Lying Lyme Liars

I’m supposed to write about how the Lyme crooks knew that OspA could never have been a vaccine before they in fact called it a vaccine. You may be thinking, this has nothing to do with me. I never got the Lyme vaccine. Bear with me, because this is one of the most important things you can know about this disease.

 
I’ll explain what the organism does, and then you tell me if a vaccine is possible. Then I’ll explain why this fact is so important.

 

 

The crooks say that “Lyme disease” borrelia are different from relapsing fever borrelia. It’s a lie. All borrelia are relapsing fever organisms. They lied about it because they were literally creating an industry (“a deep vein of gold from which to mine virulence determinants”) for tick-borne disease vaccines, and test kits of the sort that you could pick up at Walgreens after pulling a tick off your ass. The more bugs they patented, the more vaccines, test kits and theoretically, eventually, pharmaceutical remedies that they could sell.

 

 

Alan Barbour, who owns more than 30 patents in this commercial space, insists to this day that there should be a separate genus called “Borreliella” for “Lyme” and “Lyme-like” organisms, and that the genus Borrelia should be reserved for relapsing fever organisms. This is so dumb, one wonders if perhaps he was marching against himself.

 

 

Here’s how the CDC defines “relapsing fever.”:

 

 

“Relapsing fever spirochetes have a unique process of DNA rearrangement that allows them to periodically change the molecules on their outer surface. This process, called antigenic variation, allows the spirochete to evade the host immune system and cause relapsing episodes of fever and other symptoms.”

 
Yep, that’s what Borrelia burgdorferi do. This is so well known, such ancient history, that to claim otherwise should be grounds for expulsion from Chemistry Club and revocation of a medical license. But, notice that the CDC doesn’t list burgdorferi there. Let’s give them the swift boot, too, since they don’t do science, but protect their own lying, profiteering officers from prosecution for scientific fraud that has caused countless deaths and devastation to potentially millions of lives.

 
ALL Borreliae do this (antigenic variation), and when they do so, they shed their outer surface in these little blobs called blebs. The blebs are covered in toxic lipoproteins, which are the actual cause of disease. Look at how many blebs there are here (in Alan Barbour’s micrograph), relative to the number of spirochetes:

 

 

We Lymish are told that our horrifying array of symptoms are caused by tiny corkscrews drilling into all of our tissues. They’re not. They’re *initially* caused by what’s on those blebs–the lipoproteins, AKA outer surface proteins, or “Osps.” The spirochete is simply a vehicle for dissemination.

 
Here are two reports from Rocky Mountain Laboratories, a division of the National Institutes of Health (NIH), that explain how these blebs cause disease.
1990 (pre-LYMErix):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC184538/pdf/aem00087-0464.pdf

 

1993 (during LYMErix trials):

https://www.ncbi.nlm.nih.gov/pubmed/8454350

 

 

So these blobby little blebs that are covered in Osps (like OspA, OspB) travel to the brain and inflame it (Cadavid), disseminate to organs and lymph nodes, and eventually ruin the immune system. They gum up the immunity works, so antigen is no longer presented, meaning that the immune system doesn’t even have a chance to produce antibodies. (Watch Khan Academy videos for an introduction to this science. See the first Cryme 101 video here https://www.truthcures.org/videos.)

 

 

The Osps cause global immunosuppression (tolerance and cross tolerance) resulting in the reactivation of latent viruses, like EBV, CMV, HHV-6, etc. THESE are what is causing the illness. Chronic Lyme is like AIDS, and is technically the same as “Post Sepsis Syndrome.” The NIH agrees with this, and has many times reported it. See the Charge Sheets on TruthCures.org.

 

 

Here are the two reports by Martin and Marques at the NIH’s NINDS’ *Lyme and MS Division* that say OspA is responsible for causing nearly complete immunosuppression, in the end:

 

J Neuropathol Exp Neurol. 2006 Jun;65(6):540-8. Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.

https://www.ncbi.nlm.nih.gov/pubmed/16783164

 

J Infect Dis. 2006 Mar 15;193(6):849-59. Epub 2006 Feb 8. Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes. Cabral ES1, Gelderblom H, Hornung RL, Munson PJ, Martin R, Marques AR.

https://www.ncbi.nlm.nih.gov/pubmed/16479520

 

 

Here’s Allen Steere in 1988 describing the immune wreckage and cancer-like result of OspA injection. He was later sent to Europe to conduct “research” that would result in these outcomes no longer being part of the disease definition.

