TRUTH and Lyme Vaccines


A vaccine to prevent Lyme disease is being fast-tracked for approval by the U.S. Food and Drug Administration to address what public health officials say is the most rapidly growing vector-borne disease in the United States.

Currently, there is no Lyme vaccine for humans, although one is available for dogs. The human vaccine being expedited for approval by the FDA is known in its preapproval phase as VLA15, a product of French vaccine-maker Valneva. Only 180 participants in a preliminary clinical trial have received the inoculation so far.

Valneva has been authorized to move its research into the FDA’s program called Fast Track. Designated products are aimed at unmet medical needs, agency officials said.

“The incidence of Lyme disease has increased dramatically,” said Dr. Benjamin Luft, the Edmund D. Pellegrino Professor of Medicine at Stony Brook University and a specialist in infectious diseases. He said the number of people who have contracted Lyme disease and other tick-related illnesses has risen as the bugs have expanded their range.

The Borrelia burgdorferi bacterium, which causes Lyme disease, is shown in this electron micrograph image. Photo Credit: Alamy Stock Photo / RGB Ventures

Luft, who himself has developed a Lyme vaccine, said that any inoculation aimed at Borrelia burgdorferi — the bacterium that causes Lyme disease — must address the variations seen in the organism. Otherwise, he said, the vaccine is of no benefit to those who receive it.

( See Antigenic Variation below )

Luft’s vaccine was licensed to the Illinois-based Baxter pharmaceutical company, but the license now is held by Shire Plc, he said.

Shire, with headquarters in Dublin, Ireland, acquired Baxter’s biopharmaceutical division last year.

Valneva officials, meanwhile, said their vaccine appears to be effective against the six most common types of B. burgdorferi that are prevalent in the United States and Europe. Under the fast-track designation, the company will advance to a larger clinical study of the vaccine early next year.

Dr. Benjamin Luft, the Edmund D. Pellegrino Professor of Medicine at Stony Brook University and a specialist in infectious diseases, is shown on Sept. 6, 2016. Photo Credit: Ed Betz



Before you and your loved ones start lining up, you may want to take a look back at it’s predecessor LYMErix.

Antibody is taken up into tick and bacteria destroyed in vector. 0, 1 and 12 months. As of February 25, 2002 LYMErix™ off the market.
Lyme Disease Vaccine (Recombinant OspA)
LYMErix [Lyme Disease Vaccine (Recombinant OspA)] is a
noninfectious recombinant vaccine developed and manufactured by SmithKline Beecham Biologicals. Thecausative agent of Lyme disease is Borrelia burgdorferi; in
North America, all Lyme disease is due to Borrelia burgdorferi sensu stricto. The vaccine contains lipoprotein OspA, an outer surface protein of Borrelia burgdorferi sensu stricto ZS7, as expressed by Escherichia coli. Lipoprotein OspA is a single polypeptide chain of 257 amino acids with lipids covalently bonded to the N terminus. No substance of animal origin is used in the commercial manufacturing
process. Fermentation media consist primarily of inorganic salts, and vitamins, with small quantities of antifoam (contains silicon), kanamycin sulfate (anaminoglycoside
antibiotic), and yeast extract. Silicon and kanamycin are removed to levels below detection ( <7 ppm and <10 ppb,respectively). The vaccine is adsorbed onto aluminum hydroxide.
LYMErix is supplied as a sterile suspension in single-dose vials and prefilled syringes for intramuscular administration. The vaccine is ready for use without reconstitution; it must be shaken before administration to ensure a uniform turbid
white suspension.
Each 0.5mL dose of vaccine consists of 30 mcg of lipoprotein OspA adsorbed onto 0.5 mg aluminum as aluminum hydroxide adjuvant. Each dose of the vaccine
preparation contains 10 mM phosphate buffered saline and 2.5 mg of 2 phenoxyethanol, abacteriostatic agent.


