alpert,
editor-in-chief of the American Journal
of Medicine, and I'm here today to call
your attention to a very interesting
article in the March issue of the
journal. This article by [Halperin, who
showed that “Lyme” caused ALS, and those
ALS cases did not have the Dearborn
antibody panel, so that is a murder
charge
http://www.actionLyme.org/ALSLYME47.htm
” … And there's been a great debate as
to why these individuals have these
symptoms. ***It's still not totally
clear, and there will continue to be
research in this area, but it appears
that these individuals have either an
autoimmune activation, such as, for
example, seen in patients with lupus,***
or that the symptoms are psychosomatic.”
Wrong. These diseases are not
about “immune activation.” They
are the opposite. That is the
persistent lie.
LYMErix and “Lyme” bleb-exposure
produced no antibodies and gave most
people a disease we call “Chronic Lyme,”
the name given to 1) the un-eradicable
spirochetes, 2) the reactivation of
latent herpesviruses, plus 3) TLR2
tolerance to mycoplasma in the blood in
people without the acceptable HLAs. The
model and the mechanisms are apparently
the same in Gulf War Illness and in the
brain damage in children commonly called
“autism.”
Lupus is a condition of high
antiphospholipid antibodies, and since
Yale formerly had a “’Lyme’ and Lupus
Clinic” that later became the RICO
entity “L2 Diagnostics” (in formal,
SEC-listed partnership with Corixa and
Imugen), it would be hard for these
criminals to suddenly start denying that
“Lyme” caused all their former “New
Great Imitators,” including the
neurological outcomes. That is why
you mention only lupus in your corrected
statements. You did not mention
the multiple sclerosis outcome of “Lyme”
and LYMErix because the head of that
NIH-NINDS department at the time, Roland
Martin, quit and went home to his native
Germany once he found out LYMErix of
OspA was the cause of this MS outcome.
Apparently you and IDSA would like
everyone to forget that there was an
special division of the NINDS dedicated
to understanding why Lyme caused
multiple sclerosis. You’d probably
especially like everyone to forget that
Roland Martin quit his NIH job when he
found out LYMErix was the cause of the
MS outcome of Lyme.
As for persistence, I won’t go into that
because at least 20 times these same
criminals reported that treatment
failed:
http://www.actionlyme.org/BRAIN_PERMANENT.htm
Please also see the history of the
permanence and incurability of Relapsing
Fever since 1911, here:
http://www.actionlyme.org/RICOCHRON.htm
)
At the same time, when they weren’t
deploying their RNA/DNA shell game with
the primers to find spirochetes in ticks
to patent, but also to find “Not ‘Lyme’”
in humans:
http://www.actionlyme.org/PRIMERSHELLGAME.htm
Compare to their patents, here:
http://www.actionlyme.org/CENTRAL_LYME_RICO_PATENTS.htm
We know spirochetes are permanent and
un-eradicable. The problem is, Why
did a recombinant antigen cause the same
systemic disease?
Answer: LYMErix solved this crime for
us. If these IDSA/ALDF idiots had
not tried to force a “Lyme” vaccine onto
the market, and if they had not decided
to perform medicine by slamming their
victims with the scientifically invalid
religion of psychiatry – which excuses
psychopathic behavior like IDSA’s and
Adam Lanza’s as “normal” and “common”
because of the statistical frequency of
your debauched behaviors -- we might not
have ever solved the “Great Imitator”
mystery or the Vaccines-Acquired-Autism
crime, which is even bigger.
TABLE OF CONTENTS/THE PUBLISHED DATA ON
LYMERIX-DISEASE:
1) SCIENTIFIC DATA ON IMMUNOSUPPRESSION from fungal antigens like OspA or LYMErix,
starting with Dattwyler in 1988.
2) THE FAILED TB and HIV VACCINES and WAYS THEY FAILED: Failed Tb and HIV vaccines
& the HIV-LYMErix vaccine [Fauci and the new NIH grants to study why HIV-LYMErix failed (TLR2-agonist-induced immunosuppression)].
3) PAUL DURAY on EPSTEIN-BARR-like TRANSFORMED CELLS in CFS-”LYME” VICTIMS:
NCI’s and the US Army’s Duray and the pre-cancerous EBV-transformed-like cells in Chronic "Lyme"
victims. (2 articles)
4) Fungal-Viral Synergy (FVS): FVS, in coordination with what was revealed by Paul Duray, is evidence
for exposure to fungal antigens causing immunosuppression and simultaneously activating latent Epstein-Barr.
NOTE: There is a lot of overlap in these
first 4 chapters, but the history of
exposure to fungal antigens was warped
due to
the fact that the ALDF/IDSA crooks did
not even care what OspA was/did
(structure being function) and lied
about its results
to the public and to the FDA.
5) Seronegative Epstein-Barr, currently known as chronic fatigue syndrome (CFS/fibromyalgia
syndrome (FMS) (4 articles)
6) SIR SIMON WESSELY on the ACTIVATION of EBV from STRESS HORMONES (act like
“Lyme” and LYMErix, activating Epstein-Barr) and on pyridostigmine bromide.. Add immunosuppression also known to be caused by DEET.
7) The CDC’s “bogus article” on mycoplasma in chronic fatigue syndrome to which the eperythrozoons
adhere, causing CFS.
8) Childhood Immunizations and the brain damage that is called autism also fits this model: CDC’s and
BigPharma’s own data (5 reports), plus the NYT revelation that the thimerosal was intended to prevent mycoplasmal or fungal growth within the vials
9) CDC’s Patents with SmithKline in Europe that mention HLA-linked and non-HLA linked antibody outcomes
(5), with SmithKline, in Europe, 1992; The Dearborn stunt was for their own personal profit.
10) SECTION 10: CHRONIC FATIGUE SYNDROME as REAL and TREATABLE with anti-EBV/herpes
drugs (mabs), anti-virals -- Columbia and Johns Hopkins regarding the treatment of the pre-cancer condition of the immunosuppression diseases or the "no-antibody" diseases. Rituximab and anti-virals for Chronic fatigue syndrome (anti-EBV/anti-CD20 mab).
11) Epstein-Barr’s Famous and well-known Chronic-, Autoimmune Disease- and Cancer Associations
Status: While "Lyme,"
LYMErix, chronic fatigue syndrome and
other immunosuppressing
events/conditions are known to occur
without antibodies and despite the
crimes and idiocies of IDSA -- because
TLR2-agonists turn off the antibody
response -- the reactivation of
Epstein-Barr/herpes is being addressed
with anti-virals and rituximab, and is
even being funded by the NIH. Yet
nothing is being done about the return
of mycoplasma, describing the relapse
phenomenon in Brian Fallon’s long term
Lyme treatment patients as [well as] the
relapses seen in chronic fatigue
syndrome victims.
We have no data on what would be a
monoclonal antibody-type therapy to get
rid of TLR2-tolerance. We have no
recent data on the current success of
the Chinese with an anti-OspA/gp120
cationic defensin. We just know
we’re still trying to have the likes of
you and the CDC/ID$A clowns indicted for
performing the Dearborn $tunt for their
VBD$ monopoly on grant$, patent$, test
kit$, royaltie$, and the exclusive
rights to test for all VBDs in America
and Canada once LYMErix was on the
market.
The No-HLA Diseases: What happens
to the other 85-70%?
There is a spectrum or a range, in
common diseases, from what used to be
called inflammatory (allergy) diseases
to the immunosuppression outcomes like
HIV and cancer. The NIH’s stats on
chronic fatigue syndrome (CFS) and
fibromyalgia is 4 and 8 million,
respectively (12 million). We have
no numbers on chronic “Lyme,” but we can
extrapolate from the falsified Dearborn
case definition (10 times under-reported
times 15% reportable). The
frequency of the HLA’s for MS and lupus
is approximately the same as the HLA
representation in the general US
population in RA (15-30 %). So,
what happens to the other 85-70% as a
result of the same exposures?
