06/16/2013 10:59:50
Cryme Trainer (moved)
Non-HLA-linked Diseases
And Mold-Related illnesses (like
LYMErix-Disease, Lyme, CFIDS/FM, and Gulf War Illness)
=======
References for psychotropics-induced brain damage
Older data on the incurability of Relapsing Fever
1986, McSweegan trashes Navy for $$$ for ALDF.com
1988, Dattwyler & about immune-suppressing, seronegative Lyme
1990, CDC: "Diagnose Lyme as if it was Relapsing Fever."
Allen Steere "NeuroLyme won't test positive," 1990.
1992, CDC officer Allen Steere falsifies testing in Europe
1992, CDC patents with SmithKline show 2 kinds of Lyme
Compare the 2 kinds of Lyme in the RICO complaint
1994, CDC's Dearborn Booklet .pdf
CDC's invitation to participate in Dearborn .pdf
Evidence Lyme criminals knew LYMErix produced the same "multisystem disease" as "Chronic Lyme"
LYMErix Damage Coverup (short)
1998, CIA Oilmen & Israelis plan to overthrow Saddam for the oil.
Bush/Gore Oil/War-(Oct,2000)
Bush's own explainer (Oct
2000) re:
Iraq Oil
Search for "Radolf, 1990" in this page with your browser search feature for the biochemical studies which show what OspA/Pam3Cys is and how Radolf determined that that's what OspA is, a tripalmitic, 3 palmitate groups. It was since blown up by the Koreans with Mass Spec and so most people believe this is the structure of the synthetic HIV gp120/41 (although gp120 seems to be OspA in triplicate) and OspA. It was originally intended to be, behaviorally, an analog of E. coli Lipid A. Real scientists understand that structure is function, and thus, via their FUNCTION - handled by TLR2 - we can speak of these antigens mechanistically, or, "What is the DISEASE(S) it creates?"
The Lyme crooks falsely assert that one can only have a "disease" "if they have inflammation." Please see 101016.htm for an expansion of the abundant evidence that such a statement is a blatant and ridiculous lie.
See the Wayback Machine for the first ActionLyme website, Chapter 4, "Sigal and Shapiro, Lying to the Press":
http://web.archive.org/web/20010429213719/http://www.geocities.com/kmdickson0308/lyme-dilemma.htmlhttp://web.archive.org/web/20030620031132/www.geocities.com/kmdickson0308/1-4.txt
"SHAPIRO: What some people would have you believe is that there are two different diseases.
"SHAPIRO: Somehow, for that form of the disease, antibiotics are effective. They do fine. But then there's some other form of the disease which is, you can't put your hand around it. They don't have objective findings of inflammation, which is the way bacteria cause disease..."
Of course, there ARE two different diseases: the imaginary "Lyme Disease" invented by Allen Steere, alone, in Europe, and then there's this, Pam3Cys-induced immune dysregulation, or the Pam3Cys- or OspA-induced New Great Imitator outcomes:
http://www.actionlyme.org/101016.htm
http://www.actionlyme.org/PLUMSTUPID.htm or the Plum Stupid Accidental Release and the Insurance Companies-induced Hysteria Vaccine. -- 101128,KMD.
PAM3CYS_IMMUNE_SUPPRESSION.htm First published in March 2008, as part of the online book, CRYME_DISEASE.htm
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/PPT_PAM_1/PresPam16.ppt ◄ Download
See also, PIIB, the Plum Island Chapter of Cryme Disease for the work of Justin Radolf, et al re the immunosuppression caused by TLR2-agonists like OspA.
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
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).
THE PRESENTATION WITH HYPERLINKED REFERENCES:
SLIDE 1John 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)
http://newjournal.kcsnet.or.kr/main/j_search/j_archives_sub.htm?qpage=j_search&spage=b_bkcs&dpage=ar&year=1996&vol=17&no=11Characterization 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/pubmed/2464607
“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.”
1992, Pam3Cys structure, again, on a hypothetical HIV vaccine, Defoort, et al, PubMed #1478779, 1992… ????
http://www.ncbi.nlm.nih.gov/pubmed/1478779
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
OspA/Pam3Cys/HIV gp41/120 are analogs 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/pubmed/6347861
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/pubmed/15294986
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/pubmed/15294986
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/pubmed/15294986
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/pubmed/15294986
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/pubmed/15294986
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/pubmed/15294986
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/pubmed/15294986
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/pubmed/15294986
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/F1Halperin 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 timehttp://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
http://groups.google.com/groups/search?hl=en&q=submitted+to+FDA+with+supporting+documentation&qt_s=Search+Groups
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
2004, 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/pubmed/15294992
“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.
2004, 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/pubmed/15294986
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),…”
2004, 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/pubmed/15331449
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.”