Remember OspA is a Triacylated-lipoprotein, Pam3cys! It is a TLR2/1 agonist or a fungal toxin, which turns off the immune response to prevent death from septic shock. OspA can not be a vaccine because it is what causes the disease, not the spirochetes! If you have [Lyme], you have LYMErix, if you had LYMErix, you have [Lyme].

and they shed their outer surface in a mechanism called blebbing.


Through “antigenic variation,” or the ability to modify their outer surface proteins (Osps), the organism causes “relapsing fever.” Because the host immune response, (your immune system), must constantly address the variable antigens, (an antigen is a harmful substance that causes the body to produce antibodies). For this reason, it is not possible to vaccinate against borrelia.

“1986, Alan Barbour. Spirochetes bleb or pinch off bits to release its surface proteins stealth bombing or turning off the immune system. “It’s using some sort of stealth-bomber-type mechanism,” he says. Or, using another diversionary tactic called blebbing, the spirochete can pinch off bits of its membrane in order to release its surface proteins. “It’s like a bacterial Star Wars defense program.”


     Both the vaccine and Borrelia Burgdorferi contain OspA, a highly toxic immune-suppressing triacyl lipoprotein, (“a lipoprotein is a biochemical assembly whose purpose is to transport hydrophobic lipid (a.k.a. fat) molecules in water, as in blood or extracellular fluid.”).Lipoproteins in bacteria: structures and pathways

LYMErix Vaccine Adverse Events Reports

Below is a diagram of the new Lyme vaccine VLA15. Look carefully and see if anything looks familiar. No, you don’t need to be a chemist to see it.

Pic 1 lyme vaccine

Figure 1. Localization of the stabilizing disulfide bonds and schematic representation of the heterodimers.
Left panel: Part of the OspA serotype 1 crystal structure showing the monomer protein (Protein Data Bank accession 1OSP [34]). Locations of the five modifications: “A” (aa 141∶ 241), “B” (aa 182∶ 269), “C” (aa 244∶ 259), “D” (aa 165∶ 265) and “E” (aa 182∶ 272) are indicated as dotted lines between the β-carbon atoms of the corresponding residues. Right panel: Schematic illustration of two stabilized monomers joined with a linker sequence to form one heterodimer. The α-helix at the C-terminal end of the first monomer is joined with the β-sheet at the N-terminal domain of the second monomer using a linker sequence derived from burgdorferi OspA serotype 1 (L1; aa 43–53 with modification [D53S] and L2; aa 65–74). The heterodimer is expressed with a posttranslationally attached N-terminal lipid moiety, indicated in line drawing. The positions of the disulfide bonds for stabilization “B” in both OspA monomer subunits are indicated in magenta. Abbreviations: N-terminal (N-term.), C-terminal (C-term.).



A fragment of a molecule, especially one that comprises an identifiable unit, e.g. an acetyl or pyridoxal phosphate group, a regulatory subunit.

Lipids: The Essential Metabolites

Lipids are hydrophobic or amphipathic small molecules which include fats, waxes, sterols, fat-soluble vitamins (such as vitamins A, D, E and K), monoglycerides, diglycerides and phospholipids. The crucial role of lipids in a cell, tissue and organ physiology is evident by their unique membrane organizing properties that provide cells with functionally distinct subcellular membrane compartments.

The main biological functions of lipids include:

  1. Energy storage and structural components of cellular membranes.
  2. Cell signaling (e.g. phospholipase C and phospholipase A2 in modulating immunological responses).
  3. Endocrine actions (e.g. steroid hormones)
  4. Essential role in signal transduction, membrane trafficking and morphogenesis.

Classification of Lipids

Lipids can be classified into 8 classes based on their chemical structure:

1. Fatty Acyls [FA]
 Fatty Acyls - Structure of Palmitic Acid The fatty acyls are a diverse group of molecules synthesized by chain elongation of an acetyl-CoA primer with malonyl-CoA (or methylmalonyl-CoA) groups that may contain a cyclic functionality and/or are substituted with heteroatoms.
Ex: Palmitic Acid

Did you figure it out yet?