Note that at the CDC’s 1994, Dearborn,
MI, “consensus” conference where the
Steere-falsified testing for “Lyme” was
“approved,” despite none of the
participants agreeing with Steere’s
research-fraud proposal for an antibody
profile for a “positive” “case” for
relapsing fever, the average approval
rate of the attendees was only 15%.
That is, tested in the field, the
participating, invited labs at the
Dearborn conference, said this of
Steere’s proposal for a “case”:
http://www.actionLyme.org/DEARBORN_PDF.pdf
The accuracy assessments of the
Dressler/Steere proposal at the Dearborn
(based
on research fraud) stunt were:
15% (Wormser),
14% (Imugen),
22% (Lutheran Hosp),
8% (Igenex)
15% (Ron Schell, State of Wisconsin)
The above accuracy-rate of Steere’s
bogus Dearborn panel matched the
frequency of these arthritis and even
MS/lupus HLAs in the general population
(about 15%). Eight-Five percent of
us, upon the same infectious or
hypervaccination or autovaccination (Osp
blebbing by spirochetes) exposures, will
not have an HLA-linked outcome that is
detectable with antibody testing.
It’s the same number, 85, for the
“safety and efficacy” of the falsified
OspA vaccines outcomes, by the way,
which is no coincidence (76 and 92%).
SECTION 1: SCIENTIFIC DATA ON
IMMUNOSUPPRESSION
Dattwyler (again):
http://www.actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm
"Modulation of Natural Killer Cell
Activity by Borrelia burgdorferi†
http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1988.tb31843.x/abstract
"Seronegative Lyme disease.
Dissociation of specific T- and
B-lymphocyte responses to Borrelia
burgdorferi.
http://www.nejm.org/doi/full/10.1056/NEJM198812013192203
Dattwyler’s references (please refer to
the 1976 publication):
http://www.actionlyme.org/101016.htm
Harding and Radolf on OspA-induced
Immunosuppression (no antibodies), J
Immunol. 2001:
Toll-like
receptor 2-dependent inhibition of macrophage class
II MHC expression and antigen
processing by 19-kDa lipoprotein of Mycobacterium
tuberculosis
"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. This
mechanism may allow intracellular MTB to
evade immune surveillance and maintain
chronic infection."
http://www.ncbi.nlm.nih.gov/pubmed/11441098
Clifford Harding, 2010, on the 35 year
old mystery of "Steere's Bad Knees":
”Mycobacterium tuberculosis
synergizes with ATP to induce release of
microvesicles and exosomes containing
major histocompatibility complex class
II molecules capable of antigen
presentation.”
http://www.ncbi.nlm.nih.gov/pubmed/20837713
And the above mechanism of “shed
HLA-antigen complex as a unique antigen”
has had some follow up with Brucella
(Pollak et al, PLoS One, 2012):
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3506553/
It also explains a lot of strange
immunity like the anti-myelin
oligodendrocyte basic protein (MOBP)
antibodies produced from
exposure to OspA found in “Lyme”/LYMErix
victims reported by Mark Klempner
(Nature Medicine, 1999):
http://www.nature.com/nm/journal/v5/n12/full/nm1299_1346.html
Pages of Huber and Klempner’s report
scanned in showing autoimmunity in the
CNS from OspA:
http://www.actionLyme.org/KFORSCHNER_DISCOVERS_LYME_TOXIN.htm
and the other well-known mechanisms of
“mistaken self” as autoimmunity.
If Lyme and LYMErix detonate EBV, then
could the so-called HLA-antigen complex
“autoimmunity” diseases of MS and Lupus
as outcomes of Lyme and LYMErix be to
[do] with EBV/other herpes antigens and
not necessarily Lyme antigens?
Does the HLA-antigen complex theory
explain Steere’s bizarre theory about
OspA causing autoimmunity against
lymphocytes that only attack the knee?
How much time should someone spend
trying to unscramble what Allen Steere
has had to say for the last 38 years?
Even SmithKline made fun of Allen
Steere’s preposterous proposal at the
2001 FDA Meeting on LYMErix:
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_02_lobet.pdf
"- Identity of the auto-antigen
"− TRLA is observed in one (few)
joint(s), while hLFA-1 is present on
cells throughout the body”
Biofilms are covered in SLYMErix
(TLR2-agonists), but you can look that
up for yourself on PubMed. I
personally find no reason to think small
clusters of bacteria cause the systemic
disease known as “Lyme” or CFS.
Instead, these diseases are undoubtedly
about something in the blood plus some
disordered immunity in the central
nervous system, such as per NIH’s former
employee, Roland Martin,…:
“We found 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."
http://www.ncbi.nlm.nih.gov/pubmed/16783164 ),
…plus the delirium/hypoxia signs detectable with PET and SPECT imaging. The model of CFS-Lyme appears to be chronic
cerebrovascular dysimmunity and hypoxia without blatant anemia from mycoplasmally-disrupted erythrocyte membrane potential.
SECTION 2: THE FAILED TB and HIV
VACCINES and WAYS THEY FAILED:
A) Yeremeev VV et al (Russia),
Clin Exp Immunol. 2000:
The 19-kD antigen and protective
immunity in a murine model of
tuberculosis
“These results are consistent
with a model in which the presence of
the 19-kD protein has a detrimental
effect on the efficacy of vaccination
with live mycobacteria. Targeted
inactivation of genes encoding selected
antigens represents a potential route
towards development of improved vaccine
candidates."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10792376&dopt=Abstract
B) Post et al (South Africa),
Infect Immun. 2001:
Mycobacterium tuberculosis
19-kilodalton lipoprotein inhibits
Mycobacterium smegmatis-induced cytokine
production by
human macrophages in vitro
"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."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11179309&dopt=Abstract
C) Avi-Hai Hovav et al, Infect Immun.
2003:
"The Mycobacterium tuberculosis
recombinant 27-kilodalton lipoprotein
induces a strong Th1-type immune
response deleterious to protection ”
"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. We are
currently studying how the 27-kDa
antigen modulates the mouse immune
response."
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12761093
D) Anthony Fauci on the failed
HIV-”LYME”rix vaccine, producing no
antibodies, N Engl J Med 2008:
"The initial empirical approach of
immunizing with VaxGen's AIDSVax, a
recombinant form of the outer glycoprotein-120
(gp120) portion of the HIV envelope,
which was based on a strategy that was
successful with hepatitis B, failed to
protect volunteers from infection,
apparently because the vaccine did not
induce broadly neutralizing antibodies."
http://www.nejm.org/doi/full/10.1056/NEJMp0806162#t=article
E) NIAID 2012 awarded grant (Bonaldo) re
HIV-LYMErix vaccine making people
sicker, like the failed Tuberculosis
TLR2-agonist vaccines:
"After the failure of the merck STEP
trial [which was OspA] that appears to
have enhanced the rate of infection in
vaccinees, ... "
http://projectreporter.nih.gov/project_info_description.cfm?aid=8307107&icde=14976345&ddparam=&ddvalue=&ddsub=&cr=1&csb=default&cs=ASC
F) NIAID 2012 awarded grant to Mark
Klempner’s partner, Linden Hu, (together
they performed the “retreatment” trial
of people
who had never had ceftriaxone before as
the basis of IDSA’s “guidelines”) to
study this now well known phenomenon of
TLR2-tolerance or immunosuppression
caused by “Lyme” or LYMErix:
”PUBLIC HEALTH RELEVANCE: The innate
immune system is one of the most
important lines of host defense against
microbial invaders, but it can also
cause illness when stimulated
inappropriately or too vigorously. In
this proposal, we examine the mechanisms
by which a specific component of the
innate immune system, toll-like receptor
2, recognizes its targets and causes
inflammation. A better understanding of
the workings of innate immunity is
important for developing therapies for
diseases such as “Lyme” disease ***
where either an ineffective*** or an
over-exuberant immune response causes
the symptoms of illness.
