What is Lyme?




By: RJ James & Kelly Irene

“The case against science is straightforward: much of the scientific literature, perhaps half, may simply be untrue,” Dr. Horton


Lyme Borreliosis is a multi-systematic disease that's transmitted primarily through the bite of an infected tick, other insect vectors and maternal–fetal transmission (1). Originally, Borrelia was known as a relapsing fever organism because of it’s ability to undergo constant antigenic variation (modify their different outer surface proteins) (2). Unlike most bacteria, they are their own phylum that sheds it's outer membrane lipoproteins to evade the immune system (3). The shed lipoproteins are known as Outer Surface Proteins (Osps) and Variable Major Proteins (Vmps).  Borrelia modify their Osps (blebbing) as a means of evading a host immune response, making it difficult to detect through standard serology (besides an anti-flagellar (band 41) antibody method that is patented by Yale and no longer used (4)). Only those with HLA -linked hypersensitivity responses (~15%) to Borrelia test positive on current testing methods.

These shed blebs are called OspA (5). OspA is a molecule that stops the typical immunity chain reaction (6). It's a triacylated lipoprotein that's managed by toll-like receptors (TLR) 2 and 1 (TLR2/1) (7).TLR’s play a critical role in the innate immune system as they are first-line of defence against invading pathogens. The TLR’s job is to recognize the distinct molecular structure of pathogens so that they can disable or destroy them. TLR2/1 manages mycobacteria or fungal endotoxins (8). They are the same TLR's that manage mycoplasma, mycobacterium, m. tuberculosis, brucella and other fungal antigens..

In addition to being a major lipoprotein shed by spirochetes, OspA was also the antigen used in the LYMErix vaccine. Since it is a fungal – like endotoxin, it is much more toxic and stealth compared to most typical bacteria (TLR4, lipopolysaccharides). OspA or TLR2/1 agonists are so toxic, that the body shuts down the immune system to avoid a septic cytokine storm (9). OspA has the ability to cause permanent global immunosuppression in those who are infected (10).

OspA tolerizes the immune system making it unable to produce antibodies against pathogens that are managed by TLR 2/1 receptors (11). In addition, TLR’s 7/9 also shut down in a mechanism that is known as cross-tolerance whereby the immune system becomes unable to fight other viral, parasitic and bacterial pathogens. Thus, Epstein-Barr, herpesviruses, cytomegalovirus, coxsackie, zoster, etc.) and secondary infections (candida, fungi, mycoplasma, streptococcus, etc.) become the driving force in this neurological chronic fatiguing disease.

The mechanisms listen above occur within the first week of  infection once the Spirochetes disseminate to the lymph nodes (12). B-cell germinal centers collapse (13) and prevent B-cells from properly maturing (leading to a reduction in detectable antibodies). As a result, the host ends up suffering from global immunosuppression and low-grade inflammation of the brain (14). This resembles Pseudolymphoma and Leukemia (15). Chronic Lyme disease is really a B-cell (non – HIV) AIDS whereby sufferers are left with global immunosuppression and reactivated viruses
Even the NIH and Gary Wormser says OspA alone causes permanent immunosuppression (16,17,18). Since OspA is the main driver of disease, you do not need to be exposed to spirochetes to suffer from “Chronic Lyme” (OspA via tick bite or vaccine). Given this information, why is it that Steere purposely removed OspA from the diagnostics at the same time the vaccine was on trial? Namely because, it would make their vaccine look far more effective.

Firstly, you cannot vaccinate against relapsing fever organisms due to its ability to undergo antigenic variation. Secondly you cannot inject people with fungal - like antigens because they can cause immunosuppression and post-septic shock. All fungal bearing vaccine attempts managed by TLR2/1 (Tuberculosis, Brucella,  HIV etc.). were epic failures because they caused the same outcome that they were "intended" to prevent (19).

Raymond Dattwyler, Professor of Microbiology and Immunology from New York Medical College said that "Individuals with a poor immune response tend to have worse disease" (20). Chronic neuro Lyme produces low to no antibodies. In analytical testing you are supposed to look for the lowest antibody concentration possible. However, researchers at the CDC did the opposite. In Dearborn Michigan, 1994, the “scientists” from the CDC/ALDF/Yale committed research fraud by falsified the testing and case definition to detect only a high antibody concentration. This was intended to make their vaccine look far more effective by excluding all neurological immune suppressed cases from the diagnostics. Making both OspA shed by Spirochetes  and LYMErix victims undetectable with current analytical testing.

HIV-AIDS destroys T-cells
LYME-AIDS renders B-cells immature and useless
Both are Acquired Immune Deficiencies.


1. Maternal-fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi. https://www.ncbi.nlm.nih.gov/pubmed/4003991

2. Selection of Variant Borrelia burgdorferi Isolates from Mice Immunized with Outer Surface Protein A or B http://www.ncbi.nlm.nih.gov/pmc/articles/PMC173206/pdf/631658.pdf|

3. Characterization of multiprotein complexes of the Borrelia burgdorferi outer membrane vesicles. https://www.ncbi.nlm.nih.gov/pubmed/21875077

4. Antigenic variation in vector-borne pathogens. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627965/?tool=pubmed

5. Action of penicillin on Borrelia hermsii. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC182019/

6. Fungal Recognition by TLR2 and Dectin1 https://www.ncbi.nlm.nih.gov/m/pubmed/18071656/

7. Tripalmitoyl-S-Glyceryl-Cysteine-Dependent OspA Vaccination of Toll-Like Receptor 2-Deficient Mice Results in Effective Protection from Borrelia burgdorferiChallenge http://iai.asm.org/content/71/7/3894.abstract

8. TLR2

9. Endotoxin Tolerance Inhibits Lyn and c-Src Phosphorylation and Association with Toll-Like Receptor 4 but Increases Expression and Activity of Protein Phosphatases.

10. Human Lipopolysaccharide-binding Protein (LBP) and CD14 Independently Deliver Triacylated Lipoproteins to Toll-like Receptor 1 (TLR1) and TLR2 and Enhance Formation of the Ternary Signaling Complex* https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617275/

11. Lyme Diseases Greatest Mystery: Understanding Tolerance and Cross Tolerance in the Immune System Caused by Outer Surface Proteins Shed by Borrelia

12. Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102705/

13. Suppression of Long-Lived Humoral Immunity Following  Borrelia burgdorferi Infection. http://journals.plos.org/plospathogens/articl=10.1371%2Fjournal.ppat.100497

14. Bacterial lipoproteins can disseminate from the periphery to inflame the brain. https://www.ncbi.nlm.nih.gov/pubmed/20431027


16. Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.

17. Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA). https://www.ncbi.nlm.nih.gov/pubmed/1086517

18. The Toll of a TLR1 polymorphism in Lyme disease: A tale of mice and men http://onlinelibrary.wiley.com/doi/10.1002/art.34386/a

19. Fungal Bearing Failed Vaccine Parallel Models - Like LYMErix http://truthbetoldx81.blogspot.com/2017/07/fungal-bearing-failed-vaccine-parallel.html


By: Kelly and RJ

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