The Great Imitator: Part 2

by Dottie L. Heffron

In the first part of this three part series, I wanted you to see how important it was for doctors to keep on top of the latest medical technology. Doctors should do their own research instead of relying on information peddlers, especially from pharmaceutical companies. Drugs only mask certain health problems and there is always an underlying problem causing your ailment. The aspirin rids you of a headache while the real problem might be a narrowed artery ready to aneurysm or inflamed nerves. 
I also asked you to look around at the rest of the worlds' view of "Lyme disease." I am sure you have seen that other countries were no longer calling it "Lyme disease." They have always called it Neuroborreliosis. Many world scientists saw that many major U.S. universities and doctors who once got big dollars in grants to study "Lyme disease" no longer were being funded. The funding has for the past 3 years gone to different entities. 

We also revealed OspA is "The Greatest Imitator." Please recall that recombinant OspA is Yale University's LYMErix vaccine patent. Many researchers know it to be synthetic tripalmitoyl cystine (Pam3Cys), an activator of latent viruses. It also tolerizes the immune system to similar antigens, meaning they won't be recognized as dangerous and antibodies will not be produced. 
In this section, part 2, we will explore the works of Justin Radolf, Janet Weis, Schröder and Schumann, Weissmuller and his group in Germany and other renowned scientists and show you our mode of discovery that led us to believe OspA is a synthetic Pam3Cys. This is the "true science" of Lyme disease.

In our discovery, we first note that Dr. Mario T. Philipp, Professor of Microbiology and Immunology at Tulane Medical School revealed in 1998 that OspA is a Tripalmitoyl Cystine (Pam3Cys)[1]. Since we knew LYMErix was recombinant OspA, a lipoprotein vaccine, we decided to take look at the other lipoprotein vaccines to see what the similar lipoprotein vaccines outcomes were. 

To our astonishment, the tuberculosis vaccine had the same outcomes and adverse events as the LYMErix vaccine. They seemed to make existing infections worse. "In these areas, the present vaccine - Mycobacterium bovis bacillus Calmette-Guérin (BCG) - is failing. Progressive tuberculosis occurs because the potentially protective T helper 1 (TH1)-cell response is converted to an immunopathological response that fails to eliminate the bacteria." [2] 

Physicians, "Masters of Public Health," and researchers were begging for new vaccines against TB. [3] How could this be? There just had to be some common link between all this. We kept searching for answers. 

We looked over the Pam3cys/OspA data again and wondered what does this do mechanistically? We already knew Pam3Cys is managed by TLR2 (Toll-Like Receptor 2) and according to some, also TLR1 or TLR6. The research on Toll-like receptors’ role in our immune system is ongoing as of today. [4] 

"Lyme neuroborreliosis is likely caused by inflammatory effects of the tick-borne spirochete Borrelia burgdorferi on the nervous system. Microglia, the resident macrophage cells within the central nervous system (CNS), are important in initiating an immune response to microbial products. In addition, astrocytes, the major CNS glial cell type, also can contribute to brain inflammation. TLRs (Toll-like receptors) are used by glial cells to recognize pathogen-associated molecular patterns (PAMPs), mediate innate responses, and initiate an acquired immune response. Here we hypothesize that because of their PAMP specificities, TLR1, -2, -5, and -9 may be involved in the pathogenesis of Lyme neuroborreliosis." [5]

Please refer to Figures 1 and 2, they will give you a better idea of what and where they are located on the cells. 
We were studying about other effects of lipoproteins, macrophage activity and the toxicities associated with the free-radical degradation products. Of course the makers of LYMErix would never mention or thought it would be recognized that mycoplasma and mycobacteria have the same type of antigens as Borrelia. 

We can not say for certain the members of the American Lyme Disease Foundation ever even looked at other similar vaccines outcomes considering their backgrounds. It is possible that they would not have had the scientific wherewithal to even consider doing such a history and background. 