SECTION 3: PAUL DURAY on
EPSTEIN-BARR-like TRANSFORMED CELLS in
CFS-”LYME” VICTIMS:
A), 1989, in Infectious Disease Reviews
(IDSA’s former journal)
"Immature B cells can also be seen in
the spinal fluid. These cells can
appear quite atypical- not unlike
those of transformed or neoplastic
lymphocytes." --
http://www.ncbi.nlm.nih.gov/pubmed/2814170
B) Paul
Duray chapter (NCI, NIH, Ft.
Detrick,) at the 1992 Cold
Spring Harbor Crooks' Conference summary
, published by
Steve Schutzer in Lyme Disease:
Molecular and Immunologic Approaches.
1992- "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." -
New, re “immature immune cells” in
chronic TLR2 exposure (Seeboth et al,
Vet Res. 2012):
The fungal T-2 toxin alters the
activation of primary macrophages
induced by TLR-agonists resulting in a
decrease
of the inflammatory response in the pig
"By contrast, the activation
of TLR7 by ssRNA was not modulated by
T-2 toxin pre-treatment. In conclusion,
our results suggest that ingestion of
low concentrations of T-2 toxin affects
the TLR activation by decreasing pattern
recognition of pathogens and thus
interferes with initiation of
inflammatory immune response against
bacteria andviruses. Consequently,
mycotoxins [OspA
exposure, either thru blebbing or
vaccination-KMD] could increase the
susceptibility of humans and animals to
infectious diseases."
“Furthermore, T-2 toxin reduces
lymphocyte proliferative response [8,9]
and ***disturbs the maturation process
of dendritic cells [10]*** suggesting
its immunosuppressant potency [7,11]”
”Indeed Li et al. [15] showed that
systemic T-2 exposure increases the
severity of respiratory
***reovirus***infection with marked
exacerbation of bronchopneumonia and
modulation of cytokine responses in mice
alveolar macrophages.
NOTE: The above sounds quite a bit like
how to make a pandemic flu, don’t it?
Sounds quite a bit like, to me, that
Lyme
Cryme victims, rather than becoming
walking canisters of tick disinfectant
(according to the alleged modality of
Lyme
“prevention” by the Yale criminals with
their OspA vaccines), instead will
become the next Pandemic Flu/Other
Typhoid
Marys. We’re the Hostesses with
the Mostesses and we are also quite
certain the antics of Yale and IDSA will
backfire in a
bigger way than the 10 lost years of the
HIV-LYMErix vaccine.
ARTICLE CONTINUES: ”Moreover, similar
distribution of TLR on human and swine
cells, unlike rodents, has been
previously
described [48]
http://www.veterinaryresearch.org/content/pdf/1297-9716-43-35.pdf
And this, above, is why all mouse
studies of “Lyme” where the molecular
mice are not transfected with human TLR2
can be thrown out. All infectious
diseases studies where mouse TLR2 was
used to measure the antibody response
can be thrown out. All
antibody-associations to all diseases
data can be thrown out. Only
non-Primershellgame DNA/RNA and properly
defined biomarkers are acceptable for
correlations.
SECTION 4: FUNGAL-VIRAL SYNERGY (FVS) --
FVS, in coordination with what was
revealed by Paul Duray, is evidence for
exposure to fungal antigens causing
immunosuppression and simultaneously
activating latent Epstein-Barr.
This is from the 1950s, where we see
that fungal antigens like LYMErix or
OspA or Borrelial outer surface proteins
are known to activate viruses via
immunosuppression:
"In Swiss mice, animals with high
natural resistance to hepatitis virus,
the pathogenicity of this agent was
markedly enhanced by combined infection
with eperythrozoa. Eperythrozoa were
maintained throughout 18 successive
passages in normal Princeton and Swiss
weanlings with intact spleens. The
combined infection of Princeton mice
with eperythrozoa and the virus
component of Gledhill, Dick, and
Andrewes, which is nearly inactive when
injected alone, resulted in acute
hepatitis with fatal outcome."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136329/?tool=pubmed
NOTE: Later we see the CDC throw out the
red blood cells to which mycoplasma
adhere when determining whether or
not mycoplasma is involved in Chronic
fatigue syndrome. It’s cute.
It’s cute what the CDC does. Which is
why
DARPA
now wants nothing to do with the CDC.
OspA Inhibits Apoptosis in
“Lyme”-infected cells (and there are
many more besides the following report
by Power et al, J Immunol. 2004):
Bacterial lipoprotein [OspA] delays
apoptosis in human neutrophils through
inhibition of caspase-3 activity:
regulatory
roles for CD14 and TLR-2.
“In this study, we demonstrate that
BLP inhibits neutrophil mitochondrial
membrane depolarization with a
subsequent reduction in caspase-3
processing, ultimately leading to a
significant delay in PMN apoptosis.”
http://www.ncbi.nlm.nih.gov/pubmed/15470068
Here are 130 more PubMed entries on
this:
http://www.ncbi.nlm.nih.gov/pubmed?linkname=pubmed_pubmed&from_uid=15470068
You’ve heard of BCL2-analogs and the
fact that some organisms have their own
such genes to help with their parasitic
and disease activities? OspA
behaves like a BCL2-analog in that the
end result is the same. OspA is not a
program like BCL2, it’s just that the
result is the same. OspA is
associated with the porin P66, so its
function is apparently to help
spirochetes attach to and suck
membranes. One can assume OspA
might have the same function as a free
antigen inside a cell, attaching to
membranes and perhaps depolarizing the
internal structures/membranes/cell
machinery, like mycoplasma do to red
blood cells. OspA is “sticky” says
CDC officer and OspA patent owner,
Alan Barbour.
More on gumming-up the immunity process
by, again, Harding (J Immunol. 2012):
TLR2 signaling depletes IRAK1 and
inhibits induction of type I IFN by
TLR7/9
"Pathogens may signal through multiple
TLRs with synergistic or antagonistic
effects on the induction of cytokines,
including type I IFN (IFN-I). IFN-I is
typically induced by TLR9, but not TLR2.
Moreover, we previously reported that
TLR2 signaling by Mycobacterium
tuberculosis or other TLR2 agonists
inhibited TLR9 induction of IFN-I and
IFN-I-dependent MHC-I Ag cross
processing. The current studies revealed
that lipopeptide-induced TLR2 signaling
inhibited induction of first-wave IFN-α
and IFN-β mRNA by TLR9, whereas
induction of second-wave IFN-I mRNA was
not inhibited. TLR2 also inhibited
induction of IFN-I by TLR7, another
MyD88-dependent IFN-I-inducing receptor,
but did not inhibit IFN-I induction by
TLR3 or TLR4 (both Toll/IL-1R
domain-containing adapter-inducing IFN-β
dependent, MyD88 independent). The
inhibitory effect of TLR2 was not
dependent on new protein synthesis or
intercellular signaling.
IL-1R-associated kinase 1 (IRAK1) was
depleted rapidly (within 10 min) by TLR2
agonist, but not until later (e.g., 2 h)
by TLR9 agonist. Because IRAK1 is
required for TLR7/9-induced IFN-I
production, we propose that TLR2
signaling induces rapid depletion of
IRAK1, which impairs IFN-I induction by
TLR7/9. This novel mechanism, whereby
TLR2 inhibits IFN-I induction by TLR7/9,
may shape immune responses to microbes
that express ligands for both TLR2 and
TLR7/TLR9, or responses to
bacteria/virus coinfection."
http://www.ncbi.nlm.nih.gov/pubmed/22227568
Older published works in this area:
de Waal Malefy et al, J Exp Med. 1991.