Yup, they both have Triacyl (meanining 3) fatty acids or lipoproteins, Pam3cys, fungal antigen, immunosuppresive, TLR2/1 agonists attached to the N-terminals. 

Did you know;

CDC officers falsified research to fraudulently qualify the LYMErix vaccine.  They used high-passage, plasmid-dropping strains (leaving out antigens OspA and B) and knowingly raised the cutoff for the ELISA, leaving out all the neurological cases. This effectively changed the definition of the disease, from relapsing fever Borreliosis to Steere’s Knees, a purely arthritic knee outcome. The sickest people cannot get a diagnosis, and the arthritis cases likely are not looking for one! This is proven by publicly available information from the 1994 Dearborn conference along with a parallel, secret report that illustrates how the research fraud was perpetrated. We want nothing less than USDOJ prosecution of these heinous acts.




As the saying goes, “Those who fail history are destined to repeat it”. I say those who repeat it are destined to fail.

I don’t know about you but I’m not getting in line.







Of Tolerance and TRUTH

          Have you ever heard the saying, “What you don’t know can’t hurt you”, or, “Ignorance is bliss”? Well I’m here to tell you it’s a lie. [Lyme Disease], or more correctly Relapsing Fever Borrelliosis/Post-Sepsis Syndrome does hurt in more ways than one. It’s real! The physical, mental and financial toll it takes. The lives of millions that are destroyed. Most likely what you do know from either your own experience or from what you have been told is only the tip of the iceberg.

Oh, and there’s so very much more underneath. Deliberately being hid from you so that the crooks who changed the case definition could profit off of testing and vaccines at your expense. Yup, lies upon lies, upon lies.


Did you know that spirochetes attack and permanently destroy your immune system? Did you know that their outer surface proteins (Osps), are shed and are variable, so as to evade your immune system? It’s to keep your body from making antibodies. The 2-tiered test was designed to only detect 15% of those who have a HLA-linked gene, not the 85% of us with debilitating neurologic symptoms and immunosuppression.

How many really understand what this damage does, and how it is basically permanent and the allusion to a cure from such as ILADS is false? To fully understand how your immune system is damaged you must look below the surface of lies and the fraud of the perpetrators of the LYME CRYME against humanity. Of misinformed, (however well-meaning ), friends, doctors, and yes, Facebook “Experts”.

You have to follow the science, connect the dots and think critically for yourself. Your life as well as countless others depends on it.

A Osp is an outer surface protein on a spirochete.  They are labeled alphabetically, coincidentally the first one OspA is the most important to understand.  OspA is band 31 on a western blot and it was the antigen of choice for the late (and not so great) vaccine. The western blot is measuring antibodies, so band 31 is the antibody that your body produces against OspA.

When you look at the structure of OspA, it is Pam3Cys.  A triacyl lipoprotein.


It has a tri-acyl (3 fatty acids) structure.  Pam3cys is a molecule that when inside the body it basically STOPS the typical immunity chain reaction and ends in immune suppression and immune tolerance.  Immune tolerance is when your body stops recognizing all kinds of pathogens. It’s basically an AIDS (ACQUIRED immune deficiency) in most of us. Pathogens that were once kept at bay by a healthy immune system now become rampant. They are called opportunistic infections because that’s what they do. They take the opportunity to attack due to a damaged immune response and wreak havoc in our bodies. Epstein-barr, the Herpes viruses like HHV-6, Parvo, Cytomegalovirus, systemic Candida, even cancer such as Lymphoma are some opportunistic pathogens.

     HIV-Aids affects the T cells while Lyme-Aids affects the B cells of the immune system.

