Lyme Disease: The Case of the Missing Antibodies

“Scientific fraud, plagiarism, and ghostwriting are increasingly being reported in the news media, creating the impression that misconduct has become a widespread and omnipresent evil in scientific research” – Heinrich Rohrer

HIV-AIDS is a disease that destroys T – Cells

LYME-AIDS leads to immature B-cells and unhealthy antibody production

Both are Acquired Immune Deficiencies.

Left untreated, Lyme Disease can become a multi-systemic infection that can cause serious damage to the immune system. Although primarily transmitted through an infected tick bite, Lyme Disease may be transmitted in several other ways.

For instance, the CanLyme website states that “it’s possible to contract Lyme disease from blood-sucking insects” (Wilson, n.d., p. 1). In 1988, Paul Duray and CDC “expert” Dr. Allen Steere conducted a study on maternal transmission of Lyme Disease. In their paper titled, Clinical Pathologic Correlations of Lyme Disease by Stage, they listed their findings. Duray and Steere concluded that “It is clear that B. burgdorferi can be transmitted in the blood of infected pregnant women across the placenta into the fetus” (Duray & Steere, 1988, p. 77). Furthermore, they concluded that congenital Lyme has “now been documented with resultant congenital infections and fetal demise” (Duray & Steere, 1988, p. 77). Steere and Duray (1988) found that “Spirochetes can be recovered or seen in the infant’s tissues including the brain, spleen and kidney” (p. 77). At this time, doctors like Allen Steere published several studies on how Lyme Borreliosis was a relapsing fever organism.  

Before 1994, Borrelia was known as relapsing fever organism because of its ability to undergo antigenic variation (Barthold et al, 1995). Antigenic variation “or antigenic alteration refers to the mechanism by which an infectious agent such as a protozoan, bacterium or virus alters the proteins or carbohydrates on its surface and thus avoids a host immune response” (Antigenic variation, 2019, p.1). Therefore, making spirochetes part of a unique family of bacterium. 

Spirochetes are unique, because they are their own phylum that has the ability to shed its outer membrane lipoproteins as a means of evading the immune system (He et al, 2011). The lipoproteins shed by Spirochetes are known as Variable Major Proteins (Vmps) and Outer Surface Proteins (Osps). Borellia’s ability to modify their Osps and Vmps make it difficult to detect through the standard serological testing that is currently being used to detect Lyme Disease (Barbour & Restrepo 2000).

The most accurate test on Lyme Disease, which used an anti-flagellar band (band 41) was patented by Yale and is no longer being used (Berland & Flavell, R. (n.d.). In order to get a serodiagnosis of Lyme Disease, one must have an HLA-linked hypersensitivity response to Borrelia burgdorferi sensu lato.

The immune system has Toll-Like Receptors (TLR) that play a critical role in the innate immune system as they are the first line of defense against infectious pathogens. The TLR’s job is to recognize the distinct molecular structure of pathogens so that they can disable and/or destroy them.

Lyme Disease is a triacylated lipoprotein that is managed by TLR 2/1 (Heilbrun et al, 2003). One of the Blebs shed by Borrelia sp. is called Outer Surface Protein A (OspA)  (Barbour, Dunn & Lade, 1990). More specifically, OspA is a molecule that stops the typical immunity chain reaction (Kirby, Lloyd & Wills, 2018). One of the key purposes of TLR 2 is to manage fungal endotoxins and mycobacteria when they enter the bloodstream (TLR2, 2019). For example, TLR 2/1 receptors are responsible for managing Tuberculosis, Brucella, mycoplasma, and fungal antigens (i.e. Candida).  

OspA is a TLR 2 agonist (chemical that binds to a receptor and activates the receptor to produce a biological response), making it far more toxic than typical bacteria (TLR 4, lipopolysaccharides). The toxicity of OspA or TLR 2/1 agonists are so vast, that the immune system shuts itself off to avoid septic shock (cytokine storm) (Chang et al, 2015).
Therefore, because OspA is a TLR 2 agonist, it has the ability to cause permanent immunosuppression in many who become infected (Kelley Ranoa & Tapping, 2013). 
In sum, OspA causes the immune system to become tolerant (unable to recognize and produce an effective antibody response) to pathogens that are managed by TLR 2/1 receptors (See other blogs on site). 

In a process known as cross-tolerance, OspA inhibits TLR 7/9 (which manage intracellular pathogens) ability to fight several other viral, bacterial, and parasitic infections. This is one of the key reasons why Epstein-Barr, herpesviruses, cytomegalovirus, coxsackie, zoster, etc.) and secondary infections (candida, fungi, mycoplasma, streptococcus, etc.) are prominent in almost everyone who has been infected with Spirochetes. 