[LYMErix/ OspA and IL-10 perhaps
independently inhibiting apoptosis in
EBV infected cells
as the main mechanism of induction of
the New Great Imitators With Or Without
HLAs -], cited over 100 times:
“Interleukin 10 (IL-10) and viral IL-10
strongly reduce antigen-specific human T
cell proliferation by diminishing the
antigen-presenting capacity of monocytes
via downregulation of class II major
histocompatibility complex expression.”
“… Collectively, our data indicate that
IL-10 and v-IL-10 can completely prevent
antigen-specific T cell proliferation by
inhibition of the antigen-presenting
capacity of monocytes through
downregulation of class II MHC antigens
on monocytes.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118975/
IN BETWEEN (besides Paul Duray’s
observation of EBV-transformed-like
cells in chronic “Lyme”):
Hulínská D et al, Folia Biol (Praha),
2003:
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
for 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.
http://www.ncbi.nlm.nih.gov/pubmed/12630667
And here is Gary Wormser, again, in
2000, while LYMErix was still on the
market, on immunosuppression from OspA
exposure:
Modulation of lymphocyte proliferative
responses by a canine Lyme disease
vaccine of recombinant outer surface
protein A (OspA)
”OspA interferes with the response of
lymphocytes to proliferative stimuli
including a blocking of cell cycle phase
progression.”
http://www.ncbi.nlm.nih.gov/pubmed/10865170
And here is Dave Persing, one of the
“Lyme” crooks and owner of the Corixa
RICO (No-OspA-B in the spirochete)
patent:
Molecular evidence and clinical
significance of herpesvirus coinfection
in the central nervous system
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC230077/
By the way, Persing is not the only
“Lyme” crook who apparently has
only two areas of interest -- “Lyme” and
Epstein-Barr:
http://www.action”Lyme”.org/120420_AUWAERTER.htm
This also holds true for Paul “I don’t
know what OspA is” Auwaerter, Adrianna
Marques (NINDS, former partner of Roland
Martin’s), and Brigitte Huber (former
partner of Steere’s who now agrees with
us and not Steere). Auwaerter, I
guess is interested in nf-kappa events –
immunosuppression:
Epstein-Barr virus BGLF4 kinase
downregulates NF-κB transactivation
through phosphorylation of coactivator
UXT
http://www.ncbi.nlm.nih.gov/pubmed/22933289
Much like “Lyme” and LYMErix exposure:
"Induction of in vitro reprogramming by
Toll-like receptor (TLR)2 and TLR4
agonists in murine macrophages: effects
of
TLR "homotolerance" versus
"heterotolerance" on NF-kappa B
signaling pathway components.
“LPS-induced NF-κB DNA binding, c-jun
N-terminal kinase (JNK) kinase activity,
and TNF-α secretion were significantly
inhibited in murine macrophages
pre-exposed to a mycoplasma lipopeptide,
macrophage-activating lipopeptide
(MALP)-2, which signals through TLR2 (19).”
http://www.jimmunol.org/content/170/1/508.long
Synergy and Cross-Tolerance Between
Toll-Like Receptor (TLR) 2- and
TLR4-Mediated Signaling Pathways
“A family of Toll-like receptor (TLR)
mediates the cellular response to
bacterial cell wall components; murine
TLR2 and TLR4
recognize mycoplasmal lipopeptides
(macrophage-activating lipopeptides, 2
kDa (MALP-2)) and LPS, respectively.
Costimulation of mouse peritoneal
macrophages with MALP-2 and LPS results
in a marked increase in TNF-α
production, showing the synergy between
TLR2- and TLR4-mediated signaling
pathways. Macrophages pretreated with
LPS show hyporesponsiveness to the
second LPS stimulation, termed LPS
tolerance. The LPS tolerance has
recently been shown to be primarily due
to the down-regulation of surface
expression of the TLR4-MD2 complex. When
macrophages were treated with MALP-2,
the cells showed hyporesponsiveness to
the second MALP-2 stimulation, like LPS
tolerance. Furthermore, macrophages
pretreated with MALP-2 showed reduced
production of TNF-α in response to LPS.
LPS-induced activation of both NF-κB and
c-Jun NH2-terminal kinase was severely
impaired in MALP-2-pretreated cells.
However, MALP-2-pretreated macrophages
did not show any reduction in surface
expression of the TLR4-MD2 complex.
These findings indicate that LPS-induced
LPS tolerance mainly occurs through the
down-regulation of surface expression of
the TLR4-MD2 complex;
in contrast, MALP-2-induced LPS
tolerance is due to modulation of the
downstream cytoplasmic signaling
pathways.”
http://www.jimmunol.org/content/165/12/7096.abstract?ijkey=e865b5a3430b7e0af43a112e93d68f2bf4f35081&keytype2=tf_ipsecsha
2005, re the two sides of the same
fungal/viral coin -- cancer and its
opposite -- diseases with antibodies:
”Phosphorylation of NF-kappaB and
IkappaB proteins: *** implications in
cancer and inflammation. ***”
“Nuclear factor-kappaB (NF-kappaB) is a
transcription factor that has crucial
roles in inflammation, immunity, cell
proliferation and apoptosis. Activation
of NF-kappaB mainly occurs via IkappaB
kinase (IKK)-mediated phosphorylation of
inhibitory molecules, including
IkappaBalpha. Optimal induction of
NF-kappaB target genes also requires
phosphorylation of NF-kappaB proteins,
such as p65, within their
transactivation domain by a variety of
kinases in response to distinct stimuli.
Whether, and how, phosphorylation
modulates the function of other
NF-kappaB and IkappaB proteins, such as
B-cell lymphoma 3, remains unclear. The
identification and characterization of
all the kinases known to phosphorylate
NF-kappaB and IkappaB proteins are
described here. Because deregulation of
NF-kappaB and IkappaB phosphorylations
is a hallmark of chronic inflammatory
diseases and cancer, newly designed
drugs targeting these constitutively
activated signalling pathways represent
promising therapeutic tools.
http://www.ncbi.nlm.nih.gov/pubmed/15653325
Fungal Antigen Effect on Caspases:
”Bacterial lipoprotein delays apoptosis
in human neutrophils through inhibition
of caspase-3 activity: regulatory roles
for CD14 and TLR-2.”
http://www.ncbi.nlm.nih.gov/pubmed/15470068
http://www.jimmunol.org/content/173/8/5229.long
You should be sure to read that one, the
full text link, above, through
thoroughly and study all the citations,
too.
And you can follow up on what causes
EBV’s and OspA’s inhibition of
apoptosis, IL-10 induced changes and
TLR2 agonist “TOXINS’” changes to immune
cells on your own.
SECTION 5: SERONEGATIVE EPSTEIN-BARR,
currently known as chronic fatigue
syndrome (CFS)/fibromyalgia syndrome
(FMS) (4 articles)
1) Down-regulation of MHC class II
expression through inhibition of CIITA
transcription by lytic transactivator
Zta during
Epstein-Barr virus reactivation
http://www.ncbi.nlm.nih.gov/pubmed/19201831
2) Innate immune modulation in EBV
infection
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3063194/?tool=pubmed
3) The lytic cycle of Epstein-Barr virus
is associated with decreased expression
of cell surface major histocompatibility
complex class I and class II molecules
http://www.ncbi.nlm.nih.gov/pubmed/12134023
4) Epstein-Barr virus evasion of CD8(+)
and CD4(+) T cell immunity via concerted
actions of multiple gene products
“Synthesis of new MHC class I molecules
is blocked by BGLF5. Viral-IL10 causes a
reduction in mRNA levels of TAP1 and
bli/LMP2, a subunit of the
immunoproteasome. MHC class I molecules
present at the cell surface are
downregulated by BILF1. Also the antigen
presenting capacity of MHC class II
molecules is severely compromised by
multiple EBV lytic gene products,
including gp42/gH/gL, BGLF5, and vIL-10.
