The TruthCures Science is Not a Theory. OspA is Pam3Cys.

OspA is Pam3Cys.  Always has been, always will be.

Pam3Cys is a molecule that shuts down the typical chain reaction of immunity.  All Lyme patients, or rather tick bite sepsis patients, know that spirochetes cause immune suppression and that is why we don’t test positive by having a ridiculous amount of antibodies required for the CDCs surveillance data scheme.  But we forego asking why that happens.  So here it is, folks.  The proof.

Spirochetes are covered in blebs and those are covered in outer surface proteins (Osps) and that is what the Western Blot is trying to detect antibodies against.


The way spirochetes cause disease is by stealth bombing these toxic blebs that have Pam3Cys on them and they poison and render the host incompetent to fight other pathogens.  OspA is a TLR 2 agonist, the shut down spreads to other TLRs and eventually you can’t respond to anything.  This is immune tolerance and cross tolerance.  This is not fixed by killing unkillable spirochetes.

Before we move on to OspA being Pam3Cys I am going to copy in a recent post from my friend called “THIS is Lyme”.  Click the link and read all of the references listed.  This is a VERY serious disease.

“Spirochetes disseminate to the lymph nodes, bone marrow, spleen and brain within a week of infection (1). Lymph node germinal centers, where B cells are supposed to mature and be assigned an immune system function, are rendered incompetent (2). Meanwhile, the toxic triacyl lipoproteins that are shed by spirochetes on blebs of their outer surface get to work causing tolerance and cross tolerance (2,3,4), AKA shutting down the immune system (5,6). There is generalized immune suppression at the same time there are brain inflammation and neurologic complications (7,8,9,10). Opportunistic infections take hold and herpesviruses reactivate (11,12). Half the cases don’t recover fully, regardless of treatment (13,14,15). The outcome is cancer-like (16,17).”

All of us Lymish at times aggressively refute what the doctors who deny us say because they don’t have their facts straight.  So when you see a TruthCures supporter aggressively defending facts, it’s the same thing.  We are constantly attacked as the messenger by people who have never even looked at the data to see the truth for themselves.  That pesky TruthCures link gets shared on so many posts because the answer to nearly everything really is in it.  But you won’t know for yourself until you actually look.  Every single person who has looked at this and understands it has come to the same conclusion-

  1. This is a CRYME.
  2. OspA is Pam3cys
  3. If the vaccine caused the same disease without spirochetes, then tick bite victims problem is not actually spirochetes but instead the disastrous effects of the toxic triacylated lipoproteins shed by spirochetes.
  4. We are filled with outrage at the reason why we, everyone else, and especially our children are being left to be slowly tortured to death and we want everyone else to be empowered by the truth that can free us all from this bondage.


Okay, now onto the proofs that OspA is Pam3Cys (tripalmitoyl cysteine), a fungal-like antigen, triacylated lipoprotein managed by TLR 2/1 that causes immunosuppression.



“Here are the NIH’s 2 reports that say OspA (TLR2-agonist) is the cause of the MS/CFIDS/EBV-reactivated kind of Lyme (that also causes humoral immunosuppression),… and that as a result of exposure to OspA-like antigens (shed constantly in a process called blebbing, as revealed by CDC officer Alan “Stealth Bomber” Barbour), you might not even have anti-flagellar antibodies (TLR5-agonists):” –KMD

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

Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes.


“TLR2 mediates inflammatory responses to a wide variety of lipidated microbial components, including bacterial lipoproteins, atypical lipopolysaccharides, and lipomannans (26–28). Among these microbial agonists, bacterial lipoproteins are by far the most potent (26, 29–31).”

“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.”

“We have previously demonstrated that proteins of B. burgdorferi are capable of modulating human cellular immune responses [7]. Suppression of in vitro mitogen- or antigen-mediated proliferative responses of lymphocytes and reduced production of interleukin-2 (IL-2) from lymphocytes were demonstrated using protein extracts of B. burgdorferi. These early studies were confirmed by a report of de Souza et al. [8], who observed that B. burgdorferi infection in mice resulted in impaired T and B cell proliferation to mitogens and reduced IL-2 and IL-4 production. The nature of the B. burgdorferi proteins responsible for suppression of cellular immunity has not been defined. In this study we examined the modulating activity of a recombinant outer surface protein A (OspA) vaccine preparation on cellular immune responses.”

