The Greatest Imitator ~ Il più grande Imitatore

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Stanchezza Cronica-Fibromialgia-Guillain-Barré-Sclerosi Multipla-Artrite reumatoide-Morbo di Lou Gehrig (SLA)-Alzheimer-Morbo di Parkinson = Queste sono le malattie non da soli ..... questi sono solo i risultati di una infezione batterica che chiamavano "la malattia di Lyme ".... Dr. Judith Miklossy della Svizzera dissezionato 50 cervelli Alzheimer e trovato Borrelia Burdorferi (agente eziologico in malattia di Lyme) in tutti i 50 cervelli

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By: FreethinkerX (40 month(s) ago)

Presentazione Descrizione: Presentazione Panoramica perché la struttura è la funzione che abbiamo cercato di condividere ciò che si sa su Pam3Cys o OspA: 1) Storia e struttura 2) strutture ipotetiche di gram negativi lipoproteine ​​batteriche 3) la ricerca Pubblicato il immunosoppressione da antigeni fungini (TLR2 TLR4 vs) 4) Come e quando l'Università di Yale e membri ALDF sapeva OspA/Pam3Cys non era un vaccino

Presentation Transcript

Slide 1:

The presentation you are about to view contains the published mechanisms of immune suppression associated with OspA or the LYMErix vaccine.

“The Greatest Imitator”:

“The Greatest Imitator” Brought to you by ~ Concerned Citizens

Presentation Overview:

Presentation Overview 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 Yale University and ALDF members knew OspA/Pam3Cys was not a vaccine

We can not find any evidence that anyone really knows what OspA looks like scientifically:

We can not find any evidence that anyone really knows what OspA looks like scientifically You can not recrystallize a lipid (fat, oil, fatty acid, margarine, motor oil, hydrogenated-like grease…). Pam3Cys or OspA, mycoplasmal and spirochetal lipoproteins are LIPO proteins. It is 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 :

John Dunn at Brookhaven Department of Energy Report Untangling the Structure of Lyme Disease 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 :

John Dunn at Brookhaven Department of Energy Report "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 :

John Dunn at Brookhaven Department of Energy Report “ 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 :

John Dunn at Brookhaven Department of Energy Report “ 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 :

John Dunn at Brookhaven Department of Energy Report “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 .”

Nothing new about it…:

Nothing new about it… 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 . There was Brookhaven unable to re-crystallize OspA in order to shoot it with X-Rays because you can not freeze lipids. They don’t have the real structure.

X-Ray Diffraction and Generating an Image:

X-Ray Diffraction and Generating an Image

Structure of Tripalmitoyl Cysteine (Bulletin of Korean Chem Society, 1996, Vol. 17, No. 11):

Structure of Tripalmitoyl Cysteine (Bulletin of Korean Chem Society, 1996, Vol. 17, No. 11) A synthetic lipopeptide

Tri - Palmitic - Acid:

Tri - Palmitic - Acid

The curious case of HIV antibodies against Pam3Cys [PMID# 2464607] :

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. “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.”

Slide 15:

Pam3Cys structure, again, on a hypothetical HIV vaccine, Defoort, et al, 1992… ????

Slide 16:

Pam3Cys - structure first found on the web in a Korean Chemistry Journal (We have since found it elsewhere).

The Korean Chemists say…:

The Korean Chemists say…

Slide 18:

Analog of E. coli "lipid A" PubMed # 259838 Pam3Cys is synthetic (Manmade; is analogous to)

E. coli Lipid A:

E. coli Lipid A

Wiesmüller, 1983, synthesizing Pam3Cys, PubMed ID 6347861:

Wiesm ü ller, 1983, synthesizing Pam3Cys, PubMed ID 6347861

This report is from Schröder and Schumann 2004 PubMed ID# 15294986:

This report is from Schr ö der and Schumann 2004 PubMed ID# 15294986

What do these membrane components do? :

What do these membrane components do? Graphic courtesy of Duke University (Raetz) on E. coli membrane structure

E. coli membrane:

E. coli membrane (Graphic courtesy of Duke)

ActionLyme.org:

Summarized the immune suppression data that has been available on Pam3Cys. They also have shown how the Tuberculosis vaccines, as well as the Lyme vaccines failed. Since the summer of 2003 to the fall of 2005, when these were revealed there has been more interest in this phenomenon. Therefore there is more data available in 2009. ActionLyme.org

Best Science/Scientist Sources for Pam3cys:

Best Science/Scientist Sources for Pam3cys The best sources are Justin Radolf, Janis Weis, Schr ö der and Schumann, Wiesm ü ller and his group in Germany, and now Duke Biochemistry Department. (There are also jobs out there for Lipid Biochemists, we noted.) This is a hot field now , because everyone sort of found out that Yale fibbed about their LYMErix vaccine outcome. OspA did not prevent Lyme. It caused Chronic Pam3Cys or OspA-Immune-Suppression Syndrome, and the New Great Imitators.