In this review, we discuss how concerted
actions of these EBV lytic proteins
result in highly effective interference
with CD8(+) and CD4(+) T cell
surveillance, thereby providing the
virus with a window for undisturbed
generation of viral progeny.”
http://www.ncbi.nlm.nih.gov/pubmed/18977445
None of this is new. We could keep
going. The point is that
Epstein-Barr-antibody and
mycoplasmal-antibody studies in CFS,
”Lyme” - and everything else - can all
be thrown out.
We can call these sick people who have
been both abandoned and tortured by the
so-called medical community, “The
Pre-
cancerous-, Non-HLA-linked-,
Non-antibody-linked-, MS-Related
Diseases,” for short. We can even
suggest that the
lack of progress in tuberculosis,
“Lyme,” HIV, and these other “waste
basket" diagnoses that typically have
the stigma of
somatization attached to them thanks to
the medical elites (and thus this
incorrect information trickles down to
even the smallest of country doctors'
practices), was deliberate, even so far
as to assume that the failed HIV-LYMErix
vaccine trial was deliberate. We
are talking about the CDC, various other
US government departments, and we are
talking about Yale -- all well-known
purveyors of prevarications, be it
weapons of mass destruction (WMDs) in
Iraq, the Gulf of Tonkin, the 3-for-2
airplane episode in NYC with the 7
second (acceleration of gravity)
collapse of Building 7, or the fake
Yellowcake Letter and the subsequent
persecution of Joe Wilson.
In truth, we’re actually not the
Dahmer-Lanzas of the world. That’s
you and your,.. what is a non-slang word
for “handlers?” That’s the
so-called professionals, rife with
conflicts of interest, who project onto
us some psychic ability to cause
ourselves all the scientifically valid
and verifiable illness signs,
particularly all of IDSA’s own published
valid biomarkers of disease:
http://www.actionLyme.org/BIOMARKERS.htm
With no scientific talent, monotonous,
transparent skits and stunts, and now
bankrolled yet bankrupt, to trust a US
(dot)gov at this juncture one would have
to be severely lacking in IQ.
=================
SECTION 6: SIR SIMON WESSELY on the
ACTIVATION of EBV from STRESS HORMONES
(act like “Lyme” and LYMErix,
activating Epstein-Barr) and on
pyridostigmine bromide.
Recently Knighted professor of
psychiatry at the Institute of
Psychiatry, King's College London, and
director of the King's Centre for
Military Health Research, Simon Wessely
seemingly has the world in the palm of
this hand. Now if we could just get him
to start telling the truth.
Wessely reports with the Pentagon that
vaccination in the Gulf is associated
with Gulf War Illness (GWI)/fatigue:
Wessely, 2000:
"Role of vaccinations as risk factors
for ill health in veterans of the Gulf
war: cross sectional study
CONCLUSION (Wessley’s): “There was a
specific association between the timing
of multiple vaccines and ill health:
personnel who received multiple vaccines
before deployment were not at increased
risk, whereas those who had received
them during deployment were.”
http://www.bmj.com/content/320/7246/1363?view=long&pmid=10818024
Wessely later reported that he threw out
such data to invent the theory that one
can later throw out the same data, and
instead blame the victims, and thus
everyone will admire him and crown him
King. Or at least, Knight:
”Something old, something new, something
borrowed, something blue: The true story
of Gulf War Syndrome”
Wednesday,
25 January 2006
http://www.gresham.ac.uk/lectures-and-events/the-true-story-of-gulf-war-syndrome
SAYS WESSELY: "One other thing that many
people told us was that they had
received a lot of vaccines in a short
space of time. Of course this was
because it was a bit of a rush, as these
things always are, and we had not just
the biological vaccines, we had the
other, more routine, vaccines that had
to be given as well. There is no
particular reason to suspect that that
would be associated with ill health.”
What Knight Wessely fails to mention
here is his own former data with the
Pentagon where he showed that there was
an association with vaccines and the GWI
outcome. "King-Me!!"
CONTINUES WESSELY: “We did, however,
also look at the central nervous system
- that’s the brain, basically. One way
of doing that is through neuro-imaging,
but we didn’t get the money to do that,
so instead we have used sophisticated
neuro-psychological testing, which has
been largely normal in this group as
well.”
There happens to be no such thing as
"sophisticated psychological testing."
There is the only scientifically valid
testing, as per the FDA’s rules on the
validation of an analytical METHOD used
to determine scientifically valid
OUTLIERS in human biochemistry and
physiology parameters, such as IDSA’s
Biomarkers of Chronic Lyme and the New
Great Imitators: SPECT scans, spinal
fluid analyses for the likes of signs of
degradation of the central nervous
system found by Mark Klempner (MMP-130)
and Robert Schoen (Gfap), QEEG (Sigal),
etc. These valid illness signs
would be considered Organic brain
compromise. And there is B), a
verifiable history of Trauma, and there
C) is cognitive testing which, for
example, can pick up the Genetic likes
of VIQ>>> PIQ in high-functioning autism
like Einstein’s, or its reverse,
Asperger’s. The only valid axes
are Genetic, Organic, and Traumatic, but
there is no “psychological” testing
because psychology is not real:
Here is why:
New York Times (Tierney, 2008):
Deep Down, We Can’t Even Fool Ourselves
”But as useful as hypocrisy can be, it’s
apparently not quite as basic as the
human instinct to do unto others as you
would have them do unto you. Your mind
can justify double standards, it seems,
but in your heart you know you’re
wrong.”
http://www.nytimes.com/2008/07/01/science/01tier.html?_r=0
New York Times (Carey and Hartocollis):
Psychiatry admits they do not identify
evil, re the Sandy Hook Massacre
Warning Signs of Violent Acts Often
Unclear
"The sort of young, troubled males who
seem to psychiatrists most likely to
commit school shootings — identified
because they have made credible threats
— often do not qualify for any
diagnosis, experts said. They might have
elements of paranoia, of deep
resentment, or of narcissism, a
grandiose self-regard, that are
noticeable but do not add up to any
specific “disorder” according to strict
criteria."
http://www.nytimes.com/2013/01/16/health/breaking-link-of-violence-and-mental-illness.html?_r=0
Self-worship is "not a disorder,"
according to psychiatry, which, many
fail to realize, is a belief system and
not science. Putting yourself
above others is “normal,” says
psychiatry.
But you know it in your heart when you
do something wrong, they also claim,
above, using actual analytical methods.
The so-called courts also agree that
there is some element of the human Will
at work in human behavior (let’s call
that, Organic, Traumatic, Genetic, the
human Will…as the verifiable axes).
But at the same time, these
psychiatrists claim “wrong” is so common
that it is “normal,” and therefore
acceptable. Can we suppose there
is yet a fifth element or force at work?
One that explains a cumulative history
of decisions to harm people making it
easier and easier to continue to do so
on a daily basis and even with “MD”
after one’s name? Does psychopath
describe “walking Evil?” Can a
psychopath more easily pass a lie
detector test? There is
other evidence that Evil is as
verifiable as Robert Schoen’s Gfap – or
Glial Fibrillary acidic protein in the
CSF of “Lyme” victims.