Spirochetes shed (or bleb) their Osps as a way to evade to your immune cells.  So you have all these little lipoproteins floating around.  The blebs have the Osps on them.  Immune cells, like B cells, come along and eat these lipoproteins up. OspA and the other Osps are triacyl, which means FUNGAL (due to the fact that they are managed by TLRs 2 and 1), so when an immune cell eats this up it effectively turns the cell off and renders it useless.  Imagine an immune cell as a little ball  with little spiky things sticking out of it. The spiky things are called TLR’s which stand for Toll-Like Receptors.  The job they do is recognizing pathogens and telling everyone else about the invader.  They are all numbered 1, 2, 3, 4…..etc.

spirochetes shed highly acylated TLR2/1 agonists, turning off the immune system, AKA “Post-Sepsis Syndrome

spirochete with blebsOspA = pam3cys = unfixable immune suppression = immune tolerance to other pathogens = reactivated viruses + opportunistic pathogens = Post Sepsis Syndrome.  Life ruined.  Antibiotics can’t fix this.  EBV mostly causes the “Great Imitator” outcomes, think the likes of MS, ALS, etc .  No treatment because “Lyme disease” is only a bad knee. (More about this another day).

          OspA is a TLR 1/2 agonist. Which is exactly what it sounds like, bad.  Once an immune cell eats up these lipoproteins it is broken. More  IMPORTANTLY , Immune tolerance spreads to your other TLRs (cross-tolerance). All the different TLR’s recognize different stuff.  So TLR 1/2 deals with fungi, and humans just can’t take fungi. We say it is a fungal-like antigen because of what TLR manages it. Immune tolerance means that your immune system is broken in a very general sense.  It means that you can’t recognize or kill germs of all different kinds.So, now you have incompetent immune cells – almost like STUNNED or zombie  immune cells – floating around, because the Osps are fungal-ish or triacylated lipoproteins.  It is immune-suppressive because of what it does to your TLR’s; it creates cross-tolerance to other TLR’s.  So eventually its an AIDS outcome.  This damage is what CANNOT be fixed by standard ILADS treatments like antibiotics or herbal protocols.  It just won’t.  If patients initially feel better with these types of treatments?  Well, that’s anecdote.  Hearsay.  At best it’s just taking out whatever other pathogens they have and providing temporary relief.  Not the majority or we would have known about it by now and the mechanism for these cures would be published. Symptoms will naturally wax and wane anyway as spirochetes are Relapsing Fever organisms, and especially due to the opportunistics like mycoplasma and the reactivated herpesviruses.
Medvedev and Cross-Tolerance; Medvedev talking about Immunosuppression from Post-Lyme and Post-LYMErix Sepsis (TLR2-agonists or Pam3Cys is OspA or shed borrelial antigens)

IRAK4 kinase activity is not required for induction of endotoxin tolerance but contributes to TLR2-mediated tolerance

“Development of endotoxin tolerance following the initial “cytokine storm” phase of sepsis is thought to protect the host from an overexuberant immune response and tissue damage but at the same time, may render the host immunocompromised and more susceptible to secondary infection [18,–20]. …

“Reprogramming [21] of TLR4 signaling in endotoxin-tolerant monocytes and macrophages does not occur as a result of decreased TLR4 expression but involves altered recruitment, tyrosine phosphorylation, and K63-linked polyubiquitination of proximal receptor-adapter-kinase complexes [22,–27] and induction of negative regulators IRAK-M, SHIP1, and A20 [24, 25, 28]. Although a few studies have sought to dissociate kinase and adapter functions of IRAK4 in IL-1R/TLR signaling, albeit with conflicting results [13,–16, 29,–31], it is unclear how IRAK4 kinase activity affects induction of TLR2 and TLR4 homo- and heterotolerance. To address these questions, we used IRAK4KDKI mice to determine the impact of kinase deficiency of IRAK4 on the induction of TLR tolerance. Our data showed comparable induction of endotoxin tolerance in WT or IRAK4KDKI PMs and BMDMs, as judged by attenuated MAPK phosphorylation, inhibited expression of proinflammatory cytokines and chemokines, and up-regulation of negative TLR regulators, A20 and IRAK-M. Notably, IRAK4 kinase activity was found to be a prerequisite for conferring inhibition of LPS-inducible JNK and p38 MAPK activation following prior exposure to Pam3Cys. These results represent the first systematic analyses of the role of IRAK4 kinase activity in TLR homo- and heterotolerance and pave the way for improved understanding of how IRAK4 kinase dysregulation may underlie immunocompromised states in late sepsis.”