 

“The immune response involves virtually all of the organs and structures of the reticuloendothelial system including the bone marrow, and clinical pain and discomfort seems to correlate with hyperplasia of lymph nodes and spleen and bone marrow. Diffuse visceral involvement in this acute stage mimics infectious mononucleosis or disseminated viral syndromes. These include conjuctivitis, pharyngitis, pneumonitis with dry cough and mild pleuritic pain, hepato-splenic tenderness, lymph node swelling of the neck and groin, and orchitis. There is lymphoid hyperplasia of the lymph nodes and spleen consisting of prominent germinal centers and numerous perifollicular lymphocytes, with proliferation of plasma cell precursors and mature plasma cells. The plasma cell precursors are large, appear tumor-like, and can resemble Reed-Sternberg cells. Others look like typical immunoblasts (FIG. 1). In one example, cervical lymph nodes show cell degeneration with karyorrhexis and nuclear debris of lymphoid elements. This patient had repeated high fevers and marked discomfort of neck nodes. Large atypical immunoblasts can also be seen in the spleen and bone marrow. The red pulp of the spleen is congested, not unlike that seen in infectious mononucleosis.”

 
This cascade of events is caused by the Osps, alone. Not by the spirochetes drilling into tissues; not by “biofilms” that must be busted; not by a magical combination of “coinfections” that must be killed in a magical sequence. Certainly not by mutant amber bacteriophages that are actually viruses–no, wait–they’re cross-kingdom-stealth DNA…No, not that. OspA causes the disease all by itself.

 

 

So, if you were to put a bunch of OspA into a syringe and inject it into people who expect to be protected against “Lyme disease,” what do you suppose would happen?

 

Would OspA be a vaccine? Would it protect people from spirochetes? Would it promote the production of antibodies that are capable of killing spirochetes?

 
(No.)

 

 

THIS is the essence of the Cryme. CDC officers, the American Lyme Disease Foundation (ALDF), Yale researchers and others, to whom we refer collectively as “the cabal,” claimed that OspA was a vaccine when CLEARLY it was not. That’s why Barbara J. B. Johnson, head of CDC’s vector-borne diseases division, convened the Dearborn conference in 1994. She and the cabal used their position of power to dictate a new testing scheme (two-tier ELISA + Western blot serology) that excludes the immunosuppression form of disease from diagnosis. This allowed them to falsely say that the insidious, chronic, AIDS-like adverse events of the LYMErix trials were not really adverse events. And it also means that since 1994, those disease outcomes have not been considered part of the definition of “Lyme disease.”

 
They redefined Lyme disease to mean ONLY a genetically linked hypersensitivity (abundant antibody) response. Late Lyme arthritis. Autoimmune. A swollen knee. The 15%-or-so of the population who do produce the antibodies and are competent to fight the disease.

 
By the way, Yale owns both the original LYMErix patent AND a valid test method (that would detect ALL cases, not just the swollen knees), but they did not use this valid test method (US patent 5,618,533) to assess the victims of the LYMErix trials. They used the new “Dearborn” method, instead.

 
Additionally, it should be noted that *BECAUSE* all borrelia are relapsing fever organisms (shedding Osps on blebs, producing new Osps that require different antibodies), it’s ridiculous to claim that antibodies against one Osp–OspA, for example–can prevent spirochetal infection and subsequent dissemination of Osp-covered blebs.

 
Mark Klempner, who is part of the cabal and who committed research fraud with his $4.7 million-grant-funded fake retreatment study, now is claiming that such an antibody product is viable as a sort of prophylactic treatment. It’s as if he’s clinging to the edge of a cliff with the cops waiting for him at the bottom, saying, “OspA really WAS a vaccine, but since that failed, here: inject some of the OspA antibodies directly and act like Lyme borrelia are really “Borreliella” and don’t shed toxic, immune-suppressing Osps.”

