Helpin Anthony Fauci unnastan whut HIV gp120 is.
Mort Zuckerman
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Subject: Helpin Anthony Fauci unnastan whut HIV gp120 is.
Date: Oct 5, 2009 8:44 AM
Dear Ton'
Here's what we think the gp120
Tri-ad looks like:
http://www.actionlyme.org/Pam3Cys_Version15.htm
Recall that the Fauc, head of NIAID
has no clue how science is done, which
is why he did not know LYMErix was
made of the same antigen as the
HIV vaccines:
16) Anthony Fauci
http://content.nejm.org/cgi/content/full/359/9/888
"Determining the structure of the trimeric form of the envelope
protein is currently a research priority and is expected to yield
additional insights."
http://www.actionlyme.org/Pam3Cys_Version15.htm
If youz come up wid anudder structure,
we would like to see it :)))
Kathleen M. Dickson
http://www.actionlyme.org
REFERENCES FOR "The Greatest Imitator" or OspA or Pam3Cys-induced
immunosuppression PPpresentation,
now auto-run and narrated by Dottie Heffron: http://www.LymeCryme.com,
Pam3Cys (OspA) -induced immune suppression) LymeCryme.com
http://www.actionlyme.org/PresPam14.htm ◄View the latest version
online
http://www.actionlyme.org/PPT_PAM_1/PresPam16.ppt ◄ Download
PAM3CYS_IMMUNE_SUPPRESSION.htm First published in March 2008, as part
of the online book, CRYME_DISEASE.htm
Brought to you by ~ Concerned Citizens
Overview of this OspA/Pam3Cys presentation
Because structure is function we have attempted to share what is known
about Pam3Cys or OspA:
1) History and structure,
2) Hypothetical structures of gram negative bacterial lipoproteins
3) Published research on immunosuppression from fungal antigens (TLR2
vs TLR4)
4) How and when the Yale/ALDF.com Lyme cabal knew OspA/Pam3Cys wasn’t
a vaccine (was not proven to prevent “Lyme Disease”).
We can find no evidence that anyone really knows what OspA looks like
Recall from the Powerpoint Presentation on Scientific Validity, that
you can’t crystallize a lipid (fat, oil, fatty acid, margarine, motor
oil, hydrogenated-like grease…).
PPT Presentation 2, Scientific Validity
http://www.actionlyme.org/SV_PPT_2.htm
So, since Pam3Cys or OspA or tripalmitoyl cysteine or mycoplasmal and
spirochetal lipoproteins are LIPOproteins, it’s almost impossible to
see the real structure, especially of the free antigens (and not their
membrane-bound arrangement of atoms).
John Dunn at Brookhaven Department of Energy Report [SUBROUTINE
JD@BHDOE, slide 1]
http://www.actionlyme.org/JohnDunn_Brookhaven.htm
Untangling the Structure of Lyme Disease
http://www.eurekalert.org/pub_releases/2001-02/BNL-Bsdk-2702101.php
by Michaela Mann, ENERGY SCIENCE NEWS
“The Department of Energy's National Synchrotron Light Source at
Brookhaven National Laboratory helped researchers discover new
information about the bacterium that causes Lyme disease. Their work
may lead to an effective vaccine and new treatment protocols.
“Ixodes scapularis (deer ticks) are the most common vector for
Lyme disease. Larval and nymphal ticks are no bigger than the eye of a
common sewing needle. Adult ticks are about the size of a small apple
seed.
John Dunn at Brookhaven Department of Energy Report [SUBROUTINE
JD@BHDOE, slide 2]
"It's the perfect stealth bacteria," says one frustrated
physician. He's talking about Borrelia burgdorferi, the bacterium that
causes Lyme disease. This illness, which is often mistaken for
diseases ranging from multiple sclerosis to Lupus, can inflict
excruciating headaches and muscle pain, affect the brain and nervous
system, attack major organs, and inflame joints. Although there have
been more than 100,000 reports of the tick-borne Lyme disease in the
U.S. since 1982, researchers are still struggling to create vaccines
and treatments that are effective against B. burgdorferi.
John Dunn at Brookhaven Department of Energy Report [SUBROUTINE
JD@BHDOE, slide 3]
“New findings may explain vaccine failure, suggest treatment
approaches Investigators are particularly pleased with two recent
discoveries made using the Department of Energy's National Synchronous
Light Source (NSLS) at Brookhaven National Laboratory. The uniquely
refined images they were able to create demonstrated the bacterium
changes its outer surface protein according to its host, and that
different strains of the bacterium have different electrical charges,
which may determine their ability to cause disease.”
John Dunn at Brookhaven Department of Energy Report [SUBROUTINE
JD@BHDOE, slide 4]
“Understanding the structure is the key The new understanding of
the structure was made possible by the protein fixation and imaging
techniques at NSLS. The NSLS permits researchers to focus and control
light beams such that images can be seen at resolutions as fine as 2 A-
near atomic resolution.
“It is no easy matter to concoct fragile organic matter, such as
protein chains, into crystals that can withstand the powerful
radiation bombardment of the NSLS and yet retain their original
structure.
John Dunn at Brookhaven Department of Energy Report [SUBROUTINE
JD@BHDOE, slide 5]
“To do this, the Brookhaven team drew upon available nuclear
magnetic resonance (NMR) information to identify the least stable
areas of the OspC protein—the C and N termini. They truncated the
protein to remove these termini and improve their chances of
crystallizing portions of the protein into a stable, viewable form.
They then expressed and purified the protein to ensure homogeneity,
and grew them as crystals.”
Silly
The truth is that this is nothing new, and that there was never a “key
to vaccine failure” until we learned about immune suppression due to
synthetic Pam3Cys or the OspA vaccines. Relapsing Fever was always
known to be Relapsing Fever, that the protein ends of the lipoproteins
underwent “antigenic variation” or “antibody selection pressure,” that
the nature of relapses is that antibodies, and vaccines do no good due
to the antigenic variation.
But ANYWAY… There was Brookhaven unable to re-crystallize OspA in
order to shoot it with X-Rays because you can’t freeze lipids. They
don’t have the real structure.
X-Ray Diffraction and Generating an Image
Structure of Tripalmitoyl Cysteine (Bulletin of Korean Chem Society,
1996, Vol. 17, No. 11)
Characterization of Extremely Hydrophobic Immunostimulatory Lipoidal
Peptides by Matrix Assisted Laser Desorption Ionization Mass
Spectrometry
http://newjournal.kcsnet.or.kr/main/j_search/j_download.htm?code=B961118
Jung-Suk Jang, Sung-Taek Lee, Yoon-Seok Chang*
Abstract | Full Text: HTML, PDF
Tri - Palmitic - Acid
The curious case of HIV antibodies against Pam3Cys PMID 2464607
1988 Distinction between HIV-1 and HIV-2 infection using novel
synthetic lipopeptide conjugates as antigens in enzyme immunoassays.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=2464607[uid]
“A novel immunoassay technique using synthetic lipopeptide (Pam3Cys-
Ser) linked to immunodominant peptide domains of HIV-1 and HIV-2
envelope proteins as an antigen adsorbent has been developed.
Attachment of peptides to microtiter plates can be considerably
improved with this method by employing the hydrophobic properties of
lipopeptide. From the sera of 121 HIV-1 infected patients 117 reacted
with Pam3Cys-Ser-[HIV-1(598-609)cyclic disulfide]. Five of 5 HIV-2
positive sera were positive with Pam3Cys-Ser-[HIV-2(593-603)cyclic
disulfide]. Control sera failed to react with these conjugates.”
Pam3Cys structure, again, on a hypothetical HIV vaccine, Defoort, et
al, PubMed #1478779, 1992… ????
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=1478779[uid]
Slide 16-- Pam3Cys - structure first found on the web in a Korean
Chemistry Journal (We have since found it elsewhere).