The mechanisms listed in the previous paragraphs can occur soon as spirochetes disseminate to the lymph nodes (> 1week) (Barthold et al, 2011). Once the B-cell germinal centers collapse, B-cells are unable to properly mature (mature B-cells produce healthy antibodies) leading to a reduction in detectable antibodies (Baumgarth, Elsner,  Hastey & Olsen, 2015).
Simply put, the immune deficiency with Lyme Disease isn’t a shortage of B-cells; rather, it consists of an abundance of immature B-cells unable to produce an efficient antibody response from the affected TLRs. 

In the end, those who are infected with Lyme end up suffering from antibody related immunosuppression and low-grade inflammation of the brain (Cadavid & Londoño, 2010). Duray and Steere (1988) concluded in their studies that Lyme Disease resembles Leukemia and Pseudolymphoma (p. 67). Thus, the problem about ‘Chronic Lyme Disease’ so much the persistence of spirochetes; rather, it’s more about the immunosuppression, reactivated viruses and opportunistic infections. 

Since OspA is one of the primary lipoproteins shed by Borrelia sp., CDC researchers decided to use it in their LYMErix vaccine. Which makes no sense, because even the NIH and CDC officials like Gary Wormser knew that OspA can cause permanent damage to the immune system (Cabral et al, 2006).  In the end, they knew that using OspA in a vaccine was a terrible idea as OspA is a fungal-like endotoxin that causes permanent immune damage. Because of OspA’s immunosuppressant properties, using it in a vaccine is nothing short of insane. The results of this vaccine say it all: 

https://drive.google.com/file/d/1vwBdBnXlzaNN8kdBUfOxMKrRh_0h5dPR/view?fbclid=IwAR3UwQyc1D249tBMQ8MFpFltRk-E9SgPkSwEUK__CYlYx3ImtXiPsSm9SZs

The worst part about all of this, is that Steere purposely removed OspA from the diagnostics at the same time the vaccine was on trial. Namely because they knew the LYMErix vaccine look far more effective if they removed the driving force behind ‘Chronic Lyme’ (OspA) of the diagnostic standard.

There are two key reasons why OspA should never have been used as a vaccine adjuvant.
Firstly, due to antigenic variation, it is impossible to vaccinate against relapsing fever organisms. Secondly, it is extremely dangerous to inject people with TLR 2 agonists (fungal endotoxins) because of its ability to initiate septic shock and immunosuppression. 

Overall, public health officials have never had any success when it comes to immunizing against organisms managed by TLR2/1 (i.e. Tuberculosis). Immunizations against these pathogens fail often because they give recipients the same outcome that the vaccine was intended to prevent (Abou-Zeid et al, 2000). This is especially important information when it comes Valneva’s new Lyme vaccine as it contains OspA, which as you can clearly see, can cause permanent immunosuppression.

Now that this blog has discussed the mechanisms of Lyme and OspA, it is easy to understand how the current Lyme tests are based off of fraud. For decades, the CDC/NIH/ALDF have known that Lyme is a disease of immunosuppression. They knew that when it comes to analytical testing for Lyme Disease, that you should look for the lowest antibody concentration possible. Instead, researcher at the CDC/NIH/ALDF did the complete opposite. 

In 1994, these so called “experts” committed research fraud at a conference in Dearborn, Michigan. They falsified the testing and case definition to detect only a high antibody concentration. All designed to make their vaccine more effective by excluding all neuro-immune cases of Lyme Disease from the case definition and testing kits.  The removal of Osps from the case definition, left both those who were bitten by ticks and LYMErix victims undetectable on standard testing. Therefore, victims and their families of this crime against humanity have not only been left invalidated; they have also been left to suffer and die. 

References

Abou-Zeid, C., Apt, A., Inwald , J., Lyadova , I., Nikonenko, B., Yeremeev, V., & Young, D. (2000). The 19-kD antigen and protective immunity in a murine model of tuberculosis. Clinical and Experimental Immunology, 120(2), 274–279. doi: 10.1046/j.1365-2249.2000.01212.x


Antigenic variation. (2019, May 12). Retrieved October 21, 2019, from https://en.wikipedia.org/wiki/Antigenic_variation.