“During natural infection, initiation of the host response begins with CD14 recognition of triacylated borrelial lipoproteins and subsequent activation of TLR-2 in partnership with TLR-1. Such bacterial recognition activates the NF-κB, phosphatidylinositol 3-kinase/Akt, and p38 MAPK pathways. The ensuing signaling cascades initiate inflammation-associated gene activities responsible for host defense, as well as negative regulatory pathways intended to mitigate the severity and duration of the inflammatory response to spirochetes. The latter goal is achieved, in part, through the action of p38 MAPK–induced suppressors of cytokine signaling (SOCS), which down-regulate inflammation by targeting various points in the NF-κB pathway.”

The Dattwyler OspA-is-Pam3Cys patent is actually against inhalation Inhalation Bubonic Plague.

“A lipidation/processing reaction has been described for the intact OspA gene of B. burgdorferi. The primary translation product of the full-length B. burgdorferi OspA gene contains a hydrophobic N-terminal sequence, of 16 amino acids, which is a substrate for the attachment of a diacyl glyceryl to the sulflhydryl side chain of the adjacent cysteine (Cys) residue (at position 17). Following this attachment, cleavage by signal peptidase II and the attachment of a third fatty acid to the N-terminus occurs. The completed lipid moiety, a tripalmitoyl-S-glycerylcysteine modification, is termed Pam3Cys (or is sometimes referred to herein as Pam(3)Cys or Pam3Cys). It has been suggested that the lipid modification allows membrane localization of proteins, with polypeptide portions exposed as immune targets. In addition to serving as targets for the immune response, Pam3Cys-modified proteins, such as OspA, have been reported to act as potent inflammatory stimulants though the toll-like 2 receptor mechanism (TLR2).”

“The N-terminal tripalmitoyl-S-glyceryl-cysteine (Pam3Cys) lipid moiety was absolutely required.”

Tripalmitoyl-S-Glyceryl-Cysteine-Dependent OspA Vaccination of Toll-Like Receptor 2-Deficient Mice Results in Effective Protection from Borrelia burgdorferi Challenge

19 studies-

… immune suppression induced by Borrelia-infection.

In addition, regulatory T cells might also play a role, by immunosuppression, in the development of chronic Lyme borreliosis.

These results have demonstrated an immune suppressive mechanism of B. burgdorferi.

These results demonstrate that B. burgdorferi can stimulate the production of an antiinflammatory, immunosuppressive cytokine in naive cells

OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression.

we characterized tolerance induced by B. burgdorferi, describing a model of desensitization which might mirror the immunosuppression recently attributed to the persistence of Borrelia in immunocompetent hosts.

It has been established that interleukin-10 (IL-10) inhibits inflammatory cytokines produced by macrophages in response to Borrelia burgdorferi or its lipoproteins.

viable B. burgdorferi can suppress early primary macrophages Mφ responses during infection by causing increased release of IL-10.

it is necessary to use the westernblot test which could prove the presence of specific antibodies. It is probably due to the very low production of specific antibodies caused also by the status of immune deficiency detected in all our patients (32 patients)

… a novel evasion strategy for B. burgdorferi: subversion of the quality of a strongly induced, potentially protective borrelia-specific antibody response via B. burdorferi’s accumulation in lymph nodes.

Similar results were obtained using sonicated spirochetes or lipoprotein as stimulants. Our data show that IL-10 alters effectors induced by B. burgdorferi in macrophages to control concomitantly elicited inflammatory responses. Moreover, for the first time, this study provides global insight into potential mechanisms used by IL-10 to control Lyme disease inflammation.

The data further suggest that B. burgdorferi infection drives the humoral response away from protective, high-affinity, and long-lived antibody responses and toward the rapid induction of strongly induced, short-lived antibodies of limited efficacy.

Here are 560 more examples.

PubMed Search.png


And they called this crap a vaccine..  If it causes immune *suppression* that makes it the opposite of a vaccine.

Please visit for more information than you’ll see anywhere else about this disease and others that find themselves being thrown into the waste basket by the medical community.


Holla if you wanna be a blogger.

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