Lipopolysaccharide Binding Protein Binds to Triacylated and Diacylated Lipopeptides and Mediates the Immune Responses, 2004 Schröder… PubMed ID# 15294986:

Lipopolysaccharide Binding Protein Binds to Triacylated and Diacylated Lipopeptides and Mediates the Immune Responses , 2004 Schr öder … PubMed ID# 15294986 “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…”

Slide 27:

The Journal of Immunology , 2004, 173: 2683-2691. Copyright © 2004 by The American Association of Immunologists Lipopolysaccharide Binding Protein Binds to Triacylated and Diacylated Lipopeptides and Mediates Innate Immune Responses 1 PubMed ID# 15294986 Nicolas W. J. Schröder 2 ,*, Holger Heine , Christian Alexander , Maria Manukyan , Jana Eckert*, Lutz Hamann*, Ulf B. Göbel* and Ralf R. Schumann 3 ,* * Institut für Mikrobiologie und Hygiene, Charité University Medical Center, Humboldt University, Berlin, Germany; and Junior Research Group Innate Immunity, and Division of Immunochemistry Research Center Borstel, Leibniz Center for Medicine and Biosciences, Borstel, Germany

Continuing background PubMed ID# 15294986:

Continuing background PubMed ID# 15294986 “…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 ( Pam 3 Cys ) moiety at the N terminus ( 19 ), a feature that was previously described for the Braun lipoprotein from Escherichia coli ( 20 ). Because the N-terminal Pam 3 Cys modification is essential for immunoactivation caused by lipoproteins of B. burgdorferi as well as of another spirochete, Treponema pallidum ( 21 ),…”

Continuing background on what this compound is…:

Continuing background on what this compound is… “…subsequent studies investigating immune responses to spirochetes used synthetic lipopeptides ( 22 ). The Pam 3 Cys 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 ),…”

Slide 30:

Graphic taken from the full-text version The Journal of Immunology , 2004, 173: 2683-2691. Copyright © 2004 by The American Association of Immunologists Lipopolysaccharide Binding Protein Binds to Triacylated and Diacylated Lipopeptides and Mediates Innate Immune Responses 1 PubMed ID# 15294986

Once scientists realized that the Tuberculosis vaccines failed because they were lipoproteins… PubMed ID# 15294986:

Once scientists realized that the Tuberculosis vaccines failed because they were lipoproteins… PubMed ID# 15294986 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), “ it appeared to make the existing infections worse.”

Continuing …. Schröder, et al PubMed ID# 15294986 :

Continuing …. Schr öder, et al PubMed ID# 15294986 “…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 (Pam 2 Cys) lipid anchor structure at the N terminus. Following studies revealed the presence of closely related compounds in other Mycoplasma spp. ( 26 ).”

2004, Schröder, et al PubMed ID# 15294986:

2004, Schr ö der, et al PubMed ID# 15294986 “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) PubMed ID# 15294986:

(continued) PubMed ID# 15294986 “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” PubMed ID# 15294986 :

“Contaminating bacterial lipoproteins” PubMed ID# 15294986 “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 ).” References 11 and 12 refer to the works in 1999 of Radolf and Weis as regards to Borrelia burgdorferi: 11 Toll-like Receptor 2 Functions as a Pattern Recognition Receptor for Diverse Bacterial Products , 1999, Radolf, et al, PMID #10559223 12 Cutting Edge: Inflammatory Signaling by Borrelia burgdorferi Lipoproteins Is Mediated by Toll-Like Receptor 2 1, 1999, Weis, PubMed ID #10452971

Slide 36:

The “contaminating compounds” were probably from mycoplasma. We really do not 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 personnel 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:

Steere and The T-cell proliferative assay in the diagnosis of Lyme disease. PUBMED ID: 1883122 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: PMID#7103461 :

1982, Alan Barbour on what happens when you treat Relapsing Fever spirochetes with antibiotics: PMID#7103461

Review:

Review

Reference 19 from the Schröder report = Justin Radolf, 1990, PMID: 2318538 :

Reference 19 from the Schr ö der report = Justin Radolf, 1990, PMID: 2318538

Continuing Justin Radolf, 1990 PMID # 2318538 :

Continuing Justin Radolf, 1990 PMID # 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 :

Continuing Justin Radolf 1990, PMID # 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

Radolf, et al, 1990, 2318538 :

Radolf, et al, 1990, 2318538 Justin Radolf in 1990 extracted the lipids and was able to use heavy hydrogen 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.