Why call it Post-Sepsis Syndrome?

Due to the intense inflammatory response of the body caused by an infectious process, a phenomenon called endotoxin tolerance takes place in order to prevent acute organ failure and death.

“In response to tissue damage or an infection, innate immune cells will secrete many
inflammatory mediators to produce an inflammatory response. This occurs through innate cells, such as macrophages, due to the pattern recognition receptors (PRR) they possess on their surface. Toll-like receptor 4 (TLR4) is a member of the PRR family which is responsible for recognising gram-negative bacteria and their endotoxins, such as Lipopolysaccharide (LPS). This recognition allows the initiation of the inflammatory response that is firmly regulated throughout the immune system to prevent uncontrolled inflammation, which can lead to endotoxic shock, tissue damage and pathologies (Beutler, 2004).
The immune system has developed a defence mechanism against endotoxic shock thus preventing harmful pathologies like sepsis. Defined as a temporary hypo-responsiveness, endotoxin tolerance (ET) is known as one of these mechanisms (Ishiyama et al, 2006).
ET is characterised by a reduced production of cytokines when a pro-inflammatory stimulusis incurred. It occurs after an initial low dose of an endotoxin which renders the cell unresponsive when endotoxin is encountered for the second time(Biswas & Lopez-Collazo, 2009). This reduces the toxic effect of high levels of inflammatory mediators (Ishiyama et al, 2006).
“….immunosuppression that is present in sepsis has its purpose, which is to eliminate the significant proinflammatory activity initiated by the infectious agent….”

Immunotherapy of Sepsis: Blind Alley or Call for Personalized Assessment? (PDF Download Available). Available from: [accessed Aug 19, 2017].

“In a rapid and strong inflammatory response
such as during infections leading to sepsis, the role of adaptive
immunity might be lost due to the prompt development of events
plus the fact that their responses may be impaired due to the
profound depletion of T and B cells (68), leaving endotoxin
tolerance as the main mechanism to control inflammation.
Nevertheless, this suppressed-inflammatory/wound-healing state
would likely be dangerous if sustained for a prolonged period, as
the strong immunosuppression might lead to susceptibility to
secondary infections, increasing the risk of death.”

“Endotoxin tolerance protects the host by limiting excessive ‘cytokine storm’ during sepsis, but compromises the ability to counteract infections in septic shock survivors. It reprograms Toll-like receptor (TLR) 4 responses by attenuating the expression of proinflammatory cytokines without suppressing anti-inflammatory and antimicrobial mediators, but the mechanisms of reprogramming remain unclear. In this study, we demonstrate that the induction of endotoxin tolerance in human monocytes, THP-1 and MonoMac-6 cells inhibited lipopolysaccharide (LPS)-mediated phosphorylation of Lyn, c-Src and their recruitment to TLR4, but increased total protein phosphatase (PP) activity and the expression of protein tyrosine phosphatase (PTP) 1B, PP2A, PTP nonreceptor type (PTPN) 22 and mitogen-activated protein kinase phosphatase (MKP)-1. Chemical PP inhibitors, okadaic acid, dephostatin and cantharidic acid markedly decreased or completely abolished LPS tolerance, indicating the importance of phosphatases in endotoxin tolerization. Overexpression of PTPN22 decreased LPS-mediated nuclear factor (NF)-x03BA;B activation, p38 phosphorylation and CXCL8 gene expression, while PTPN22 ablation upregulated LPS-induced p65 NF-x03BA;B and p38 phosphorylation and the expression of TNF-α and pro-IL-1β mRNA, indicating PTPN22 as an inhibitor of TLR4 signaling. Thus, LPS tolerance interferes with TLR4 signaling by inhibiting Lyn and c-Src phosphorylation and their recruitment to TLR4, while increasing the phosphatase activity and expression of PP2A, PTPN22, PTP1B and MKP1.