More on stress-activated Epstein-Barr,
which is clearly an outcome of the
reversed placebo effect of Wessely’s now
obviously criminally fraudulent
accusations against Gulf War Illness
Veterans (2 reports, one on heart
disease):
Stowe et al, Psychosom Med. 2001:
Elevated stress hormone levels relate to
Epstein-Barr virus reactivation in
astronauts
http://www.ncbi.nlm.nih.gov/pubmed/11719627
Uchakin et al, Interdiscip Perspect
Infect Dis. 2011:
Fatigue in medical residents leads to
reactivation of herpes virus latency
http://www.ncbi.nlm.nih.gov/pubmed/22229027
Yang et al, Brain Behav Immun. 2010:
Glucocorticoids activate Epstein Barr
virus lytic replication through the
upregulation of immediate early BZLF1
gene expression
http://www.ncbi.nlm.nih.gov/pubmed/20466055
Science Daily, 2013:
Viral [EBV] Reactivation a Likely Link
Between Stress and Heart Disease
http://www.sciencedaily.com/releases/2013/01/130122162331.htm
Back to Wessely and how nerve agent
antidote causes immunosuppression:
Peden-Adams et al, Immunopharmacol
Immunotoxicol. 2004:
Pyridostigmine bromide (PYR) alters
immune function in B6C3F1 mice
”Exposure to PYR did not alter splenic
and thymus weight or splenic
cellularity. However, 20 mg PYR/kg/day
decreased thymic cellularity with
decreases in both CD4+/CD8+ (20
mg/kg/day) and CD4-/CD8- (10 and 20
mg/kg/day) cell types. Functional immune
assays indicated that lymphocyte
proliferative responses and natural
killer cell activity were normal;
whereas exposure to PYR significantly
decreased primary IgM antibody responses
to a T-cell dependent antigen at the 1,
5, 10 and 20 mg/kg treatment levels for
14 days. This is the first study to
examine the immunotoxicological effects
of PYR and demonstrate that this
compound selectively suppresses humoral
antibody responses.”
http://www.ncbi.nlm.nih.gov/pubmed/15106728
There are other reports regarding the
toxicity of PYR on MedLine.
I am claiming, since it is already
claimed by these labs, that
immunosuppression-plus-hypervaccination
in the Gulf could be contributing
factors in Gulf War Illness. And
Simon Wessely is a tool deployed against
both GWI and CFS/myalgic
encephalomyelitis (ME) victims in the
UK, much like the Munchausen’s and
Shaken Baby false accusations have been
flung at the parental victims of
vaccines that cause encephalitis and
hemorrhage and death. I propose
that these outcomes, GWI and “autism,”
mimic both the HLA(strange immunity)-
and non-HLA- models of LYMErix disease.
SECTION 7: The CDC’s “bogus article” on
mycoplasma in chronic fatigue syndrome;
CDC throws out the red blood cells, to
which the eperythrozoons adhere, causing
CFS:
”Absence of Mycoplasma species DNA
in chronic fatigue syndrome.”
http://jmm.sgmjournals.org/content/52/11/1027.full.pdf+html
CDC centrifuges the blood, throws out
the erythrocytes to which the
eperythrozoons adhere, mentions that
these patients have no antibodies which
is to be expected after chronic exposure
to fungal antigens as shown by Harding
and Radolf, above, and subsequent
related studies like the no-antibodies
from the HIV-”LYME”rix exposure, as
explained by Anthony Fauci (above).
1992; “[The effect of Eperythrozoon suis
infection on the osmotic fragility of
erythrocytes]”
"Osmotic fragility of erythrocytes was
tested in weaned pigs experimentally
infected with Eperythrozoon (E.) suis.
Acute
eperythrozoonosis of splenectomized pigs
***led to an increase of osmotic
fragility.*** It is supposed that E.
suis infection
causes a structural change in
erythrocyte membrane. Possible
mechanisms of this cell membrane injury
are discussed.
http://www.ncbi.nlm.nih.gov/pubmed/1471973
And you can follow up on ^^^ that.
Do the RBC-zoons or the mycoplasma cause
fatigue in animals? The PubMed
crystal
ball says yes:
http://www.ncbi.nlm.nih.gov/pubmed?term=eperythrozoon%20and%20lethargy%20and%20animals
No longer can anyone claim that “no
antibodies means no organism,” or “no
disease,” nor can they claim “mycoplasma
are absent from the erythrocytes of CFS
victims.”
-------------------------------------
8) Childhood Immunizations and the brain
damage that is currently called autism
also fits this model – CDC’s and
BigPharma’s own data (5 reports), plus
the NYT revelation that the thimerosal
was intended to prevent mycoplasmal or
fungal
growth within the vials (you can’t
autoclave a vial with a rubber septum,
obviously).
A) – BigPharma: "Finally, there is the
risk that the virus may not be fully or
completely inactivated or attenuated and
thus, the
vaccine may actually cause disease."
http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=7%2C632%2C510.PN.&OS=PN%2F7%2C632%2C510&RS=PN%2F7%2C632%2C510
B) CDC:
”Measles, Mumps, and Rubella -- Vaccine
Use and Strategies for Elimination of
Measles, Rubella, and Congenital Rubella
Syndrome and Control of Mumps:
Recommendations of the Advisory
Committee on Immunization Practices
(ACIP)
"Updated information on adverse events
and contraindications, particularly for
persons with severe HIV infection,
persons with a g allergy or gelatin
allergy, persons with a history of
thrombocytopenia, and persons receiving
steroid therapy [are
immunosuppressed- KMD]."
http://www.cdc.gov/mmwr/preview/mmwrhtml/00053391.htm
C) CDC: Human Exposure to Brucella
abortus Strain RB51 -- Kansas, 1997
http://www.cdc.gov/mmwr/preview/mmwrhtml/00051495.htm
In the above, an immunosuppressed
pregnant cow was given a Brucella
(“LYME”rix-like) "live attenuated"
vaccine and the baby cow ended up with
the disease, which then was transferred
to the humans handling the cow and her
dead baby. This parallels what is
happening to children who are vaccinated
while immunosuppressed, or who receive
mycoplasmally (“LYME”rix-like)
contaminated vaccines.
D) in the case of pandemic MRSA, as we
have seen, the vaccine didn't work
because TLR2 agonists (lipoproteins)
suppress the immune system. We
also learned from the MRSA vaccine
patent, that:
"Several established vaccines consist of
live attenuated organisms where the risk
of reversion to the virulent wild-type
strain exists. In particular in
immunocompromised hosts this can be a
live threatening scenario.
Alternatively, vaccines are administered
as a combination of pathogen-derived
antigens together with compounds that
induce or enhance immune responses
against these antigens (these compounds
are commonly termed adjuvant), since
these subunit vaccines on their own are
generally not effective."
http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=7,771,728.PN.&OS=PN/7,771,728&RS=PN/7,771,728
E) "The effect of exogenous
corticosterone on West Nile virus
infection in Northern Cardinals
(Cardinalis cardinalis)
“Corticosterone was administered at
levels that individuals enduring chronic
stressors (i.e ., long-term inclement
weather, food shortage, anthropogenic
pollution) might experience in the wild.
Corticosterone greatly impacted
mortality: half of the
corticosterone-implanted cardinals died
between five - 11 days post-inoculation
whereas only one of nine sham-implanted
(control) birds died.
”No differences were found in viral
titer between corticosterone- and
sham-implanted birds. However, cardinals
that survived
infections had significantly higher
average body temperatures during peak
infection than individuals that died.