The Korean Chemists say…
http://newjournal.kcsnet.or.kr/main/j_search/j_download.htm?code=B961118
Analog of E. coli "lipid A" PubMed # 3281910
E. coli Lipid A
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=3281910[uid]
Wiesmüller, 1983, synthesizing Pam3Cys, PubMed ID 6347861
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=6347861[uid]
Slide 21 -- Through the years, we were trying to find background data
on this structure (function). This report is from Schröder and
Schumann, 2004… PubMed ID# 15294986
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294986[uid]
http://www.jimmunol.org/cgi/content/full/173/4/2683
What do these membrane components do? Stealing a graphic from Duke
(Raetz) on E. coli membrane structure
http://www.biochem.duke.edu/faculty/christian-raetz/research-interests
Zooming in on the E. coli membrane (Duke)
The Best Scientist Sources - 1
It’s only been in the past few years since ActionLyme summarized the
immune suppression data available on Pam3Cys and on how the
Tuberculosis vaccines, as well as the Lyme vaccines failed. Since
mid-2003 to the fall of 2005, when lipoprotein vaccines and Pam3Cys
related immune suppression was revealed by ActionLyme, there has been
more interest in this phenomenon. Therefore there is more data now, in
2009.
Best Science/Scientist Sources - 2
The best sources (recommended by ActionLyme) are Justin Radolf, Janis
Weis, Schröder and Schumann, Wiesmüller and his group in Germany, and
now Duke Biochemistry Department. (There are also jobs out there for
Lipid Biochemists, we noticed.)
This is a hot field now, because everyone sort of found out that Yale
LIED about their LYMErix vaccine outcome. OspA did not prevent Lyme.
It caused Chronic Pam3Cys or OspA-Immune-Suppression Syndrome, and the
New Great Imitators.
Slide 26, Continuing from Slide – 21; Lipopolysaccharide Binding
Protein Binds to Triacylated and Diacylated Lipopeptides and Mediates
the Immune Responses, 2004 Schröder, 15294986[uid]…
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294986[uid]
http://www.jimmunol.org/cgi/content/full/173/4/2683
“Lipoproteins and lipopeptides have been identified in a large number
of microorganisms, the most prominent ones being mycobacteria,
mycoplasms, and spirochetes. They have been found to exhibit both a
strong innate inflammatory response in the host and an enduring
adaptive immune response in mammalian hosts (16). The strong
proinflammatory capacities of lipoproteins were first described for
outer surface proteins A and B of Borrelia burgdorferi, which are also
highly…”
Continuing background 15294986[PMID]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294986[uid]
http://www.jimmunol.org/cgi/content/full/173/4/2683
“…immunogenic (17) and have lately been the basis for a Lyme disease
vaccine development (18). These compounds exhibit an triacylated lipid
anchor structure comprising an N-palmitoyl-S-[2,3-bis(palmitoyloxy)-
(2RS)-propyl]-(R)-cysteinyl (Pam3Cys) moiety at the N terminus (19), a
feature that was previously described for the Braun lipoprotein from
Escherichia coli (20). Because the N-terminal Pam3Cys modification is
essential for immunoactivation caused by lipoproteins of B.
burgdorferi as well as of another spirochete, Treponema pallidum (21),
…”
Continuing background 15294986[PMID] on what this compound is…
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294986[uid]
http://www.jimmunol.org/cgi/content/full/173/4/2683
“…subsequent studies investigating immune responses to spirochetes
used synthetic lipopeptides (22). The Pam3Cys moiety was also reported
to be present in cytokine-inducing lipoproteins of Mycobacterium and
Mycoplasma spp. (23, 24); thus, it can be regarded as a highly
conserved molecular motif among different classes of bacteria. In
Mycoplasma fermentans, the presence of a macrophage stimulating
lipopeptide, termed 2-kDa macrophage-activating lipopeptide (MALP-2),
…”
Once the Actual Scientists realized that the Tuberculosis vaccines
failed because they were lipoproteins…
ActionLyme reported a series of research articles on the failures of
the Tuberculosis lipoprotein vaccines (19kD, 27kD) in 2003. They all
seemed to fail in the exact same way LYMErix appeared to fail, which
was (as reported by KMDickson to the FDA Vaccine Committee in January,
2001), in that it appeared to make the perhaps existing infection(s)
worse.
[UConn’s Justin Radolf and Yale’s Erol Firkig are Actual Scientists;
although they’re the only ones in Connecticut. But they’re not
squawking about these crimes. So we wonder what that mentality is,
where you know stuff is scientific BS but you don’t say anything
publicly. And if we can’t find the DSM entry for that “Does Not Speak
to the Scientific BS” mental illness, we will make it up and submit
it.]
Continuing intro for Schröder, et al, PubMed ID# 15294986
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294986[uid]
http://www.jimmunol.org/cgi/content/full/173/4/2683
“…was observed, being stimulatory active at picomolar concentrations
(25). This compound, in contrast to the predominant lipopeptide
structures present in lipoproteins of E. coli, B. burgdorferi, and
mycobacteria, lacks the N-palmitoyl group, thus containing a
diacylated (Pam2Cys) lipid anchor structure at the N terminus.
Following studies revealed the presence of closely related compounds
in other Mycoplasma spp. (26).”
2004, Schröder, 15294986[uid] continued
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294986[uid]
http://www.jimmunol.org/cgi/content/full/173/4/2683
“The innate immune system is represented by both humoral and cellular
elements (1, 2). Soluble CD14 (sCD14)4 and LPS binding protein (LBP)
are major serum factors with the ability to bind pathogens and
initiate innate immune responses (3, 4). The cellular, so-called
pattern recognition receptors include the recently identified family
of TLRs (2). TLRs are germline-encoded receptors exhibiting homologies
to Toll, which is involved in embryogenesis and host defense against
Gram-positive bacteria and fungi in Drosophila (5, 6). TLR-2 was
originally described to recognize LPS, a major constituent of the
outer membrane of Gram-negative bacteria (7, 8), whereas later studies
identified TLR-4 as the central transmembrane component of the LPS
receptor (9, 10).”
(continued, 15294986[uid])
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294986[uid]
http://www.jimmunol.org/cgi/content/full/173/4/2683
“The reason for this discrepancy was that LPS preparations used
contained contaminating bacterial lipoproteins, which later were
identified to be highly active TLR-2 agonists (11, 12). TLR-2 also has
been shown meanwhile to interact with numerous ligands of mainly
bacterial origin, including peptidoglycan and lipoteichoic acid (LTA)
of Gram-positive bacteria (13, 14) and spirochetal glycolipids (14,
15).”
“Contaminating bacterial lipoproteins”
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294986[uid]
http://www.jimmunol.org/cgi/content/full/173/4/2683
“The reason for this discrepancy was that LPS preparations used
contained contaminating bacterial lipoproteins, which later were
identified to be highly active TLR-2 agonists (11, 12).” --15294986
[uid]
References 11 and 12 refer to the works in 1999 of Radolf and Weis as
regards Borrelia burgdorferi:
Toll-like Receptor 2 Functions as a Pattern Recognition Receptor for
Diverse Bacterial Products*, 1999, Radolf, et al, PMID #10559223
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=10559223[uid]
Cutting Edge: Inflammatory Signaling by Borrelia burgdorferi
Lipoproteins Is Mediated by Toll-Like Receptor 21, 1999, Weis, PubMed
ID #10452971
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=10452971[uid]
The Plot Thickens…
But the “contaminating compounds” were probably from mycoplasma.
We really don’t think everything is contaminated with Borrelia
burgdorferi spheroplasts, just because antibiotic treatment forces
these organisms into the spheroplast form (Barbour, 1982) which are
regenerative (Everybody, including Russell Johnson, Willy Burgdorfer
and all the ALDF/Yale gang who referenced the URI research where “the
spheroplasts regenerated into intact spirochetes within one minute of
addition of whole rabbit blood,” not to mention Allen Steere’s “4/9
lab workers” who apparently inhaled these airborne cyst forms of
spirochetes but “tested positive to the Seronegative Lyme T – cell
assay used by Allen Steere.”).
Steere and The T-cell proliferative assay in the diagnosis of Lyme
disease. PUBMED ID: 1883122
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=1883122[uid]
Allen Steere’s “4/9 lab workers” apparently inhaled these airborne
cyst forms of spirochetes but “tested positive to the Seronegative
Lyme T – cell assay used by Allen Steere.”