© 2015 S. Karger AG, Basel.

          When they made the vaccine, LYMErix, they also made the disease. The disease is the vaccine the vaccine is the disease. That’s why a brave whistleblower came forward, that’s why it was really removed from the market! It’s not [LYME]! It really never was and if you look at the pre-1994 research by these same criminals you can read, ( in their own words ), what it was and STILL is!
          In 1994 in Dearborn, Michigan the diagnostic criteria for Relapsing Fever Borrelliosis [Lyme Disease], was changed.

          Pam3Cys is the basic molecule of LYMErix or OspA and others shed by Borrelia:
A20 is critical for the induction of Pam3CSK4-tolerance in monocytic THP-1 cells.

“A20 functions to terminate Toll-like receptor (TLR)-induced immune response, and play important roles in the induction of lipopolysacchride (LPS)-tolerance. However, the molecular mechanism for Pam3CSK4-tolerance is uncertain. Here we report that TLR1/2 ligand Pam3CSK4 induced tolerance in monocytic THP-1 cells. The pre-treatment of THP-1 cells with Pam3CSK4 down-regulated the induction of pro-inflammatory cytokines induced by Pam3CSK4 re-stimulation. Pam3CSK4 pre-treatment also down-regulated the signaling transduction of JNK, p38 and NF-κB induced by Pam3CSK4 re-stimulation. The activation of TLR1/2 induced a rapid and robust up-regulation of A20, suggesting that A20 may contribute to the induction of Pam3CSK4-tolerance. This hypothesis was proved by the observation that the over-expression of A20 by gene transfer down-regulated Pam3CSK4-induced inflammatory responses, and the down-regulation of A20 by RNA interference inhibited the induction of tolerance. Moreover, LPS induced a significant up-regulation of A20, which contributed to the induction of cross-tolerance between LPS and Pam3CSK4. A20 was also induced by the treatment of THP-1 cells with TNF-α and IL-1β. The pre-treatment with TNF-α and IL-1β partly down-regulated Pam3CSK4-induced activation of MAPKs.

Furthermore, pharmacologic inhibition of GSK3 signaling down-regulated Pam3CSK4-induced A20 expression, up-regulated Pam3CSK4-induced inflammatory responses, and partly reversed Pam3CSK4 pre-treatment-induced tolerance, suggesting that GSK3 is involved in TLR1/2-induced tolerance by up-regulation of A20 expression. Taken together, these results indicated that A20 is a critical regulator for TLR1/2-induced pro-inflammatory responses.”

          TLR2/1-induced tolerance or LYMErix or Lyme tolerance is a thing, like Endotoxin Tolerance, only worse, since so far it is not reversible. In other words, IDSA and the CDC have no idea what they are talking about, and this concerns every major disease, if not every disease.        

          Patents had been bought and the process for controlling the outcome of the efficacy of a vaccine and the monopoly of Tick Borne Disease Testing was firmly in place. Rubbing their greedy hands together, they sat back and waited for the profits to come rolling in!
          I don’t know how that makes you feel? I know I’m really “ticked” off! I know I won’t stop speaking the TRUTH until these criminals are prosecuted and all involved are served JUSTICE. Then, and ONLY then, can research based on the TRUTH go forward. Only then can we receive care with dignity, with treatments that work and are covered by insurance.
          First, the TRUTH. Then, the CURE. WE must demand the DOJ prosecute the criminals!














     So what’s in a name you may ask? A lot sometimes, and othertimes, well not so much.

     [Lyme Disease] was originally known as a “relapsing fever” or borreliosis, due to the taxonomy,

(the branch of science concerned with classification, especially of organisms; systematics.

  • the classification of something, especially organisms.),

and nature of the organism that causes the disease. Spirochetes are their own phylum,



  1. a principal taxonomic category that ranks above class and below kingdom.),

 and they shed their outer surface in a mechanism called blebbing.