Slide 44:

1994, Janis Weis discovers that… [PubMed # 7927731]

Weis, 1994 “Native OspA is active at 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.:

Weis, 1994 “Native OspA is active at 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:

Mini-Review We’re trying to find out what OspA is, since structure = function . In the late 1990s, we found out that OspA is a Pam3Cys (Mario Philipp; PMID# 9864208). 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…

Where is Pam3Cys on the HIV virus?:

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 envelope glycoproteins, but other references show gp120 and gp41 themselves are Pam3Cys.

Slide 49:

Author MHC_Class_1.svg : User atropos235 on en.wikipedia derivative work: Zionlion77

Are they positive?:

Are they positive? 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…

Think Back:

Think Back Try to recall if Alan Barbour, Allen Steere, Gary Wormser, Durland Fish, Larry Zemel or Lenny Sigal… have ever mentioned what OspA is or does….

Allen Steere:

Allen Steere Originally, OspA was supposedly the thing against which persons with Lyme Arthritis had an allergic response to. (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.

Who was Allen Steere working with when he went to Europe to leave OspA-B out of the standard? :

Who was Allen Steere working with when he went to Europe to leave OspA-B out of the standard? 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 came out 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.

:

USPTO.gov Patent No. 6,045,804 “ The present invention provides a method useful to detect a B. burgdorferi infection in a subject. The method provided by the invention is particularly useful to discriminate B. burgdorferi infection from OspA vaccination, although it is sufficiently sensitive and specific to use in any general Lyme disease screening or diagnostic application. Thus, the method of the invention is particularly appropriate for large scale screening or diagnostic applications where only part of the subject population has been vaccinated or where the vaccination status of the population is unknown. “

Who is helping Dave Persing? (We will look at this again later.) [PMID 8968914]:

Who is helping Dave Persing? (We will look at this again later.) [PMID 8968914]

In 1995 and 1996 the Yale Lyme Disease grantees knew they had problems reading Western Blots in LYMErix vaccinated people. This is from the Schoen/Fikrig/Persing 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]:

In 1995 and 1996 the Yale Lyme Disease grantees knew they had problems reading Western Blots in LYMErix vaccinated people. This is from the Schoen/Fikrig/Persing 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]

Did they report these problems to the FDA when they told the FDA they had a vaccine in 1998?:

Did they report these problems to the FDA when they told the FDA they had a vaccine in 1998? No.

Slide 58:

Taken from the FDA database on LYMErix it appears that the FDA focused on Lyme arthritis instead of "multisystem complaints characteristic of later presentations of Lyme disease…” US Patent 6,045,804

Is Pam3Cys on the Syphilis spirochete as well?:

Is Pam3Cys on the Syphilis spirochete as well? Lipopolysaccharide Binding Protein Binds to Triacylated and Diacylated Lipopeptides and Mediates Innate Immune Responses 1 2004: Schroder, PMID #15294986 “Because the N-terminal Pam 3 Cys 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 ). ”

References:

References “Because the N-terminal Pam 3 Cys 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, PMID # 7927731 :

The references are 1994 & 1995, Radolf and Weis, PMID # 7927731

PMID 7927731, Weis, 1994 Abstract:

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:

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, as the outside observers can guess, is that these scientists really think these antigens are Pam3Cys.

in 2004…:

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 :

Aha! The famous Toll-Like-Receptors… PMID: 10426995

within the text of this TLR report…:

within the text of this TLR report… “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 NH 2 -terminal triacylated lipopeptide region.

. . . continuing:

. . . continuing “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 NH 2 -terminal lipopeptide of the T. pallidum 47-kD antigen activated IL-12 p40 promoter activity by a TLR-dependent mechanism ( Fig. 2 C), thereby providing evidence that TLRs serve to recognize a diverse family of microbial lipoproteins.

. . . continuing:

. . . continuing “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. 2 D). 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.

Do you understand that?:

Do you understand 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 Strain tricks in Europe to leave OspA and B out of the standard we have today.