”In sum, this study indicates that
elevated corticosterone could affect the
survival of WNV-infected wild birds,
suggesting that
populations may be disproportionately
at-risk to disease in stressful
environments.”
http://7thspace.com/headlines/410671/the_effect_of_exogenous_corticosterone_on_west_nile_virus
_infection_in_northern_cardinals_cardinalis_cardinalis.html
---------------------------
SECTION 9: CDC’s PATENTS WITH SMITHKLINE
IN EUROPE, discussing the 2 kinds of
"Lyme," A) the HLA-linked kind which is
the Dearborn kind and which is the
Clifford-Harding-Solves-Steere’s-Bad-Knees
kind, which produces antibodies, and B)
the non-HLA-linked kind which is now
called hypochondria, Munchausens, a
“pattern of protection,”
Fibro-Viagra-Deficit
(instead of a sexually transmitted
disease, fibromyalgia is the opposite)
or whatever is the next permutation of
cowardly witch hunts and victim-blaming.
Which will boomerang.
The 5 European Patents owned by CDC
staff:
http://www.wikipatents.com/CA-Patent-2135800/compositions-useful-in-diagnosis-and-prophylaxis-of-lyme-disease
In the descriptions of these 5, 1992
CDC's staff's patents with SmithKline in
Europe, CDC staff admits that Lyme
arthritis is not the only kind of Lyme:
"Summary of the Invention
"In one aspect, the invention provides
isolated B. burgdorferi antigens which
are regulated and differentiated by
growth of the B. burgdorferi in a tick
vector. Novel antigens of the invention
are listed below in Table I.
"Certain of these antigens are
characterized as being B. burgdorferi
B31 strain specific and major
histocompatibility complex (MHC)
nonrestricted. Certain other of these
antigens are characterized as being MHC
restricted...."
The Dearborn stunt excluded these
non-HLA-linked cases via research fraud
performed by Allen Steere in Europe,
where he fooled around with strains and
raised the cut-off for a positive ELISA
to 5 std and deliberately left out the
neurologic or meningitis cases.
These were the 2 reports:
Antigens in Europe and Dressler/Steere:
http://www.ncbi.nlm.nih.gov/pubmed/8106763
http://www.ncbi.nlm.nih.gov/pubmed/8380611
The research fraud committed by Steere
playing a game with the strains and the
non-lipidated recombinant antigens to
leave out OspA and B for a monopoly on
post-LYMErix testing with Imugen, Corixa
and Yale’s L2-Diagnostics:
http://www.actionlyme.org/STEERE_IN_EUROPE.htm
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)."
See the rest of the above report and the
graphic snippet of Steere’s research
fraud here:
http://www.actionlyme.org/PLUMSTUPID.htm
The intended monopoly is described in
the Corixa’s advertisements and in the
Corixa-Yale RICO patent:
Posted to the Lyme Newsgroup in 1999:
“Imugen, a lab in Norwood, MA, is in a
partnership with CORIXA another growing
biotech company...Here's why:
http://www.corixa.com/parpro/partnered.asp
”Target Product: Reference
diagnostic for detection of
certain tick-borne diseases
”Status: Development
”Partner: IMUGEN, Inc.
[Corixa and others are looking for
markers of infection; to patent other
commercially viable diagnostic test kit
antibodies/ biomolecules- KMDickson]
”From a Corixa press release,
April 7, 1998:
"...The agreement provides Imugen with
an exclusive license, including the
right to sub-license these recombinant
antigens for reference laboratory
testing in the US and Canada in exchange
for a share of revenues from any
diagnostics kits or blood screening
tests that are developed as a result of
this collaboration..."
https://groups.google.com/forum/?hl=en&fromgroups=#!topic/sci.med.diseases.lyme/cy9beTF_Uqs
Corixa's RICO Patent Claims:
http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6045804.PN.&OS=PN/6045804&RS=PN/6045804
Note the date on the patent: May, 1996.
"Additional uncertainty may arise if the
vaccines are not completely protective;
vaccinated patients with multisystem c
omplaints characteristic of later
presentations of Lyme disease may be
difficult to distinguish from patients
with vaccine failure..."
"The present invention provides a method
useful to detect a B. burgdorferi
infection in a subject. The method
provided by the invention is
particularly useful to discriminate B.
burgdorferi infection from OspA
vaccination, although it is sufficiently
sensitive and specific to use in any
general Lyme disease screening or
diagnostic application. Thus, the method
of the invention is particularly
appropriate for large scale screening or
diagnostic applications where only part
of the subject population has been
vaccinated or where the vaccination
status of the population is unknown. "
Or maybe they mean, “appropriate for a
monopoly on vaccines and testing.”
The entire Dearborn/Fake-Vaccine stunt
was
about a monopoly on vector borne
diseases grants, patents, and commercial
products like test kits and vaccines.
But Lyme is Relapsing Fever, antigenic
variation is the nature of the relapse,
and so none of this, scientifically,
could ever happen unless we are talking
about the genus/species determinant,
flagellin, for testing.
The entire crime is about the falsified
Dearborn testing. This is the
reason the IDSA cronies keep insisting
on Klempner’s bogus “long term
retreatment” trial wherein 2/3 of his
victims never had had intravenous meds
before, and which was dependent upon the
false belief that the Dearborn standard
was real. The “IDSA Guidelines”
reinforce the notion that Dearborn was
real and the notion that the Lyme crooks
all still believe it is real. We
know this is not true. Wormser was
there. Even he admitted that the
Steere proposal was way off base, too.
JJ Halperin knows the Dearborn standard
does not detect his ALS cases of Lyme.
You can look at the Western Blots in
that,
Halperin’s report:
http://www.actionlyme.org/ALSLYME47.htm
You can look at the above Western Blots
and see that these sick patients would
not test positive to the criminal
“two-tiered” criteria. This is a
murder charge and explains JJ Halperin’s
hysterical behavior – trying to get some
neurology group to come up with similar
“guidelines” - when Senator Richard
Blumenthal subpoenaed all the crooks
records in the Antitrust lawsuit against
IDSA:
http://www.actionlyme.org/080430_RICO_CABAL_CAVES.htm
Said Blumenthal in that decision:
”The IDSA portrayed another medical
association's Lyme disease guidelines as
corroborating its own when it knew that
the two panels shared several authors,
including the chairmen of both groups,
and were working on guidelines at the
same time. In allowing its panelists to
serve on both groups at the same time,
IDSA violated its own conflicts of
interest policy.”
This crazy hysterical BS that has been going in since 1990 when the American Lyme Disease Foundation (ALDF.com) was founded by the DNA patenteers and Kaiser-Permanente at New York Medical College, is all about Gary Wormser, Robert Schoen, Allen Steere, Barbara Johnson, Alan Barbour, Eugene Shapiro, Lenny Sigal, Henry Feder, JJ Halperin, J Nowakowski, Peter Krause, Mark Klempner, Edward McSweegan, Phil Baker, Durland Fish, et al, not going to jail for negligent homicide over the Dearborn stunt. And here, these patents owned by CDC officer Barbara Johnson, make clear the reason Steere went to Europe to leave out the non-HLA linked cases. You can’t sell a vaccine for a disease that is known to make no antibodies. So, they said “only people with certain HLAs are allowed to have a ‘disease.’”
SECTION 10: CHRONIC FATIGUE SYNDROME AS
REAL AND TREATABLE with
anti-EBV/herpes drugs (mabs),
anti-virals
Wall Street Journal, 2011:
Unlocking Chronic Fatigue Syndrome
http://online.wsj.com/article/SB10001424052748703858404576214443015558976.html
- "Other scientists are trying to
understand why other infections, such as
mononucleosis, appear to prompt chronic
fatigue
syndrome in some patients. And in a
program at New York's Columbia
University, researchers are seeking to
identify pathogens that may appear
prominently in patients with the
disorder. Researchers will be testing
"for all those agents that we know
affect vertebrates on this globe," says
Mady Hornig, who heads the Columbia
program….