Through “antigenic variation,” or the ability to modify their outer surface proteins (Osps), the organism causes “relapsing fever” because the host immune response, (your immune system), must constantly address the variable antigens, (an antigen is a harmful substance that causes the body to produce antibodies). For this reason, it is not possible to vaccinate against borrelia.

“1986, Alan Barbour. Spirochetes bleb or pinch off bits to release its surface proteins stealth bombing or turning off the immune system. “It’s using some sort of stealth-bomber-type mechanism,” he says. Or, using another diversionary tactic called blebbing, the spirochete can pinch off bits of its membrane in order to release its surface proteins. “It’s like a bacterial Star Wars defense program.”


     Both the vaccine and Borrelia Burgdorferi contain OspA, a highly toxic immune-suppressing triacyl lipoprotein, (“a lipoprotein is a biochemical assembly whose purpose is to transport hydrophobic lipid (a.k.a. fat) molecules in water, as in blood or extracellular fluid.”).Lipoproteins in bacteria: structures and pathways

 OspA is Pam3cys or a TLR2/1 agonist.

OspA structure: it is a triacyl lipoprotein ,as you can see below, it has 3 acyl groups.


     You got the vaccine.  Everyone with Lyme got LYMErix. This is what LYMErix is, and how this vaccine-was-the-disease works:

It’s Pam3Cys or a triacylated lipoprotein; the degree of acylation is equated with its toxicity. 

So what is acylation?  It’s the zig-zaggy lines that mean Carbon-Carbon-Carbon, yes, hydrocarbons, like margarine or octane. Exactly, the name just refers to the number of carbons in each carboxyl or acyl group.  Palmitic (the Pam in Pam3Cys) has X number of carbons, gasoline, 8, linoleic acids, like 14. Look up what are alkanes then add a COOH group and you have one of these fatty acids.
Something highly acylated like this (3 or more fatty acids hanging off) are managed by Toll-like Receptor (TLR) 2 and TLR1, together. Therefore a “TLR2/1-agonist” is another term that generally refers to lipoproteins like those from Borrelia, mycoplasma, mycobacteria, and others, like Brucella. (But they can manage other compounds.)

Pam3Cys and fungal lipid molecules like it, is shed with these blebs.

“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”

“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…”  —Energy Science News,  [full article: BrookhavenStealthBacteria]

     TLR2/1 agonists cause tolerance, (Immune tolerance. From Wikipedia, the free encyclopedia. … Immune tolerance, or immunological tolerance, or immunotolerance, is a state of unresponsiveness of the immune system to substances or tissue that have the capacity to elicit an immune response in a given organism), and cross tolerance, (extension of the tolerance for a substance to others of the same class, even those to which the body has not been exposed previously), to other TLR’s to no longer detect or fight this or other pathogens. It’s like non-HIV AIDS, where it causes immunosuppression and all the other infections that the immune system was able to keep under control are now able to rear their ugly heads and wreak havoc in your body. From HHV-6, Epstein-barr, Cytomegalovirus, Zoster, Candida, Coxsackievirus, Mycoplasma, Babesiosis, PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections), etc.. OspA is the culpret in both vaccine and Lyme. It causes permanent immunosuppression. The lymph nodes and brain are targeted, causes chronic encephalopathy, mutated B-cells and “The Great Neuro-Degenerative Imitator”…. ALS, MS, lupus, parkinsons, Autism, ADHD/ADD, dementia, alzhiemers, stroke, cancer, schizophrenia, seizure disorder, Huntington’s, mitochondrial disease, myasthenia gravis, autoimmune encephalitis, chronic fatigue syndrome, fibromyalgia, etc..

The perfect stealth pathogen because immunosuppressed victims produce no to little antibodies (think serongative test results),. The Dearborn fraud changed the testing to a high antibody concentration. So the immune-suppressed neurological B-cell AIDS victims cannot get a positive test nor a diagnosis. This was the whole purpose of Dearborn, it hid their vaccine injuries. The current definition says you can only have Lyme if you have high antibodies and arthritic Lyme with no other symptoms.