Barbour, A. J., Dunn, J., & Lade, B. G. (1990). Outer surface protein a (OspA) from the lyme disease spirochete, borrelia burgdorferi: High level expression and purification of a soluble recombinant form of OspA. Protein Expression and Purification, 1(2), 159–168. doi: 10.1016/1046-5928(90)90011-m


Barbour, A., & Restrepo, B. (2000). Antigenic Variation in Vector-Borne Pathogens. Emerging Infectious Diseases, 6(5), 449–457. doi: 10.3201/eid0605.000502


Barthold, S. S., Baumgarth, N. J., Feng, S., Hastey, C., Hodzic, E. W., & Tunev  , S. (2011, May). Lymphoadenopathy during lyme borreliosis is caused by spirochete migration-induced specific B cell activation. Retrieved October 21, 2019, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102705/.


Barthold, S., Fikrig, E., Flavel, R., & Tao, H. (1995). Selection of Variant Borrelia burgdorferi Isolates from Mice Immunized with Outer Surface Protein A or B. Infection and Immunity, 1658–1662. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC173206/pdf/631658.pdf

Berland, R., Fikrig, E., & Flavell, R. (n.d.). US5618533A – Flagellin-based polypeptides for the diagnosis of lyme disease. Retrieved February 11, 1992, from https://patents.google.com/patent/US5618533A/en

Baumgarth, N., Elsner, R., Hastey, C., & Olsen, K. (2015). Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection. PLOS Pathogens, 11(7). doi: 10.1371/journal.ppat.1004976


Cabral  , E., Cassiani-Ingoni, R., Garza, Z., Gelderblom, H., Lünemann, J., Magnus, T., … Munson, P. (2006). Borrelia burgdorferiInduces TLR1 and TLR2 in Human Microglia and Peripheral Blood Monocytes but Differentially Regulates HLA-Class II Expression. Journal of Neuropathology & Experimental Neurology, 65(6), 540–548. doi: 10.1097/00005072-200606000-00002


Cadavid  , D., & Londoño, D. (2010). Bacterial Lipoproteins Can Disseminate from the Periphery to Inflame the Brain. The American Journal of Pathology, 176(6), 2848–2857. doi: 10.2353/ajpath.2010.091235


Chang, H.-H., Ho, I.-C., Manavalan, T., Medvedev, Y., Murphy, M., Pattabiraman, G., …  Xiong, A. (2015). Endotoxin Tolerance Inhibits Lyn and c-Src Phosphorylation and Association with Toll-Like Receptor 4 but Increases Expression and Activity of Protein Phosphatases. Journal of Innate Immunity, 8(2), 171–184. doi: 10.1159/000440838


Dickson , K. (n.d.). Steere writes about deformed B cells, later shown to be an outcome of LYMErix, too: Remember, OspA is Pam3Cys. Retrieved October 21, 2019, from http://www.actionlyme.org/

Dunn, J. J., Lade, B. N., & Barbour, A. G. (1990). Outer surface protein a (OspA) from the lyme disease spirochete, borrelia burgdorferi: High level expression and purification of a soluble recombinant form of OspA. Protein Expression and Purification, 1(2), 159–168. doi: 10.1016/1046-5928(90)90011-m


Duray, P. H., & Steere, A. C. (1988). Clinical Pathologic Correlations of Lyme Disease by Stage. Annals of the New York Academy of Sciences, 539(1 ), 65–79. doi: 10.1111/j.1749-6632.1988.tb31839.x


He, M., Kariu , T., Pal, U., Promnares , K., Shroder , D. Y., Wang , Y., & Yang, X. (2011). Characterization of Multiprotein Complexes of the Borrelia Burgdorferi Outer Membrane Vesicles. J Proteome Res, 10(10), 4556–4566. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/21875077

Heilbrun, M., Kirschning, C., Ma, Y., Philipp, M., Wang, X., Weis, J., … Yoder, A. (2003). Tripalmitoyl-S-Glyceryl-Cysteine-Dependent OspA Vaccination of Toll-Like Receptor 2-Deficient Mice Results in Effective Protection from Borrelia burgdorferi Challenge. Infection and Immunity, 71(7), 3894–3900. doi: 10.1128/iai.71.7.3894-3900.2003


Kelley, S. ., Ranoa , D., & Tapping, R. (2013). 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. Journal of Biological Chemistry, 288(14), 9729–9741. doi: 10.1074/jbc.m113.453266


Kirby, A., Lloyd, V., & Wills, M. (2018). Detecting the Lyme Disease Spirochete, , in Ticks Using Nested PCR. Journal of Visualized Experiments, (132). doi: 10.3791/56471


TLR2. (2019, August 8). Retrieved October 21, 2019, from https://en.m.wikipedia.org/wiki/TLR2

Wilson, J. (n.d.). Transmission. Retrieved October 21, 2019, from https://canlyme.com/lyme-prevention/transmission/

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