Feel free to go ahead and ask Allen Steere what he was talking about
when he reported that: The T-cell proliferative assay in the diagnosis
of Lyme disease.
1982, Alan Barbour on what happens when you treat Relapsing Fever
spirochetes with antibiotics:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=7103461
Recall that in the Scientific Validity Presentation we showed that All
Borreliae are Relapsing Fever Organisms, that they are categorized by
differences in their flagellin.
And that this nonsense about “Lyme Disease” is nonsense.
Slide 37-- 1982, Alan Barbour on what happens when you treat Relapsing
Fever spirochetes with antibiotics: PMID#7103461
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=7103461[uid]
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=7103461
Slide 38 Review
We have seen what this Pam3Cys structure is, and we have seen that, to
our ability to discover, it was first synthesized in 1983.
We have seen that Brookhaven again tried to see what was the actual
structure of OspA (and the other Osps), but they could not do it
without lopping off the lipids.
We have seen that there was some confusion over which toll-like
receptors were responsible for the immune activation due to
contamination, likely with mycoplasma, but that Borrelial antigens are
believed to be handled by TLR2 and that Bb lacks LPS (managed by TLR4
and not 2)
Next we will look at Justin Radolf and Janis Weis and why they think
Bb OspA is Pam3Cys.
We are approaching WHAT could this OspA molecule be?, and HOW does it
act in the immune system? We do not know why we also see it in the HIV
vaccine. Why people with HIV have antibodies to a synthetic Pam3Cys
remains unknown.
Reference 19 from the Schröder report = Justin Radolf, 1990, PMID:
2318538
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=2318538[uid]
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=2318538
Continuing Justin Radolf, 1990, PMID # 2318538
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=2318538[uid]
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=2318538
“The OspA and OspB antigens were radioimmunoprecipitated from [3H]
palmitate-labeled detergent-phase proteins with monoclonal antibodies,
and [3H]palmitate was recovered unaltered from these proteins after
sequential alkaline and acid hydrolyses. The combined results provide
formal confirmation that the major B. burgdorferi immunogens extracted
by Triton X-114 are lipoproteins. The demonstration that B.
burgdorferi integral membrane antigens are lipoproteins may explain…
Continuing Justin Radolf 1990, PMID # 2318538
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=2318538[uid]
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=2318538
“…the basis of their immunogenicity and may help to improve our
understanding of the surface topology of B. burgdorferi. …”
(Structure is Function, or Function is Structure)
Slide 42 -- Radolf, et al, 1990, 2318538
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=2318538[uid]
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=2318538
Justin Radolf in 1990 extracted the lipids and was able to use heavy
hyrogen labeled H(3) palmitate to determine that these lipids came on
and off the spirochete intact, lending his group to believe the
lipoproteins were Pam3Cys- 3 acyl groups.
Weis, 1994 “Native OspA is active a concentrations lower than these
synthetic lipopeptides…unique modifications by the spirochete.” She is
saying that Bb may be taking up the palmitic acid groups intact, but
somehow the spirochete arranges the lipids so that they’re more toxic
when the bug produces them.
Mini-Review
We’re trying to find out what OspA is, since structure = function. In
the late 1990s, we find that OspA is a Pam3Cys (Mario Philipp; PMID#
9864208).
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=9864208[uid]
So, where does Pam3Cys come from? It’s a synthetic analog of E. coli
Lipid A and these scientists think it is also found in mycobacteria
and spirochetes…
By performing experiments to separate the lipids (Radolf, growing
bacteria in radiolabeled palmitate), the scientists think it is
Pam3Cys. Weis is not sure…
So, you may say to yourself, “Self, what could this MoFo be?”
Where is Pam3Cys on the HIV virus?
It’s pretty hard to tell because the patenteers are rather stingy with
their patent graphics. From the Koreans who blew this synthetic HIV
120/41 up as shown previously, they say these Pam3Cys structures are
the envelop glycoproteins, but other references show gp120 and gp41
themselves are Pam3Cys.
If you go to Wikipedia and steal the HIV image like we did…
http://en.wikipedia.org/wiki/HIV_structure_and_genome
Are they sure???
Is this really both OspA and the HIV glycoproteins?
Remember, Lyme has lipoproteins and HIV 120/41 are glycoproteins (but
no glycolipids, like E. coli Lipid A), and all the scientists seem
pretty convinced that this Pam3Cys is what the antigen is…
Thinkin’ ? [SUBROUTINE 2; Steere/RICO, slide 1]
Try to recall if Alan Barbour or Allen Steere or Gary Wormser or
Durland Fish or Larry Zemel or Lenny Sigal… have ever mentioned what
OspA is/does….
Slide 51-- Allen Steere’s Baby [SUBROUTINE 2; Steere/RICO, slide
2]
Originally, OspA was supposedly the thing against which persons
with Lyme Arthritis had an allergic response (too many antibodies). It
is the usual practice to assay for the efficacy of a vaccine by
testing with antigens that are different from the vaccine antigens.
Therefore, Allen Steere went to Germany in 1992 alone with bogus
“high-passage” strains and recombinant OspA-B from US strain B31 (with
no very immunogenic lipids attached) to leave OspA-B out of the
current or Dearborn diagnostic standard. (See the PPT on Scientific
Validity).
http://www.actionlyme.org/STEERE_IN_EUROPE.htm
http://www.actionlyme.org/CRYMEDISEASE_CHP3_B.htm
http://www.actionlyme.org/UCONN_NO_HOSPITAL.htm
http://www.actionlyme.org/CORIXARICO.htm
Who was Allen Steere working with when he went to Europe to leave
OspA-B out of the standard? [SUBROUTINE 2; Steere/RICO, slide 3]
OspA was intended to be the vaccine because people with Lyme
arthritis have high antibodies to OspA, and OspA was the most abundant
surface antigen on these spirochetes fresh out of a tick.
So OspA-B were left out of the diagnostic standard via some Steere
lab-and-strains shenanigans. In this way, whoever develops a test that
leaves OspA-B (they’re encoded on the same plasmid, so they’re hard to
separate.; you have to take the plasmid out) will have a monopoly on
all the national blood testing after LYMErix comes on the market…
This all would have happened if there was no Blot-Smudging problem
because you can’t test for vaccine efficacy with the same antigen as
the vaccine.
http://www.actionlyme.org/DICKSON_FDA_SUBMISSION_FULL.htm
Here are those 4 "we can't read our OspA vaccine results" reports:
1) SCHOEN and PERSING, with JOHN ANDERSON,1996 - the RICO
report:
http://jcm.asm.org/cgi/reprint/35/1/233?view=long&pmid=8968914
2) SCHOEN AND PERSING IN THEIR 1996 RICO METHOD PATENT:
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=6,045,804.PN.&OS=PN/6,045,804&RS=PN/6,045,804
3) PERSING WITH SIGAL EXPLAINING THAT THE WESTERN BLOTS WERE
UNREADABLE, 2000:
http://www.journals.uchicago.edu/doi/pdf/10.1086/313920
4) Yale's ROBERT SCHOEN in the 1998 Munchausen's Book,
instructing MDs to blow off LYMErix systemically injured people ("but
send the post-vaccination blood to the Yale L2 Diagnostics RICO lab if
you must bother to be a physician").
This is a FALSE CLAIM or a QUI TAM or FRAUD on the GOVERNMENT:
http://www.usdoj.gov/usao/eousa/foia_reading_room/usam/title9/crm00921.htm
Let’s take a look at that RICO patent and the researchers at Yale
who “helped.” [SUBROUTINE 2; Steere/RICO, slide 4]
USPTO.gov Patent No. 6,045,804:
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=6,045,804.PN.&OS=PN/6,045,804&RS=PN/6,045,804
Who is Helpin Dave Persing…? (We will look at this again later.)