- ”Dr. Montoya's team enrolled 30
patients with elevated levels of
antibodies against Epstein-Barr virus
and HHV-6, a herpes
virus, in a trial and treated them
with valganciclovir, an anti-viral
medicine. Dr. Montoya says patients on
the drug showed
improvement in cognition and fatigue.”
Norway, et al:
“Clinical impact of B-cell depletion
with the anti-CD20
antibody rituximab in chronic fatigue
syndrome: a preliminary case series.”
http://www.ncbi.nlm.nih.gov/pubmed/19566965
But why do these and the
Brian Fallon/Columbia U. Chronic Lyme
patients who received 14 weeks of
antibiotics relapse?
No drug for TLR2 tolerance. The
mycoplasma come back. The fatigue
comes back.
No drug for TLR2 tolerance. The
mycoplasma come back. And
Duray’s bad B-cells? What to do about
them? The spirochetes are un-eradicable
but the ILLNESS - the fatigue - comes
back.
SECTION 11: Epstein-Barr’s Famous and
well-known Chronic-, Autoimmune Disease-
and Cancer- Associations
A friend advises me that it is not
common knowledge that EBV causes cancer,
MS, Lupus, arthritis, et al. That means
I will briefly deploy the following
science-artillery upon your little pin
head and hope you forward it to all the
other journals, against the possibility
that such Alzheimery type “editors” are
also at their helms.
As for the so-called autoimmune
diseases:
http://www.ncbi.nlm.nih.gov/pubmed?term=EBV%20and%20arthritis
PubMed is loaded with data.
As for the Cancer outcomes of EBV:
http://www.ncbi.nlm.nih.gov/pubmed?term=cancer%20and%20herpes
Over 9000 articles.
As for Joe Tully of “Tully and Shope,
Rockefeller Institute and Yale
Bioweaponeers at Large” from the last
century?
Tully Volume 3, Number 1—March 1997
Synopsis
Mycoplasmas: Sophisticated, Reemerging,
and Burdened by Their Notoriety
http://www.cdc.gov/ncidod/eid/vol3no1/baseman.htmMycoplasmal
Diseases and Cancer
“Malignant Transformation
“As early as the mid-1960s,
mycoplasma-infected cell lines were
associated with chromosomal aberrations,
altered morphologies, and cell
transformation (77,78). These abnormal
oncogenic cell traits continued even
after the apparent elimination of
mycoplasmas, and evidence implied
increased tumorigenicity of these
transformed cells in animals. This issue
has been revisited in studies
demonstrating that longterm, persistent
mycoplasmal infection of mouse embryo
cells initiated a multistage cellular
process that resulted in irreversible
cell transformation, karyotypic
alterations, and tumorigenicity in nude
mice (6). Do these oncogenic events
associated with mycoplasma-mammalian
cell coincubation relate to the ontogeny
of human cancers?”
Tully’s reference, 18:
Murphy WH, Gullis C, Dabich L, Heyn R,
Zarafonetis CJD. Isolation of Mycoplasma
from leukemic and nonleukemia patients.
J Natl Cancer Inst.
1970;45:243–51.PubMed
Why would Joe Tully say such a thing in
the CDC’s own publication, no less?
Why would the National Cancer
Institute’s, the US Army’s and Fort
Detrick’s own Paul Duray publish such a
thing as “these look like Epstein-Barr
transformed cells” in IDSA’s own
journal.
Imagine the boldness.
Joe Tully, the bioweaponeer and
mycoplasma and tick, on MedLine:
http://www.ncbi.nlm.nih.gov/pubmed?term=tully%20jg[Author]%20AND%20%28%22mycoplasma%22[MeSH%20Terms]%20OR%20%22mycoplasma%22[All%20Fields]%29%20AND%20%28%22ticks%22[MeSH%20Terms]%20OR%20%22ticks%22[All%20Fields]%20OR%20%22tick%22[All%20Fields]%29&cmd=DetailsSe
Says Harold Varmus (have you ever heard
of Varmus, Mr. Alpert?)
“Unseen Enemies
“At a session in Orlando on the future
of cancer research, Dr. Harold Varmus,
the director of the National Cancer
Institute, described the Provocative
Questions initiative, a new effort to
seek out mysteries and paradoxes that
may be vulnerable to solution.
“In our rush to do the things that are
really obvious to do, we’re forgetting
to pay attention to many unexplained
phenomena,” he said. “Why, for example,
does the Epstein-Barr virus cause
different cancers in different
populations? Why do patients with
certain neurological diseases like
Parkinson’s, Huntington’s, Alzheimer’s
and Fragile X seem to be at a lower risk
for most cancers? Why are some tissues
more prone than others to developing
tumors? Why do some mutations evoke
cancerous effects in one type of cell
but not in others?
“With so many phenomena in search of a
biological explanation, “Hallmarks of
Cancer: The Next Generation” may
conceivably be followed by a second
sequel — with twists as unexpected as
those in the old “Star Trek” shows. The
enemy inside us is every bit as
formidable as imagined invaders from
beyond. Learning to outwit it is leading
science deep into the universe of the
living cell.”
http://www.nytimes.com/2011/08/16/health/16cancer.html?pagewanted=all
- - - - - - -
And last, but not least, let us consider
the possibility referred to by Paul
Duray, 1992 – (mouse gammaherpesviruses
and/or mouse
cytomegalovirus in ticks):
"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."
More:
”Molecular detection of murine
herpesvirus 68 in ticks feeding on
free-living reptiles.
http://www.ncbi.nlm.nih.gov/pubmed/21732020
“Block of death-receptor apoptosis
protects mouse cytomegalovirus from
macrophages and is a determinant of
virulence in
immunodeficient hosts.”
http://www.ncbi.nlm.nih.gov/pubmed/23271968
There is always the possibility that
this criminal IDSA gang is doing to the
tick borne viruses what they’re doing
with “Lyme disease” – falsely claiming
each new Borrelia is distinct, narrowing
disease definitions, limiting our
knowledge of what is in ticks to what
they have already patented (such as
Barbour’s 1996 patent for cow Relapsing
Fever, now known as Masters’ Disease –
but again, no one has it ??), and not
allowing anyone to have a disease until
the commercial product is ready. And I
am not talking about the known
co-infections, which have been discussed
openly at NIH “Rare Diseases” hearings
since the mid-1990, but nothing has been
done about them, of course.
Thirty-eight years and we’re still
wondering what the hell happens after a
tick attachment. Twenty-three years
since the ALDF was founded by
Kaiser-Permanente and the greedy DNA
patent mongers… and we know nothing
about chronic “Lyme disease” except for
IDSA’s statement, “There is no disease
for which there were two vaccine
trials.”
And now, today, Jan 2013, we are
subjected to you, Mr. Alpert, and your
corrected video announcements. Yikes.
Spare us, please, in the future, from
having to publicly point out that you
need to retire due to something like
Alzheimer’s. That is, if your
actions are not just plain criminal.
Kathleen M. Dickson
PS: I probably left some important junk
out, but ultimately, the Dearborn
booklet is scanned into my website, so
the whole world can see how we got this
ludicrous testing standard despite the
non-recommendation of the labs invited
to “participate" in the Dearborn
proceedings, all the way back in 1994.
It wasn’t really a consensus conference,
so even excluding its technical
non-merits, it needs to be investigated,
which was what I told the USDOJ when I
filed the RICO complaint in 2003.
http://www.actionlyme.org/DEARBORNINVITATION.pdf
http://www.actionlyme.org/DEARBORN_PDF.pdf
http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm
http://www.actionlyme.org/EVIDENCE_STEERESCHOEN_KNEW.htm