Mechanisms and evidence of immune suppression associated with spirochetal and mycoplasmal antigens … And the New Great Imitators:

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] 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] 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

Justin Radolf, 2001, PubMed ID # 11441098 :

Justin Radolf, 2001, PubMed ID # 11441098

Slide 72:

“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. PubMed ID # 11441098

He goes on to say…:

He goes on to say… This mechanism may allow intracellular MTB to evade immune surveillance and maintain chronic infection. PubMed ID # 11441098 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.

Slide 74:

Graphic courtesy of Duke University TLR-4

One more thing you need to know about Techniques of Self-Poisoning (by Alan Barbour) The Scientist 1996, 10(14):13 ): :

One more thing you need to know about Techniques of Self-Poisoning (by Alan Barbour) The Scientist 1996, 10(14) : 13 ): “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 ): :

Continued (Alan Barbour on Spirochetal blebbing, The Scientist 1996, 10(14) : 13 ): …. "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.

Tuberculosis Lipoprotein Vaccines Failures:

Tuberculosis Lipoprotein Vaccines Failures PubMed ID#10792376 2000 Blackwell Science Ltd The 19-kD antigen and protective immunity in a murine model of tuberculosis: “These results are consistent with a model in which the presence of the 19-kD protein has a detrimental effect on the efficacy of vaccination with live mycobacteria. “

PubMed ID 11179309 :

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. “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.”

PubMed ID # 12761093 :

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 “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 PubMed ID# 10865170 :

Gary Wormser reporting that OspA suppresses the immune response in 2000 PubMed ID# 10865170 Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA). “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.

Lest we forget, Lyme victims came under vicious attacks by Edward McSweegan of the NIH online at that time:

Lest we forget, Lyme victims came under vicious attacks by Edward McSweegan of the NIH online at that time On newsgroups 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 Lyme scientists were crazy. Anonymous internet harassment is now a federal crime.

 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.’" :

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.’"

Kathleen Dickson spoke at the FDA Vaccine Committee, Jan 31, 2001 : “THE PROBLEM IS THE DEARBORN/DRESSLER IgG STANDARD”:

Kathleen Dickson spoke at the FDA Vaccine Committee, Jan 31, 2001 : “THE PROBLEM IS THE DEARBORN/DRESSLER IgG STANDARD”

She also warned the FDA Vaccine Committee (about LYMErix):

She also warned the FDA Vaccine Committee (about LYMErix)

The main issue for this entity is that they knew they had no way to test whether they actually had vaccines or not.:

The main issue for this entity 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?

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.:

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."

Kathleen Dickson is a analytical methods development chemist and did this kind VALIDATION OF ANALYTICAL METHODS of work for a living at Pfizer.:

Kathleen Dickson is a analytical methods development chemist and did this kind VALIDATION OF ANALYTICAL METHODS of work for a living at Pfizer. 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:

No-Work McSweegan

What else does Pam3Cys OspA do?:

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 mess 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 went un-discovered as a result of Yale and Allen Steere’s OspA sham…:

Enormously important research went un-discovered as a result of Yale and Allen Steere’s OspA sham… ….as we were studying all the known mechanisms of illness associated with this disease because we real Lyme victims know we’re not messing around. We heard 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 defrauders 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 .

This is our method of discovery. We were 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…:

This is our method of discovery. We were 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…

“These look like Epstein-Barr transformed (immortalized) cells”:

“These look like Epstein-Barr transformed (immortalized) cells”

Duray, 1992, Cold Spring Harbor Conference, Transcribed::

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 latent virus infections in tissues? :

“…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 Conference , published in Steve Schutzer's Lyme Disease: Molecular and Immunologic Approaches

It looked like LYMErix somehow reactivated Lyme. That is what the LYMErix victims told us (LD Support Group Leaders) on the phone:

It looked like LYMErix somehow reactivated Lyme. That is what the LYMErix victims told us ( LD Support Group Leaders ) 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 fraudulent Dearborn conference “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.