[SUBROUTINE 2; Steere/RICO, slide 5, PMID 8968914]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=8968914[uid]
In 1995 and 1996 the Yale Lyme criminals knew they had problems
reading Western Blots in LYMErix vaccinated people. This is from the
Schoen/Fikrig/Persing RICO Method report. The point is that they never
told the FDA they could not read their Western Blots in OspA-
vaccinated people, and that they therefore had no way to tell whether
or not OspA vaccination prevented “Lyme Disease” [PubMed ID #:
8968914]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=8968914[uid]
[SUBROUTINE 2; Steere/RICO, slide 6]
Did they report these problems to the FDA when they told the FDA
they had a vaccine in 1998?
[SUBROUTINE 2; Steere/RICO, slide 7]
No.
“We focused on reports of arthritis and facial paralysis because
these have been associated with Lyme disease”
http://www.actionlyme.org/LYMErix_VAERS.pdf
Let’s go back and see if Pam3Cys really is on the Syphilis spirochete,
too.
Lipopolysaccharide Binding Protein Binds to Triacylated and Diacylated
Lipopeptides and Mediates Innate Immune Responses1
2004: Schroder, PMID #15294986
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294986[uid]
http://www.jimmunol.org/cgi/content/full/173/4/2683
Let’s look at those references
“Because the N-terminal Pam3Cys modification is essential for
immunoactivation caused by lipoproteins of B. burgdorferi as well as
of another spirochete, Treponema pallidum (21), subsequent studies
investigating immune responses to spirochetes used synthetic
lipopeptides (22).
The references are 1994 & 1995, Radolf and Weis, again PMID # 7927731
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=7927731[uid]
PMID 7927731, Weis, 1994 Abstract
“Borrelia burgdorferi lipoproteins are 50- to 500-fold more active as
cytokine inducers and B-cell mitogens than Escherichia coli
lipoproteins and synthetic peptides containing the tripalmitoyl-S-
glyceryl-cysteine moiety. To investigate the source of this unique
potency, we compared native OspA from B. burgdorferi with recombinant
lipidated OspA produced in E. coli. As little as 10 ng of either
protein per ml stimulated B-cell proliferation and production of
cytokines and nitric oxide by macrophages. The two proteins induced
comparable antibody responses in mice. Nonlipidated OspA made in E.
coli had no stimulatory activity. Thus, lipid modification is
essential both in vivo and in vitro for the immunological properties
of OspA. The lipid moiety appears equally active whether produced in
B. burgdorferi or in E. coli.”
These researchers keep cross-referencing their own reports
But are we really sure OspA and the HIV gps are really Pam3Cys??
What ways are there to tell, since you can’t recrystallize a lipid? So
these researchers simply do comparative immune response studies. The
best we, the outside observers, can guess is that these scientists
really think these antigens are Pam3Cys.
Now recall that way, way back a hundred years ago in 2004…
This thing, whatever it is, is also found in mycoplasma and
mycobacteria.
Okay, so how do we know THAT for sure?
Aha! The famous Toll-Like-Receptors… PMID: 10426995
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=10426995[uid]
http://www.sciencemag.org/cgi/content/abstract/285/5428/732?siteid=sci&ijkey=9zbxdq3GpVJqs&keytype=ref
Continuing with the text of the previous TLR report…
http://www.sciencemag.org/cgi/content/abstract/285/5428/732?siteid=sci&ijkey=9zbxdq3GpVJqs&keytype=ref
“The 19-kD M. tuberculosis lipoprotein is a member of a family of
prokaryotic lipoproteins. Lipoproteins have been found extensively in
both Gram-positive and Gram-negative bacteria, including Treponema
pallidum, Mycoplasma species, and Borrelia burgdorferi (22-24).
Profound immunoregulatory functions have been attributed to
lipoproteins, including monocyte or macrophage activation (25). The
portion of lipoprotein responsible for its immunologic activity is
located in the NH2-terminal triacylated lipopeptide region. Removal of
Continuing the TLR report
http://www.sciencemag.org/cgi/content/abstract/285/5428/732?siteid=sci&ijkey=9zbxdq3GpVJqs&keytype=ref
“Removal of this lipid element rendered the parent product
nonactivating, and synthetic lipopeptides could activate B cells and
macrophages (23, 24, 26). Studies of the B. burgdorferi OspA
lipoprotein and the 47-kD lipopeptide of T. pallidum demonstrated
lipoprotein induction of IL-12 mRNA (24, 27). We found that OspA and
the NH2-terminal lipopeptide of the T. pallidum 47-kD antigen
activated IL-12 p40 promoter activity by a TLR-dependent mechanism
(Fig. 2C), thereby providing evidence that TLRs serve to recognize a
diverse family of microbial lipoproteins.
Continuing the TLR report…
http://www.sciencemag.org/cgi/content/abstract/285/5428/732?siteid=sci&ijkey=9zbxdq3GpVJqs&keytype=ref
“A monoclonal antibody specific to human TLR-2 (28) blocked the
ability of LPS and the 19-kD lipoprotein to stimulate IL-12 production
from primary human monocytes, indicating the crucial role for TLR-2 in
monocyte activation by these microbial molecules (Fig. 2D). Because
the deacylated OspA (d-OspA) was unable to activate IL-12 production
from THP-1 cells (29), the fatty acyl moiety, which is genetically and
structurally conserved among microbial lipoproteins, appears to be
crucial for monocyte activation through TLRs.
You with that?
“Removal of this lipid element rendered the parent product
nonactivating, and synthetic lipopeptides could activate B cells and
macrophages (23, 24, 26).
Don’t remove the lipids or else you’re not going to get as serious an
antibody response, yet that’s just what Allen Steere did with his
Strains Tricks In Europe to leave OspA and B out of the standard we
now have.
Slide 69 -- Mechanisms and evidence of immune suppression associated
with spirochetal and mycoplasmal antigens … And the New Great
Imitators:
1) Justin Radolf on HLA downregulation [11441098] [slide 70]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=11441098[uid]
2) Ablation of IRAK-associated kinase [15294992]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294992[uid]
3) Inhibition of TNF-alpha induced apoptosis [15286682] (see also
Duray)
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15286682[uid]
4) Inhibition of NF-kappa [12496438]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=12496438[uid]
Alan Barbour on blebbing as autovaccination with Osps [slide 73]
http://www.actionlyme.org/BARBOURS_STEALTH_BOMBERS.htm
Tuberculosis Lipoprotein Vaccine Failures (3) [slide 75-]
Gary Wormser on OspA-induced immunosuppression [10865170] [slide 78]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=10865170[uid]
McSweegan Attacks [slide 79]
http://groups.google.com/groups/search?hl=en&q=submitted+to+FDA+with+supporting+documentation&qt_s=Search+Groups
Paul Duray and EBV-immortalized cells; MS (1989 and 1992) [slide 86]
Joseph G. Tully and mycoplasma in cancer and effect on erythrocytes
(Chronic Fatigue)
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=9126441[uid]
Mycoplasma attaching to RBCs (Chronic Fatigue)
http://iai.asm.org/cgi/content/full/76/1/71/F1
Halperin on Lyme and ALS
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=2334308[uid]
ALS and fungal antigens
Gulf War Illness and ALS (and Sam T. Donta and Mycoplasma and GWI)
The Murdered Iraqi/ Plum Island Mycoplasmal Bioweaponeer
Re-enter the very excellent scientist, Justin Radolf, 2001, PubMed ID
# 11441098 (Radolf is a jerk, but he’s a good scientist.)
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=11441098[uid]
So, Justin Radolf comes along and says…
Oh, yeah. Like the failed tuberculosis
lipoprotein vaccines – that made the
infections worse, just like LYMErix – we
find that these lipoproteins cause the cells
to stop presenting antigen (making
antibodies)… And if Lyme/LYMErix victims
are not making antibodies, they are very
Munchausery, self-poisoners,
“seronegative,” or are “women and girls.”
http://www.actionlyme.org/MUNCHAUSENS.htm
http://www.actionlyme.org/UN_PETITION.htm
No. That’s not what Radolf said. He said:
“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.
And he says…
This mechanism may allow intracellular MTB to evade immune
surveillance and maintain chronic infection.