CDC 2017 Case Definition

You can’t have a vaccine against a disease known to shed surface antigens that are fungal and known to cause immunosuppression.  Notice there are no vaccines against Tuberculosis or other fungal diseases.  To get around this scientific dilemma, CDC staff who own patents for vector borne diseases (,(American Lyme Disease Foundation, a Non-non profit), simply declared that only the hypersensitivity or HLA-linked allergy outcome would be allowed to be a “case” of “Lyme disease” at a fake consensus conference in Dearborn, Michigan, in 1994. Only 15% of cases test positive.

AND SERONEGATIVE DISEASE (Note that if Wormser owns stock in Abbott- they won’t produce a real
test for Lyme; an Abbott representative was at the Congressional Hearing 120717.):




Here we see Gary Wormser talking about immunosuppression from Lyme and LYMErix, yet how could that be if he also insists the Dearborn standard is real,… and subsequently Klempner’s Non-Retreatment non-study, upon which the

IDSA , (Infectious Disease Society of America),”guidelines” are based? IDSA guidelines for Lyme Disease

The crux of the crime is the  Dearborn diagnostic standard.


Note that Gary Wormser above discusses the mechanism of seronegative Lyme and the resultant immunosuppression
from exposure to OspA either thru blebbing or vaccination, resulting in LYMErix Disease being the same disease as Chronic Lyme/Great Imitators.

Tolerance and Cross Tolerance 
“we propose that TLR2 signaling induces rapid depletion of IRAK1, which impairs IFN-I induction by TLR7/9. This novel mechanism, whereby TLR2 inhibits IFN-I induction by TLR7/9, may shape immune responses to microbes that express ligands for both TLR2 and TLR7/TLR9, or responses to bacteria/virus coinfection.”
B-cells are mutated 
“immature B cells can also be seen in the spinal fluid.  These cells can appear quite atypical- not unlike those of transformed or neoplastic lymphocytes.”

Lymph nodes are targeted
Together, these findings suggest 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.”

Chronic Encephalopathy  
Bacterial lipoproteins can disseminate from the periphery to inflame the brain. “We conclude that some bacterial lipoproteins can disseminate from the periphery to inflame the brain”  ttps://


“Steere’s original, 1986, Lyme-diagnostic serology report which resulted in the 1990 CDC standard (and says Lyme is Relapsing Fever, and that the only valid antibody to use to detect all cases of Lyme was flagellin, or band 41):

A snippet from that 1986 report:

The above was mentioned at the 2001, Jan, FDA Meeting on LYMErix Adverse Events by Kathleen Dickson:  “The standard changed at Dearborn, Lyme used to be considered Relapsing Fever according to Allen Steere, above, people with LYMErix Disease are like chronic Lyme victims, and that could be because of the immunosuppression as per Mario Philipp (OspA results in the production of the immunosuppressive cytokine IL-10) and Ray Dattwyler’s NK cell suppression studies):

1990 CDC Serology standard (same as Steere’s 1986 report; means Lyme is Relapsing Fever):
1990 Case Definition for “Lyme Disease” was “Relapsing Fever”








Dearborn Invitations (connotes consensus, but it was not):, Who Approved:

Dearborn booklet (111 pages) showing no one agreed with Steere’s proposal and who was on all the committees

Gary Wormser’s peer-reviewed assessment of Steere’s Dearborn proposal where he says only 9/59 patients met the Steere/Dearborn  criteria for IgG (85% of cases are missed):

 Page 74 of the Dearborn booklet – Gary Wormser saying the Steere proposal sucked.  Here is the full text of that assessment:

 (missed 85% of the cases). This was deliberate so that they could say that the “vaccine” worked.

So, hopefully by now you can begin to see the BIG picture about what is, and is NOT [Lyme], and why Chronic Lyme is denied.

It doesn’t exist. No disease. No Treatment. NO CURE!

This is why the Lyme Cryme has to be prosecuted.



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