Durland Fish is an entomologist. He is a self professed cheater, exposed in The Hartford Courant. "I went to work for the state health department, totally bored out of my mind inspecting restaurants. A terrible job and I wasn't very good at it," Fish said. He hated imposing regulations on eateries just scraping by in the poor county where he was assigned. "I'm not a very good cop. ... I used to coach them on how to get by - how to cheat." [6] Once a cheater, always a cheater, my grandfather used to tell me. 
Edward McSweegan is not only not a medical doctor, he apparently never performed any lab work while either at the US Navy or the NIH. [7] Eugene Shapiro has an undergraduate degree in English Literature. Allen Steere went into Rheumatology specifically because he was told this would be a way to avoid the draft [8] and Vietnam. That is very cowardly, I believe. 
Later, in 1992, two years after the ALDF.com was founded, Steere went to Europe apparently alone to falsify the diagnostic standard; leaving out OspA and B in anticipation of a post-LYMErix monopoly on blood products (human and bacterial viral) and the free venture capital known as NIH grants. 

By accident we stumbled upon mechanisms of inhibition of the auto-kill kinase by some of these weird lipids (these seemed to behave like BLC2-class molecules or by some other means resulted in immortalized cells) and to our amazement, there it was all along. In 1989, reported that, essentially, "badly cloned B cells that looked like Epstein-Barr immortalized cells." [9] He was working for the Fox Institute Cancer Center at that time and later went on to win many awards for his service and discovery. Paul Duray worked for the US Army and the National Cancer Institute at Fort Detrick. 

We know from Mario Philipp that OspA was a Pam3Cys structure, but nowhere could we find a structure of either it or in the HIV antigens gp41 and gp120. Antibodies against Pam3Cys in HIV victims- a curiosity, since creating antibodies against HIV seems to be the problem with vaccines. 
In 1988 we read [17]:

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
We also found that in 1992, Defoort created an HIV vaccine that has this structure:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC525594/pdf/pnas01083-0219.pdf [18] 

No one can show us what OspA looks like structurally. That is to say, there is not one chemical structure available online, anywhere, which includes the free, lipid-protein adjuvant, especially such that we would know what it looks like allegedly as a free molecule. Everyone knows that you can't crystallize a lipid (meaning any fat, oil, fatty acid, margarine, motor oil, hydrogenated-like grease, et.al) [10] 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." [11] 

He goes on to say, "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." [11]

The Brookhaven team who studied the structures of OspA and C only reported the non-lipid portion of these lipoproteins because you can't re-crystallize OspA in order to shoot it with X-rays. You can't freeze (crystallize) lipids. No one knows the real structure. Remember, structure is function and function is structure, they are one and the same. The only way we know the structure of OspA, as reported by Justin Radolf, was through its function (how it behaves immunologically).
According to NIAID Director, Anthony Fauci, regarding the recently failed-and-stopped HIV vaccine trial:
"Determining the structure of the trimeric form of the envelope protein is currently a research priority and is expected to yield additional insights." [19]

There was never a "key to vaccine failure" other than the known nature of the relapse in Relapsing Fever (antigenic variation or selection pressure, or the fact that antibodies would never work as a vaccine, since they don't work to control Relapsing Fever) until we learned about immune suppression due to synthetic Pam3Cys or the OspA vaccines. 

Some of the best scientific sources that we recommend on the subject of Pam3Cys/OspA induced immunosuppression are 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.[12], Janis Weis, "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. [13]

Other notable scientists Schröder and Schumann reported, "Lipoproteins and lipopeptides have repeatedly been shown to act as potent cytokine inducers, interacting with TLR-2, in synergy with TLR-1 or -6."[14], Wiesmüller, is talking about how he added the fatty acid groups ("lipo") to the amino acids ("protein"). In the end he says he used 13C-NMR (radiolabeled carbon) and mass spectrometry to see if it all went on right… and then he separated out the components that added on wrong with HPLC (silica gell) or a SEPARATION METHOD [15]. All the scientists were cross-referencing each others work. 