So, Justin Radolf says, essentially: Vaccination with OspA will render
you unable to make antibodies against Lyme and mycoplasma and
mycobacteria.
So stop poisoning yourselves with OspA vaccination.
One more thing you need to know about Techniques of Self-Poisoning (by
Alan Barbour)
http://www.actionlyme.org/BARBOURS_STEALTH_BOMBERS.htm
“Many researchers believe that the secret to B. burgdorferi's
infectivity and inflammatory capacity lies in the interaction of its
surface proteins with the host's immunological system 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…
Continued (Alan Barbour on Spirochetal blebbing, The Scientist 1996, 10
(14):13 ):
http://www.actionlyme.org/BARBOURS_STEALTH_BOMBERS.htm
…. "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. “
This of course is the auto-vaccination with the immune suppressing
OspA-like antigens, which render you seronegative after a time.
It’s stealth bombery and Munchausery and the vaccine.
You too can be a shienticks!
Tuberculosis Lipoprotein Vaccines Failures
10792376, 2000 Blackwell Science Ltd The 19-kD antigen and protective
immunity in a murine model of tuberculosis:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=10792376[uid]
“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. “
PubMed ID 11179309
Infect Immun. 2001 Mar;69(3):1433-9.
Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits
Mycobacterium smegmatis-induced cytokine production by human
macrophages in vitro.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=11179309[uid]
“Thus, the immunosuppressive effect is dependent on glycosylated and
acylated 19-kDa lipoprotein 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.”
Slide 78 PubMed ID # 12761093
Infect Immun. 2003 Jun;71(6):3146-54. The Mycobacterium tuberculosis
Recombinant 27-Kilodalton Lipoprotein Induces a Strong Th1-Type Immune
Response Deleterious to Protection
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=12761093[uid]
“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. We are currently studying
how the 27-kDa antigen modulates the mouse immune response.”
Gary Wormser reporting that OspA suppresses the immune response in
2000 PMID# 10865170:
Modulation of lymphocyte proliferative responses by a canine Lyme
disease vaccine of recombinant outer surface protein A (OspA).
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=10865170[uid]
“After exposure to either the unaltered vaccine preparation or OspA
prepared in saline, normal lymphocyte responses to the mitogens
concanavalin A, phytohemagglutinin-M or pokeweed mitogen, or the
antigen BCG were consistently reduced. Whole cell extracts of B.
burgdorferi also modulated immune responses but required a much
greater quantity of protein than needed for the OspA preparation. The
magnitude of modulation was directly dependent on the quantity of
OspA. OspA interferes with the response of lymphocytes to
proliferative stimuli including a blocking of cell cycle phase
progression. Future studies designed to delete the particular region
or component of the OspA molecule responsible for this effect may lead
to improved vaccine preparations.
Now don’t forget, Lyme victims came under vicious attacks by the
McSweegan gang online at that time
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
On the newsgroup and elsewhere, anyone who said anything about Lyme or
the vaccines was stalked and harassed by the likes of Durland Fish and
Edward McSweegan. This can be verified in the stalking and harassment
lawsuits in addition to the fact that McSweegan was present at the
January 31, 2001 FDA Vaccine Meeting on LYMErix, and a few days later
claimed the presentation demonstrating the EXACT PROBLEM with Lyme and
LYMErix demonstrated that we Lyme scientists were crazy.
Anonymous internet harassment is now a federal crime.
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
MCSWEEGAN: “I think the only thing it accomplished was to remind the
audience that 1) easy access to scientific and medical information is
no substitute for real knowledge and 2) ‘some of these people are
nuts.’"
http://www.actionlyme.org/GOLDWATER_LETTER.htm
Says Kathleen Dickson to the Jan 31, 2001 FDA Vaccine Committee: “THE
PROBLEM IS THE DEARBORN/DRESSLER IgG STANDARD”
Kathleen Dickson also said to the FDA Vaccine Committee (LYMErix):
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
Slide 84 -- The main issue for these Lyme criminals is that they knew
they had no way to test whether they actually had vaccines or not.
They all said they could not read their Western Blots in LYMErix or
ImmuLyme (CDC officer Alan Barbour’s OspA patent) or OspA, and at
Dearborn, no one agreed with Allen Steere regarding his “5 of 10
bands” Dressler/Steere proposal (so it wasn’t even a “consensus”
conference). Steere’s Dearborn criteria was only accurate to the tune
of 15-20% or missed 85-80% of the cases, per the Dearborn submissions.
OspA Adverse Events cases, these simply blew off, lied about it to the
FDA, lied about it in the journals, and to the public.
WHY did they lie and why do they lie, still?
They’re scared to death of criminal charges because these are murder
charges.
And that’s the reason for all the stalking and harassment by the likes
of NIH’s Edward McSweegan and Yale’s Durland Fish.
NIH’s Edward McSweegan said we were “nuts” to be saying OspA wasn’t a
vaccine after Gary Wormser reported that OspA could not be a vaccine.
“Actually, it wasn't great. It was a rambling, buzzsaw critique of
the Dressler serodiagnostic criteria, with washed out, illegible black-
and-white overheads.
“Worse, it had nothing to do with the topic of meeting which was a
"Lyme Disease Vaccine Safety Update." I think the only thing it
accomplished was to remind the audience that 1) easy access to
scientific and medical information is no substitute for real knowledge
and 2) "some of these people are nuts."
But a person could always be an analytical methods development chemist
and do this kind VALIDATION OF ANALYTICAL METHODS of work for a
living, say, at Pfizer.
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
Not only is it very well-known that McSweegan does “no work” for a
living, he would not know the first thing about analytical methods
validations, not being a chemist.
While he was at the FDA (LYMErix Vaccine Meeting in Jan, 2001) he
could have asked the FDA about how it was done.
No-Work McSweegan
What else does Pam3Cys OspA do?
Okay, we know that Pam3Cys is managed by TLR2, and according to some
people, also TLR1 or TLR6. This research continues to be refined.
And we know it results in the downregulation of HLA or inhibits
antibody production. Radolf, PMID# 11441098
But how, exactly, does this lipid screw up the normal process of
antigen presentation through the HLAs? What other research is out
there about what OspA/Pam3Cys does to the immune system?
Enormously important research was un-discovered as a result of Yale’s
and Allen Steere’s OspA scam…
….We were studying all the known mechanisms of illness associated with
this disease because we real Lyme victims know we’re not fooling
around. And we were hearing from LYMErix victims that they had a
disease like Lyme (since they “had had Lyme before”). And we were
studying about other effects of lipoproteins and errant lipoproteins,
and the macrophage activity and the toxicities associated with the
free-radical degradation products (conveniently not mentioned by the
Lyme crooks as regards OspA vaccination),… and it being recognized
that mycobacteria and mycoplasma have the same type of antigens as
Borrelia… and we stumbled upon mechanisms of inhibition of the auto-
kill kinases by some of these bizarre lipids and VIOLA!
There was Paul Duray.
http://www.actionlyme.org/Duray.htm
In one of those famous epiphanous, serendipidous, singularity moments
where one makes that EUREKA!! connection (which are more likely, “I
forgot where I read it”)…
I forgot what was the clue. I think I was looking at toxic degradation
products of lipids degraded by the superoxides and quinolinic acid and
also the anti-apoptotic qualities of BCL2 promoters, quite honestly…
Of course anyone who thinks a scientist should be a left-brainer,
linear-thinker don’t know what it’s like to be a real scientist, cuz
we’re all VISUAL-SPATIAL. How could it be otherwise?
“These look like Epstein-Barr transformed (immortalized) cells”
Duray, 1992, Cold Spring Harbor Conference, Transcribed:
"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…
“…Does Bb reactivate latent virus infections in tissues?
“…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 means of tissue-based molecular probe
analysis." - Paul Duray, NCI, NIH, Ft. Detrick, at the 1992 Cold
Spring Harbor Lyme Crooks' Conference, published in Steve Schutzer's
Lyme Disease: Molecular and Immunologic Approaches.