 

http://www.fox25boston.com/news/local-researchers-hope-to-have-lyme-antibodies-available-by-2020/525800477

 

 

While we’re at it, let’s just make fun of Alan Borreliella Barbour, “Barbourella,” one more time.



Categories: Lyme 101, Lyme Disease

Tags: , , , , , ,

6 replies

  1. Ha ha ha….I love it…how you trashed that idiot Ms. Beaux Reiosis.
    “A sweet man” FTW!!…yeah sure…I d feel more confortable in a jail cell with a rapist than Barbour.
    …..we are bitter…..not because of lyme itself but because of the denial and the lies who keep prolonging uneccesary suffering and death as well.

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  2. I m not sure we will ever get to prosecute these people. Not only they are protected their power is well above that of major officials. Ex pres. G. Bush was treated in secret w an undisclosed protocol. You better beilive he was cured. They have protection of the entire US defense system because they make the laws.
    Unless more and more politicians and legislators become directly touched by this illness, I dont see a light at tge end of this dark tunnel.
    In addition, their ties with both big Pharma and GMO industry are so dense and intricated to make it nearly impossible for these criminals to b prosecuted.

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  3. OspA being Pam3Cys… causing the same near-cancer as Lyme:

    J Immunol. 2005 Jun 1;174(11):6639-47.

    Role of TLR in B cell development: signaling through TLR4 promotes B cell maturation and is inhibited by TLR2.

    Hayashi EA1, Akira S, Nobrega A.

    Author information

    AbstractThe role of TLR4 in mature B cell activation is well characterized. However, little is known about TLR4 role in B cell development. Here, we analyzed the effects of TLR4 and TLR2 agonists on B cell development using an in vitro model of B cell maturation. Highly purified B220(+)IgM(-) B cell precursors from normal C57BL/6 mouse were cultured for 72 h, and B cell maturation in the presence of the TLR agonists was evaluated by expression of IgM, IgD, CD23, and AA4. The addition of LPS or lipid A resulted in a marked increase in the percentage of CD23(+) B cells, while Pam3Cys had no effect alone, but inhibited the increase of CD23(+) B cell population induced by lipid A or LPS. The TLR4-induced expression of CD23 is not accompanied by full activation of the lymphocyte, as suggested by the absence of activation Ag CD69. Experiments with TLR2-knockout mice confirmed that the inhibitory effects of Pam3Cys depend on the expression of TLR2. We studied the effects of TLR-agonists on early steps of B cell differentiation by analyzing IL-7 responsiveness and phenotype of early B cell precursors: we found that both lipid A and Pam3Cys impaired IL-7-dependent proliferation; however, while lipid A up-regulates B220 surface marker, consistent with a more mature phenotype of the IgM(-) precursors, ***Pam3Cys keeps the precursors on a more immature stage.*** Taken together, our results suggest that TLR4 signaling favors B lymphocyte maturation, whereas TLR2 arrests/retards that process, ascribing new roles for TLRs in B cell physiology.

    https://www.ncbi.nlm.nih.gov/pubmed/15905502

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  4. He wants to maintain the pretense that the Dearborn two-tier test is valid. A separate group for Borrelia burgdorferi is meant to support the lie that Bb does not relapse and that it does not lead to severe neuro and immune related disease and it is little more than Arthritis. Why is he talking about creating a separate group for Bb now? It is because they want to bring OspA back now. Yet again, It is all about making it look like the vaccine is safe and effective when it actually leads to the severe neuro symptoms which they want to hide.

    Liked by 1 person

  5. You CANT make this up. But when the Lyme crymes are finally prosecuted, people will be lining up for the compensation from Yale and the State of CT like ENRON and Madoff.:
    https://www.linkedin.com/pulse/steere-writes-deformed-b-cells-later-shown-outcome-lymerix-dickson

    Liked by 1 person

  6. Umbelivable, but now nothing really surprises me any longer. They are layong their lyme scare marketing strategy as well. We all know the media is in bed with pharma company and the CDC. They will scare people enough to convince them that the 2nd vaccine is what they need. Note also how they are just talking about acute lyme, and they never address chronic and late stage lyme.

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