The Duke Biochemistry Department, say the "LIPO - POLY - SACCHARIDES" are components of the cell membranes and are known as endotoxins. Remember that lipids from bacteria are a problem for humans. They're immunogenic. They tell the body that there is an invader. [16]. 

We also noted there are jobs out there for Lipid Biochemists. 

This is a hot field now; scientists around the world have found out that Yale falsified their LYMErix vaccine outcomes. OspA did not prevent Lyme. It caused Chronic Pam3Cys or OspA-Immune-Suppression Syndrome, and the New Great Imitators.
In 1994 Justin Radolf reported: 

"A structural feature common to T. pallidum and B. burgdorferi is that the majority of their integral membrane proteins are lipid modified (9, 12, and 42). Compelling data have now emerged supporting that these spirochetal lipoproteins are potent immunopotentiators. Treponemal and borrelial lipoproteins have been shown to activate monocytes/ macrophages, B cells, and endothelial cells in vitro (1, 28, 29, 36, 39, 49, 56), suggesting that these molecules are inflammatory mediators in both syphilis and Lyme disease. More recently, we reported that synthetic lipohexapeptide analogs (lipopeptides) corresponding to the N termini of the native spirochetal lipoproteins could be used as lipoprotein surrogates in immune cell activation studies (16, 37). These lipopeptides, modeled after earlier studies of Bessler, Jung, and coworkers on the murein (Braun's) lipoprotein of Escherichia coli (21, 22), have been configured as N-palmitoyl-S-dipalmitoylglycerylcysteine-pentapeptides (16, 37) revealing that OspA was Pam3Cys and synthetic, and that OspA without the lipids attached - the way Allen Steere came up with the current, scientifically fraudulent CDC diagnostic standard missing OspA and B in Europe - would be how "not to create antibodies" or an immune response. [20]

Allen Steere reported in 1992, when he went to Europe [21]: 

"Supernatants from sonicated lysates of whole spirochetes were prepared as described (20). The group 1 strain of B. burgdorferi, G39/40, used in this study and in the previous study of US patients was isolated from an Ixodes damini tick in Guilford, Connecticut 921). The group 2 strain, FRG [Federal Republic of Germany], was isolated from Ixodes ricinus near Cologne (21). The group 3 strain, IP3, was isolated from Ixodes persulcatus near Leningrad (23). All three strains used in this study were high passage isolates, which were classified by Richard Marconi (Rocky Mountain Laboratory, Hamilton, MT) using 16S ribosomal RNA sequence determination as described (11, 24). The recombinant preparations of OspA and OspB used in this study were purified maltose-binding protein-Osp fusion proteins derived from group 1 strain B31 (25). The fusion proteins contained the full-length OspA or OspB sequence - without the lipid moiety or the signal sequence." 

This is the CDC standard we have in place today [22]. 

"It was recommended that an IgM immunoblot be considered positive if two of the following three bands are present: 24 kDa (OspC) *, 39 kDa (BmpA), and 41 kDa (Fla) (1). It was further recommended that an that IgG immunoblot be considered positive if five of the following 10 bands are present: 18 kDa, 21 kDa (OspC) *, 28 kDa, 30 kDa, 39 kDa (BmpA), 41 kDa (Fla), 45 kDa, 58 kDa (not GroEL), 66 kDa, and 93 kDa (2)." 

As you can see in the above paragraph, there is No OspA or B in the diagnostic standard that is in place today. This is why hardly anyone tests CDC positive, and we are all staying so sick. 

I do realize this is an abundance of data for regular people, like you and me. The information presented is very hard to understand, but if you really think about what each doctor did and then read their reports, it will become abundantly clear why they committed scientific fraud. 

I find myself so compelled to study the mechanisms that once tried to take my life. Now, it sits exposed for all to see as if the emperor was naked all along. The "true science" behind Lyme disease now is there for the taking. Please use the information to empower yourself….empower others. 

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