Pretty much, LYMErix looked like it somehow reactivated Lyme, since
that’s what the LYMErix victims told us on the phone
And Paul Duray was saying something similar. And there was published
data on OspA inducing Interleukin-10, a cytokine that tends to tame or
reduce the immune response (Mario Philipp)… It’s pretty hard to argue
that OspA was a vaccine, when all the science and all the empirical
evidence and the bogus Dearborn “science” seemed to show that there
was a real problem here, in addition to the bizarre situation of being
stalked and harassed by the likes of Edward McSweegan and Yale’s
Durland Fish.
http://www.actionlyme.org/TICK_BITE_CONSPIRACY.htm
http://www.actionlyme.org/McSweegan.htm
http://www.actionlyme.org/GOLDWATER_LETTER.htm
Tolerance Induced by the Lipopeptide Pam3Cys Is Due to Ablation of
IL-1R-Associated Kinase-11 [PMID# 15294992, 2004]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294992[uid]
“Preculture of the cells with Pam3Cys at 1 µg/ml leads to a reduced
response after subsequent stimulation with Pam3Cys at 10 µg/ml,
indicating that the cells have become tolerant to Pam3Cys. …
“LPS acts via CD14 and the associated TLR4 (19, 20, 21). In the
present study, we have investigated which mechanisms operate in
tolerance induced via TLR2 by the synthetic lipopeptide Pam3Cys. Using
this pathway of monocyte activation, an entirely different mechanism
appears to operate, because mobilization of NF- B-p50p65 heterodimers
is completely blocked. The failure to mobilize classical NF- B-p50p65
is shown to be due to a blockade at the level of IRAK-1 protein in
Pam3Cys-tolerant Mono Mac 6 cells. We also confirm that LPS tolerance
operates via induction of NF- B-p50p50 homodimers and that highly
purified (lipoprotein-free) LPS only partially inhibits IRAK-1 protein
expression in LPS-tolerant cells.
Tolerance Induced by the Lipopeptide Pam3Cys Is Due to Ablation of
IL-1R-Associated Kinase-11 [PMID#15294992, 2004]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294992[uid]
“Hence, in monocytes, different mechanisms of tolerance appear to
coexist. This indicates that it is important for the host to provide
more than one mechanism to ensure down-regulation of TNF and to
prevent the detrimental effects of excessive amounts of
proinflammatory cytokines during bacterial infection.
“It is concluded that in Mono Mac 6 monocytic cells, inhibition of
IRAK-1 expression at the mRNA and protein levels is the main TLR-2-
dependent mechanism responsible for Pam(3)Cys-induced tolerance, but
not for TLR-4-dependent LPS-induced tolerance.”
Review of where Pam3Cys is found (previous slides, slide 28, PMID
15294986, 2004)
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15294986[uid]
http://www.jimmunol.org/cgi/content/full/173/4/2683
“…subsequent studies investigating immune responses to spirochetes
used synthetic lipopeptides (22). The Pam3Cys moiety was also reported
to be present in cytokine-inducing lipoproteins of Mycobacterium and
Mycoplasma spp. (23, 24); thus, it can be regarded as a highly
conserved molecular motif among different classes of bacteria. In
Mycoplasma fermentans, the presence of a macrophage stimulating
lipopeptide, termed 2-kDa macrophage-activating lipopeptide (MALP-2),
…”
Mycoplasma fermentans inhibits tumor necrosis factor alpha-induced
apoptosis.
Mycoplasma fermentans inhibits tumor necrosis factor alpha-induced
apoptosis in the human myelomonocytic U937 cell line. [PMID #
15286682, Nov 2004]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15286682[uid]
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,
2003 PMID # 12496438
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=12496438[uid]
Slide 101 -- So, if spirochetes and the mycos (-plasma and -bacteria)
have the same antigens and we see the same outcomes (low/no
antibodies, tolerance to Pam3Cys, anti-apoptosis and handling by TLR2)
…
It became clear that probably these same type of lipoproteins were
behaving in the same way (which everyone seems to think are like
Pam3Cys or OspA) and if, as was explained to the FDA Vaccine Committee
in January 2001, the outcomes of LYMErix were exactly like “Lyme
Disease” as described by the patients who had had both, “Lyme
Disease” (not the Steere-knee-only kind of Lyme) and LYMErix, then
logically, mechanistically, empirically, and from the lab outcomes, it
appears that Chronic Lyme and LYMErix vaccination produced the same
outcomes, like Epstein-Barr-related Multiple Sclerosis, ALS, possibly
Chronic Fatigue, and cancer.
What was told to the FDA LYMErix Vaccine Committee in January 2001
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
“By what mechanism vaccination of the asymptomatic Bb infected
patients is causing the Lyme like illness, we do not know exactly.
Previous infection could be "priming" the immune system, as Denise
Huber of Tufts has suggested, in "Identification of LFA-1 as a
Candidate Autoantigen in Treatment-Resistent Lyme Arthritis" July 31,
1998, Science, Vol 281, p 703. “or the vaccine is activating a dormant
infection by the immune dysregulation it causes, as demonstrated by
the effect of Bb infection and Osp A alone, on NK cells population, T
cells, neutrophils, and the effects on the various inflammatory
regulating biomoleclues, such as IL-10. …
“We simply don't know all the variables, at present, that effect
systemic illness from immune dysregulation caused by Bb infection, and
especially the effect of a such a a large dose of a known immune
irritant, Osp A upon this system, the asymptomatic Lyme patient.
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
“It is because I have gotten so many calls from patients looking for
help because of their illness, that I am here today.”
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
“As a support group leader in Southeastern CT, I have met ~10 people,
who found my name on the internet, who had adverse events and were
ill, looking for help. After learning more about these patients, I
found that all but one of these cases had previous Lyme, and that one
got the Erythema Migrans rash during the series of vaccination. NOT
ONE SINGLE PERSON DID NOT HAVE OTHER BANDS ON FOLLOW UP WESTERN
BLOT.
“It is because I have gotten so many calls from patients looking for
help because of their illness, that I am here today.
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
We told the FDA that it looked like Chronic Lyme, not Steere’s
Imaginary “Bad Knees” Disease.
And that no one agreed with Allen Steere’s new definition of “Lyme
Disease” at the Dearborn conference among the invited labs.
http://www.actionlyme.org/DEARBORN_WHO_SAID_WHAT.htm
Mycoplasma fermentans infection promotes immortalization of human
peripheral blood mononuclear cells in culture, 2004, PMID #15331449
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=15331449[uid]
Blood, 15 December 2004, Vol. 104, No. 13, pp. 4252-4259.
http://bloodjournal.hematologylibrary.org/cgi/content/full/104/13/4252
“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.
(CANCERS and Multiple Sclerosis)
The Plum Island Murdered Iraqi scientist (do your own research on
this… Al-Aubaidi JM)
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=Al-Aubaidi+JM[Author]
Once Don C. Wiley was bumped off –literally- because he is an
influenza expert, I began to think it might be true about the bumped-
off former Plum Island Iraqi scientist. His name was Al-Aubaidi and he
was studying bovine infertility from mycoplasma.
Joseph G. Tully and Robert E. Shope (Senior and Junior). Feel free to
use PubMed and read all of his/their reports.
His interest was in mycoplasma and how immune dysregulation from
mycoplasma could play a role in cancer and the like. Now this research
is becoming popular again, so you will see a relative increase in
reports on this topic and how Epstein-Barr is involved in cancer and
Multiple Sclerosis.
Go “Tully JG” without the quotes
Tully warns about the lack of interest in Mycoplasma, PMID # 9126441
http://iai.asm.org/cgi/content/full/76/1/71/F1
Mycoplasma adhering to and distorting RBCs. We’re going to guess this
plays a role in Chronic Fatigue since CFIDS people have normal
hemoglobin, but it shore feels like you have must anemia. Dedicated
VO2-Max exercise efforts to beat the fatigue doesn’t really work… So
it’s gotta be caused by something like this (RNC membrane osmotic
potential disrupted and therefore O2 transfer is inhibited),
especially since Chronic FatigueLyme and LYMErixFatigue victims now
are tolerized to OspA/Pam3Cys and can’t beat off these fungal
infections in the blood and elsewhere, and guess what? It has nothing
to do with any antibiotic-tolerance acquired by these disgusting
suckers and their little spirally- and human-snakey-slymy-Yalie-lying-
whorey-mass-murdering partners in cryme.