Tolerance Induced by the Lipopeptide Pam3Cys Is Due to Ablation of IL-1R-Associated Kinase-11 [PMID# 15294992, 2004]:

Tolerance Induced by the Lipopeptide Pam 3 Cys Is Due to Ablation of IL-1R-Associated Kinase-1 1 [PMID# 15294992, 2004] “Preculture of the cells with Pam 3 Cys at 1 µg/ml leads to a reduced response after subsequent stimulation with Pam 3 Cys at 10 µg/ml, indicating that the cells have become tolerant to Pam 3 Cys. … “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 Pam 3 Cys. 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 Pam 3 Cys-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]:

Tolerance Induced by the Lipopeptide Pam 3 Cys Is Due to Ablation of IL-1R-Associated Kinase-1 1 [PMID#15294992, 2004] “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 PMID 15294986, 2004:

Review of where Pam3Cys is found PMID 15294986, 2004 “…subsequent studies investigating immune responses to spirochetes used synthetic lipopeptides ( 22 ). The Pam 3 Cys 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. Mycoplasma fermentans inhibits tumor necrosis factor alpha-induced apoptosis in the human myelomonocytic U937 cell line. [PMID # 15286682, Nov 2004] “To investigate the mechanism of M. fermentans antiapoptotic effect, the reduction of mitochondrial transmembrane potential (DeltaPsim) and the protease activity of caspase-8 were measured. In the infected cells, the reduction of DeltaPsim was inhibited (approximately 75%), and an approximately 60% reduction of caspase-8 activity was measured. In conclusion, M. fermentans significantly inhibits TNFalpha-induced apoptosis in U937 cells, and its effect is upstream of the mitochondria and upstream of caspase-8.”

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 :

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 “TNF-alpha secretion was also suppressed in P. gingivalis LPS-pretreated, Ec LPS-challenged cells, but not vice versa, while Pam3Cys and Ec LPS did not induce a state of cross-tolerance at the level of TNF-alpha. Experiments designed to elucidate novel mechanisms of NF-kappaB inhibition in tolerized cells revealed the potential contribution of IkappaBepsilon and IkappaBxi inhibitory proteins and the necessity of TLR4 engagement for induction of tolerance to Toll receptor-IL-1R domain-containing adapter protein/MyD88-adapter-like-dependent gene expression. Collectively, these data demonstrate that induction of homotolerance affects a broader spectrum of signaling components than in heterotolerance, with selective modulation of specific elements within the NF-kappaB signaling pathway.

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)…:

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). It 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” and LYMErix vaccine. 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.

Kathleen Dickson reported to the FDA LYMErix committee in January 2001::

Kathleen Dickson reported to the FDA LYMErix committee in January 2001: “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.”

“It is because I have gotten so many calls from patients looking for help because of their illness, that I am here today.”:

“It is because I have gotten so many calls from patients looking for help because of their illness, that I am here today.” “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 A 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

She also told the FDA that it looked like Chronic Lyme, not Steere’s Imaginary “Bad Knees” Disease.:

She also 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.

Mycoplasma fermentans infection promotes immortalization of human peripheral blood mononuclear cells in culture, 2004, [PUBMED 15331449]:

Mycoplasma fermentans infection promotes immortalization of human peripheral blood mononuclear cells in culture, 2004, [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)

The Plum Island Iraqi Scientist (Please, do your own research on this… Al-Aubaidi JM):

The Plum Island Iraqi Scientist ( Please , do your own research on this… Al-Aubaidi JM) Once Don C. Wiley suffered a mysterious demise because he is an influenza expert, we began to think it might be true about the former Plum Island Iraqi scientist. His name was Al-Aubaidi and he was studying bovine infertility from mycoplasma

Joe Tully:

Joe Tully Joseph G. Tully and Robert E. Shope (Senior and Junior). Please use PubMed and read all of his/their reports. Their interests are 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.

Tully warns about the lack of interest in Mycoplasma, PMID # 9126441:

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 sure feels like you have must anemia. Dedicated VO2-Max exercise efforts to beat the fatigue do not really work… So it has to be caused by something like this (RBC 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:

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 sure feels like you have must anemia. Dedicated VO2-Max exercise efforts to beat the fatigue do not really work… So it has to be caused by something like this (RBC 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

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.”:

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.”

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…:

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 hypothesizing (there are no other kind) trying to tell us what’s a disease.

JJ Halperin - famous promoter of 2 sets of “Guidelines” wherein the deadliest version of the disease, ALS, is not detected, since the Dearborn conference. Is only that imaginary “BAD KNEES DISEASE” that Allen Steere concocted in Europe, alone, to set up his own little monopoly with Dave Persing and Robert Schoen – talks about how Lyme results in ALS in 47% of the cases::

JJ Halperin - famous promoter of 2 sets of “Guidelines” wherein the deadliest version of the disease, ALS, is not detected, since the Dearborn conference. Is only that imaginary “BAD KNEES DISEASE” that Allen Steere concocted in Europe, alone, to set up his own little monopoly 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. “Cerebrospinal fluid was examined in 24 ALS patients--3 (all with severe bulbar involvement) appeared to have intrathecal synthesis of anti-B burgdorferi antibody. Following therapy with antibiotics, 3 patients with predominantly lower motor neuron abnormalities appeared to improve, 3 with severe bulbar dysfunction deteriorated rapidly, and all others appeared unaffected. There appears to be a statistically significant association between ALS and immunoreactivity to B burgdorferi, at least among men living in hyperendemic areas. “

We took a pencil and tried to see if 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 Allen Steere to have been exposed to Bb and he said he thought the 47% association “was significant.”:

We took a pencil and tried to see if 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 Allen Steere to have been exposed to Bb and he said he thought the 47% association “was significant.”

ALS, Mycoplasma…and Gulf War Illness Garth Nicholson [Pubmed # 12383408]:

ALS, Mycoplasma…and Gulf War Illness Garth Nicholson [Pubmed # 12383408] 1: J Clin Neurosci. 2002 Sep;9(5):525-9. High frequency of systemic mycoplasmal infections in Gulf War veterans and civilians with Amyotrophic Lateral Sclerosis (ALS). “The presence of systemic mycoplasmal infections in the blood of Gulf War veterans (n=8) and civilians (n=28) with Amyotrophic Lateral Sclerosis (ALS) and age matched controls (n=70) was investigated by detecting mycoplasma gene sequences with forensic Polymerase Chain Reaction (PCR) and back hybridization with a radiolabeled internal oligonucleotide probe. Almost all ALS patients (30/36 or approximately 83%) showed evidence of Mycoplasma species in blood samples, whereas <9% of controls had blood mycoplasmal infections (P<0.001).

Continued :

Continued 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 those deployed to the land where we sold Saddam Hussein “fungi” and other microorganisms, like Plum Island mycoplasma are more likely at risk for ALS.:

NIH determines conclusively those deployed to the land where we sold Saddam Hussein “fungi” and other microorganisms, like Plum Island mycoplasma are more likely at risk for ALS. National Institute of Neurological Disorders and Stroke, Bethesda 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 :

Plum Island Mycoplasma : 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. “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. …

Selling fungi to Saddam Hussein:

Selling fungi to Saddam Hussein Congressional Record: September 20, 2002 (Senate) Page S8987-S8998 “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 eyes and couldn’t tell that that wasn’t right at the time…:

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 eyes 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.

What else do we know about OspA and Plum Island?:

What else do we know about OspA and Plum Island?

Sam T. Donta and Gulf War Mycoplasmal OspA/Pam3Cys Illness, PMID # 12057884 :

Sam T. Donta and Gulf War Mycoplasmal OspA/Pam3Cys Illness, PMID # 12057884 “ 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.”

Members of the ALDF and Yale University knew there was a problem with Chronic Lyme-like adverse events from OspA/Pam3Cys vaccination.:

Members of the ALDF and Yale University knew there was a problem with Chronic Lyme-like adverse events from OspA/Pam3Cys vaccination. There are at least 3 major clues: 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 their own labs (Imugen and L2 Diagnostics) where they have vested interests At the FDA vaccine Committee in Jan 2001, it was reported in Dave Persing patent that vaccine failure would be indistinguishable from chronic Lyme Gary Wormser in 2001 reported immunosuppression from OspA vaccination

Guilty:

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 doctors and non-for-profits that THEY were being stalked and harassed. Which is totally hilarious considering we explained the entire crime to the FDA Vaccine Committee in Jan 2001. T here were so many public hearings including in front of Senator Dodd in 1993 where Joe Burrascano described the harassment. When ever before have the victims of a disease been so obviously persecuted along with their treating specialists???

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 labs we own and profit from….:

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 labs we own and profit from….

Do you recall from slide 54 Who was Helping Dave Persing in 1995 when he was discussing and patenting a monopoly method for vaccination???:

Do you recall from slide 54 Who was Helping Dave Persing in 1995 when he was discussing and patenting a monopoly method for vaccination???

The Persing-Schoen-Steere RICO Method Patent US Patent No. 6,045,804:

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 RICO method patent claim…:

Let’s take a closer look at that Persing 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 two 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.

Four Signs of Typical Chronic Lyme and/or LYMErix Disease:

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 :

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 “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 131:

“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.” Steere - PMID # 2172819

They haven’t only harmed tick bitees worldwide,:

They haven’t only harmed tick bitees worldwide, They have harmed us all. . . .

The Greatest Imitator:

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.”

Slide 134:

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