Slide 110-- Paul Duray in IDSA’s “Reviews,” 1989; [PMID #2814170],
Special Supplement 6 on Lyme and Spirochetal Diseases, an entire data
set that IDSA refused to turn over to the CT Attorney General in
answer to his subpoena for all of IDSA’s previous publications to see
if any were missing from the IDSA “Guidelines.”
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=2814170[uid]
If Pam3Cys suppresses the immune system response by gumming up the
auto-kill caspases and produces tolerance to mycoplasmal antigens (no
antibodies), and Paul Duray saw what looked like Epstein-Barr
immortalized (mutated, incompetent) lymphocytes, then we think Chronic
Lyme with the Chronic Barbour Star Wars Blebbing or autovaccination
with Pam3Cys is probably the cause of the immortalization. And then
cancer (leukemia). And MS. And ALS…
“It’s an hypothesis that needs to be tested,” if we could find some
real scientists to do it. Paul Duray is 70-something and deploys to
Iraq regularly. Or maybe they have scientists in Germany. Germans tend
to be smart because their language is very demanding in logic
production. In the US we have the likes of master debators (Sigal),
restaurant sanitation workers (Fish) and English Literature majors
(Shapiro) and genuine psychiatric perverts (there are no other kind)
trying to tell us what’s a disease.
Okay hooduh ferget?, Oh. JJ Halperin and ALS, and Gulf War Illness and
Mycoplasma, and Sam Donta and GWI
1) Justin Radolf on HLA downregulation [11441098] [slide 68]
2) Ablation of IRAK-associated kinase [15294992]
3) Inhibition of TNF-alpha induced apoptosis [15286682] (see also
Duray)
4) Inhibition of NF-kappa [12496438]
Alan Barbour on blebbing as autovaccination with Osps [slide 73]
Tuberculosis Lipoprotein Vaccine Failures (3) [slide 75]
Gary Wormser on OspA-induced immunosuppression [10865170] [slide 78]
McSweegan Attacks [slide 79]
Paul Duray and EBV-immortalized cells; MS (1989 and 1992) [slide 86]
Joseph G. Tully and mycoplasma in cancer and effect on erythrocytes
(Chronic Fatigue)
Mycoplasma attaching to RBCs (Chronic Fatigue)
Halperin on Lyme and ALS
ALS and fungal antigens
Gulf War Illness and ALS (and Sam T. Donta and Mycoplasma and GWI)
The Murdered Iraqi/ Plum Island Mycoplasmal Bioweaponeer
JJ Halperin - famous promoter of 2 sets of “Guidelines” wherein the
deadliest version of the disease, ALS, is not detected, since Dearborn
is only that imaginary “BAD KNEES DISEASE” that Allen Steere concocted
in Europe, alone, to set up his own little RICO with Dave Persing and
Robert Schoen – talks about how Lyme results in ALS in 47% of the
cases:
PMID: 2334308 Arch Neurol. 1990 May;47(5):586-94.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=2334308[uid]
http://www.actionlyme.org/ALSLYME47.htm
So, I took my widdle pencil and tried to see ifffin there was 5 out of
10 Dearborn bands and which 5 out of 10 bands were there… You can see
that these people do not have a case of Lyme disease, yet 9/19 were
diagnosed with ALS and later determined by this gangster to have been
exposed to Bb and he said he thought the 47% association “was
significant.”
Here are the Blots from the 2003 USDOJ RICO complaint. You can see
that, clearly, “a hypersensitivity response to OspA in a knee” will
not produce Lyme-ALS-type antibody bands and vice versa.
ALS and Mycoplasma…and Gulf War Illness and Sam T. Donta. What’s
the evidence? [SUBROUTINE ALSMYCO - slide 1] PMID 12383408, Garth
Nicholson
[SUBROUTINE ALSMYCO - slide 2]
Nicholson, Continued: “Using PCR ALS patients with a positive test
for any mycoplasmal infection were investigated for the presence of M.
fermentans, M. pneumoniae, M. hominis and M. penetrans in their blood.
All Gulf War veterans with ALS were positive for M. fermentans, except
one that was positive for M. genitalium. In contrast, the 22/28
civilians with detectable mycoplasmal infections had M. fermentans
(13/22, 59%) as well as other Mycoplasama species in their blood, and
two of the civilian ALS patients had multiple mycoplasma species (M.
fermentans plus M. hominis). Of the few control patients that were
positive, only two patients (2/70, 2.8%) were positive for M.
fermentans (P<0.001). The results support the suggestion that
infectious agents may play a role in the pathogenesis and/or
progression of ALS, or alternatively ALS patients are extremely
susceptible to systemic mycoplasmal infections.
NIH Determines Conclusively that those deployed to the land where
we sold Saddam Hussein “fungi” and other microorganisms, like Plum
Island mycoplasma we figger… [SUBROUTINE ALSMYCO - slide 3]
National Institute of Neurological Disorders and Stroke, Bethesda
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=14504315[uid]
RESULTS: Among approximately 2.5 million eligible military
personnel, 107 confirmed cases of ALS were identified for an overall
occurrence of 0.43 per 100,000 persons per year. A significant
elevated risk of ALS occurred among all deployed personnel (RR = 1.92;
95% CL = 1.29, 2.84), deployed active duty military (RR = 2.15, 95% CL
= 1.38, 3.36), deployed Air Force (RR = 2.68, 95% CL = 1.24, 5.78),
and deployed Army (RR = 2.04; 95% CL = 1.10, 3.77) personnel.
Elevated, but nonsignificant, risks were observed for deployed
Reserves and National Guard (RR = 2.50; 95% CL = 0.88, 7.07), deployed
Navy (RR = 1.48, 95% CL = 0.62, 3.57), and deployed Marine Corps (RR =
1.13; 95% CL = 0.27, 4.79) personnel. Overall, the attributable risk
associated with deployment was 18% (95% CL = 4.9%, 29.4%).
CONCLUSIONS: Military personnel who were deployed to the Gulf Region
during the Gulf War period experienced a greater post-war risk of ALS
than those who were not deployed to the Gulf. PMID: 14504315 [PubMed -
indexed for MEDLINE]
Plum Island Mycoplasma [SUBROUTINE ALSMYCO - slide 4] PMID#
6190898
: J Hyg (Lond). 1983 Jun;90(3):441-9.
Immunogenic variation among the so-called LC strains of Mycoplasma
mycoides subspecies mycoides. Smith GR, Oliphant JC.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=6190898[uid]
“Much evidence of immunogenic heterogeneity among the LC strains
of Mycoplasma mycoides ssp. mycoides emerged from cross-immunization
and -hyper-immunization experiments in mice in which three LC strains
(Vom/Plum Island, 74/2488, and Mankefår 2833) were used for challenge
purposes. All heterologous LC-strain vaccines cross-immunized against
the three challenge strains, but protection was usually only
'partial', i.e. significantly less than that given by homologous
vaccine. Cross-hyperimmunization with all heterologous LC but not SC
strains produced protection against challenge with Vom/Plum Island
that was virtually 'complete', i.e. similar to that produced by
homologous vaccine. … blah blah blah
Selling fungi to Saddam Hussein [SUBROUTINE ALSMYCO - slide 5]
Congressional Record: September 20, 2002 (Senate) Page S8987-S8998
http://www.fas.org/irp/congress/2002_cr/s092002.html
“Over the protest of some Pentagon skeptics, the Reagan
administration began allowing the Iraqis to buy a wide variety of
"dual use" equipment and materials from American suppliers. According
to confidential Commerce Department export-control documents obtained
by NEWSWEEK, the shopping list included a computerized database for
Saddam's Interior Ministry (presumably to help keep track of political
opponents); helicopters to transport Iraqi officials; television
cameras for "video surveillance applications"; chemical-analysis
equipment for the Iraq Atomic Energy Commission (IAEC), and, most
unsettling, numerous shipments of "bacteria/fungi/protozoa" to the
IAEC. According to former officials, the bacterial cultures could be
used to make biological weapons, including anthrax. …
And of course at the end of Gulf War I we all saw on CNN the US
soldiers in Iraq blowing up buried arsenal and the earth moved and
there were dust clouds… As if we didn’t see it with our own eyeballs
and couldn’t tell that that wasn’t right at the time…
We saw it on CNN. Just like we heard Henry Kissinger say on 9/11 on
CNN in a phone call from Europe about 11:30 in the morning (Eastern
USA Time) that even the “countries who harbored terrorists” would be
treated like terrorists and that the world “was either with us or
against us.”
It happened. The CNN tapes exist.
Let’s see. What else do we know about OspA and Plum Stupid Island?
Epstein-Barr and Multiple Sclerosis… HOT HOT HOT!
Sam T. Donta and Gulf War Mycoplasmal OspA/Pam3Cys Illness, PMID #
12057884
http://www.actionlyme.org/WE_DONT_KNOW_DISEASE.htm
(▲▲Sam Donta is Helpin IDSA Remembers Whats-IDSAs-We-Dont-Know)
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=12057884[uid]
“Many veterans who were deployed to the Persian Gulf during the
1990-1991 Gulf War developed multiple unexplained symptoms such as
pain, fatigue, and neurocognitive problems. This constellation of
symptoms has been termed Gulf War Veterans' Illnesses (GWVI). Although
there is no proven explanation for the cause of GWVI, one fairly
widespread explanation is systemic Mycoplasma fermentans infection."
Is there a single definite clue that the ALDF and Yale knew there was
a problem with Chronic Lyme-like adverse events from OspA/Pam3Cys
vaccination?
Actually there are at least 3 major clues:
1) Robert Schoen’s chapter in “Lyme Disease” where he reveals that
victims of LYMErix might have the exact same general symptom set as
Chronic Lyme victims claim and that per Schoen these LYMErix victims
are to either be blown off or the blood sent to the RICO labs (Imugen
and L2 Diagnostics)
2) As told to the FDA vaccine Committee in Jan 2001, Dave Persing
reported in his RICO patent that vaccine failure would be
indistinguishable from chronic Lyme
3) Gary Wormser in 2001 reported immunosuppression from OspA
vaccination
Guilty
4) The harassment and stalking of Lyme victims and especially Lyme
scientists, such as Karen Forschner, Janice Beers, Lisa Masterson,
Lida Mattman, Bowen Labs, Igenex, Kathleen Dickson, and several
others.
5) The false claims by the perpetrators of the crimes that THEY were
being stalked and harassed, which is hilarious considering we
explained the entire crime to the FDA Vaccine Committee in Jan 2001
and there were so many public hearings including in front of Senator
Dodd in 1993 where Joe Burrascano described the harassment by the
perps.
When ever before have the victims of a disease been so obviously
persecuted along with their treating specialists???
Slide 127 – 1998, Yale’s Robert Schoen to MDs: “Blow off LYMErix-
injured people with Chronic Lyme-like symptoms, but otherwise send the
blood to us, one of the RICO Method labs”
Says Schoeny-RICO-Baloney:
http://www.amazon.com/Lyme-Disease-Key-Diseases-1/dp/0943126584:
(=MUNCHAUSENS BOOK)
http://www.actionlyme.org/SCHOEN_INSTRUCTING_DOCS_TO_BLOW_OFF_LYMERIX_INJUREES.htm
“In the absence of specific clinical features [according to this RICO
crew, Lyme Disease is only a bad knee with no fatigue and dementia
signs] tell the LYMErix vaccine damaged person they’re nuts.
“Or else send the blood to the RICO Method labs, where we have the No-
OspA-B in the Western Blot mix test, something we knew about in 1995
and possibly even before Steere went to Europe, but never told the FDA
when falsely presenting LYMErix data.
“Thanks and I hope you drop dead and get out of the way (and yer dirty
little cockroach kids too!) ,
RTS
Do you recall from slide 54 Who was Helpin Persing in 1995 when he was
discussin and patentin the RICO method???
The Persing-Schoen-Steere RICO Method Patent US Patent No. 6,045,804
“Ironically, however, the availability of such vaccines may increase
the level of diagnostic uncertainty in the evaluation of patients with
presentation of a nonspecific ***flu-like illness*** after tick bite
or so-called "summer flu," the majority of which may be due to
unrelated causes, to diseases transmitted by ticks such as B. microti,
or to granulocytic Ehrlichia spp. 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
failure.
Let’s take a closer look at that Persing-Yale RICO method patent
claim…
“vaccinated patients with multisystem complaints characteristic of
later presentations of Lyme disease may be difficult to distinguish
from patients with vaccine failure.”
Translation: There are 2 sets of patients:
One set with vaccine damage that looked like chronic late Lyme, and
another set with plain old regular late chronic Lyme.
These are not “vague complaints” but the typical 1) dementia,
confusion, 2) chronic fatigue with sleep disorder, 3) severe headache,
light sensitivity, nerve pain or radiculopathy characteristic of
encephalitis with MS/Guillain-Barre, and 4) diffuse and varying
musculoskeletal pain, especially deep muscle pain and the deep bone
pain characteristic of the flu, all of which are verifiable using the
correct scientifically valid methods to detect the ALDF/Yale
Biomarkers.
Reiterating the Four Signs of Typical Chronic Lyme and/or LYMErix
Disease
These are not “vague complaints” but the typical 1) dementia,
confusion, 2) chronic fatigue with sleep disorder, 3) severe headache,
light sensitivity, nerve pain or radiculopathy characteristic of
encephalitis with MS/Guillain-Barre, and 4) diffuse and varying
musculoskeletal pain, especially deep muscle pain and the deep bone
pain characteristic of the flu, all of which are verifiable using the
correct scientifically valid methods to detect the ALDF/Yale
scientifically valid Biomarkers of Disease.
Says Allen Steere in 1989 (before Kaiser-Permanente established the
ALDF.com at New York Medical College), 22% of Chronic Neurologic Lyme
victims improve with IV treatment, but then relapse. PMID # 2172819
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=2172819[uid]
“At the time of examination, chronic neurologic abnormalities had been
present from 3 months to 14 years, usually with little progression.
Six months after a two-week course of intravenous ceftriaxone (2 g
daily), 17 patients (63 percent) had improvement, 6 (22 percent) had
improvement but then relapsed, and 4 (15 percent) had no change in
their condition. CONCLUSIONS. Months to years after the initial
infection with B. burgdorferi, patients with Lyme disease may have
chronic encephalopathy, polyneuropathy, or less commonly,
leukoencephalitis. These chronic neurologic abnormalities usually
improve with antibiotic therapy.
SLIDE 135 Pointing out that Steere at one time knew there was
something to Lyme besides the knee-disease:
“CONCLUSIONS. Months to years after the initial infection with B.
burgdorferi, patients with Lyme disease may have chronic
encephalopathy, polyneuropathy, or less commonly, leukoencephalitis.
These chronic neurologic abnormalities usually improve with antibiotic
therapy.”
SLIDE 136 They haven’t only harmed tick bitees worldwide…
It should be pretty clear by now that if by the mid-1990s, when these
ALDF/Yale Lyme crooks knew there was a problem with LYMErix causing a
Chronic Lyme-like outcome, and they instead persecuted the victims of
their crimes (while at the same time playing The Victim Card), and
that the outcomes of their crimes negatively affected discovery in
Multiple Sclerosis, ALS, possibly HIV, Gulf War Illness, Cancer
(leukemia), Chronic Fatigue from fungal infections in the blood,
cancer from fungal infections in the blood, immunization of immune-
incompetent children and finding out the hard way that the kids were
immune-incompetent for over 15 years… that it wasn’t just people who
were bitten by stealth ticks who are/were harmed and/or dead from this
crime.
SLIDE 137 The Greatest Imitator
“vaccinated patients with multisystem complaints characteristic of
later presentations of Lyme disease may be difficult to distinguish
from patients with vaccine failure.”
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci