The criminals knew the entire time that OspA could never have been a vaccine.

My goal is to show that they KNEW before they started injecting people with the endotoxin OspA that it could never have been a vaccine, and that you could never vaccinate against a relapsing fever germ in the first place.  This is due to antigenic variation, which means that the organism is capable of changing its outer surface proteins, which means in turn the immune system has to constantly adapt to the changes or variability of outer surface proteins (Osps).  So antibodies against only one or two of the Osps are completely useless.

LymeRix gave people the same disease as “Chronic Lyme”.

OspA = 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.  No treatment because “Lyme disease” is only a bad knee.

But most importantly- we are victims of a prosecutable crime.

We refer to the cryme as “Dearborn” and the criminals as “the Cabal”.  The case definition for “Lyme disease” was changed in 1994 at a conference set up by Barbara Johnson in Dearborn, Michigan.  Prior to this conference Allen Steere traveled to Europe to commit research fraud by changing the diagnostic criteria for the disease.  The changes that were made is the addition of the ELISA and to drop OspA and OspB (major diagnostic antigens) from western blots.  His intention was to use the ELISA to rule out all of the chronic neurologic cases (85% of patients by the way) and collude with other members of the Cabal to make sure that none of the sickest patients were included in the definition of “Lyme disease”.  We are still stuck with this two-tier testing method today.  This was all done so that they could make money by commercializing tick borne diseases, test kits, and vaccines.  If they narrowed the case definition to only the 15% bad knee type outcome then they could say “Hey, we have an 85% effective vaccine!”.

Remember, there are two completely separate outcomes of Borrelia in humans.  The problem today as we all know is that most of us cannot get diagnosed.  This is the Cryme Now onto the disease.

They are the same thing, you cannot have one without the other.

OspA is pam3cys.

pam3cys image

We’ve known for over 100 years that Relapsing Fever germs relapse and remit.  It’s what they do.  Here is a great breakdown of  The History of Relapsing Fever .

Now we will go through what the Cabal admitted to knowing prior to injecting people with triacylated lipoproteins and destroyed a bunch of lives.

Here is Allen Steere:

J Clin Invest. 1986 Oct;78(4):934-9.

Antigens of Borrelia burgdorferi recognized during Lyme disease. Appearance of a new immunoglobulin M response and expansion of the immunoglobulin G response late in the illness.

Craft JE, Fischer DK, Shimamoto GT, Steere AC.

“… Using immunoblots, we identified proteins of Borrelia burgdorferi bound by IgM and IgG antibodies during Lyme disease. In 12 patients with early disease alone, both the IgM and IgG responses were restricted primarily to a 41-kD antigen. This limited response disappeared within several months. In contrast, among six patients with prolonged illness, the IgM response to the 41-kD protein sometimes persisted for months to years, and late in the illness during arthritis, a new IgM response sometimes developed to a 34-kD component of the organism. The IgG response in these patients appeared in a characteristic sequential pattern over months to years to as many as 11 spirochetal antigens. The appearance of a new IgM response and the expansion of the IgG response late in the illness, and the lack of such responses in patients with early disease alone, suggest that B. burgdorferi remains alive throughout the illness.

Notice the date on that.  This is what pre-Dearborn guidelines were based off of.  So first he says that the antibodies keep changing, spirochetes remain alive during the entire process, and both IgG and IgM responses are most reliably to 41 KDa.  The antibodies vary over time because the Osps are variable.  Yale owns the only valid test, which is an antibody test to flagella (band 41 KDa), since it is so specific to spirochetes and doesn’t change, or vary.  Here are the guidelines that were used in 1990:

“Laboratory criteria for diagnosis
”• Isolation of Borrelia burgdorferi from clinical specimen, or
“• Demonstration of diagnostic levels of IgM and IgG antibodies to the spirochete in serum or CSF, or ”                                                                                                                                              • Significant change in IgM and IgG antibody response to B. burgdorferi in paired acute – and convalescent-phase serum samples.”



VERY different compared to what we have today.

Here is Steere talking about seronegativity in patients with neurologic symptoms:

Steere seronegative lyme

So Steere admits that patients can be seronegative and still sick and talks about how the antibody bands on western blots fluctuate over time.  Patients are seronegative because OspA is pam3cys and causes immune suppression and cross tolerance in the immune system.  He knew that antibodies to OspA and OspB alone was completely moronic and could never have been a vaccine.  Let’s continue.

Here is Barbour in 1992 talking about antigenic variation:

Screen Shot 2017-07-06 at 6.19.59 PM.png

Dattwyler in 1988 proving that fungal supernatants (like LymeRix) cause immune suppression:

“……[Figure 4] demonstrates that when lymphocytes are cultured in the presence of growing B. burgdorferi (in BSKII media) there is a marked inhibition ( p < .0005) of NK activity on days 3, 5, and 7 when compared to lymphocytes cultured in BSKII media in the absence of spirochetes. This effect is not due to a selective depletion of or toxicity to endogeneous NK since viability studies and monoclonal antibody studies demonstrate no significant changes after culture with the organism (FIG.5). The inhibition is directly attributable to the organism or its products, since supernatants from the organism cultures also inhibit endogeneous NK without prior exposure (data not shown).”

Here is Fikrig saying the same thing, that due to antigenic variation or “selection pressure” you can’t vaccinate against Borrelia Burgdorferi:

Selection of variant Borrelia burgdorferi isolates from mice immunized with outer surface protein A or B.

“A nonclonal population of Borrelia burgdorferi N40 (passage 3) that survived protective immunity following challenge inoculation of outer surface protein (Osp) A- or B-hyperimmunized mice were characterized for the molecular basis of evasion of immunity. Two of six B. burgdorferi isolates, cultured from OspA-immunized mice, had antigenic diversity in the carboxyl terminus of OspA and did not bind to the protective OspA monoclonal antibody designated IXDII. However, OspA-immunized mice challenged with these variants were fully protected. Moreover, B. burgdorferi isolates with a point mutation in ospB, which results in a truncated OspB that does not bind to protective OspB monoclonal antibody 7E6C, were frequently enriched after infection of OspB-immunized mice. These studies suggest that the incomplete efficacy of an OspA- or OspB-based vaccine may be partly due to immunomediated in vivo selective pressure, resulting in the persistence of some spirochetes that do not bind to protective antibodies.”

Another from Fikrig:

The Lyme disease vaccine takes its toll.

“Vaccination with Borrelia burgdorferi outer surface protein (Osp) A can induce a protective response against Lyme disease and serves as a model to understand the generation of protective immune responses against the spirochete. The innate response to pathogens is activated by specific Toll-like receptors (TLRs) that recognize distinct pathogen-associated molecular patterns. TLR2 is of particular interest for B. burgdorferi research because TLR2 recognizes several pathogen-associated molecular patterns, including lipoproteins. TLR2 may form heterodimers with TLR6 to identify diacylated lipoproteins, while TLR2 works in concert with TLR1 to recognize triacylated lipoproteins such as OspA. We will discuss the role of TLR1/2 in the development of responses to OspA in TLR1-and TLR2-deficient mice, and in selected individuals that received the OspA vaccine. While > 95% of human OspA-based Lyme disease vaccine recipients develop OspA antibodies, a very small group of individuals did not develop detectable humoral responses against OspA. We demonstrated that this hyporesponsiveness to OspA vaccination was associated with decreased cell surface expression of TLR1. Moreover, TLR1- and TLR2-deficient mice did not develop significant levels of OspA antibodies following vaccination with OspA, providing a correlation with human hyporesponsiveness to OspA. These data suggest that defects in the TLR1/2 signaling pathway are associated with an impaired ability to generate antibodies following immunization with OspA lipoprotein.

One more from Fikrig:

Hyporesponsiveness to vaccination with Borrelia burgdorferi OspA in humans and in TLR1- and TLR2-deficient mice.

“The Lyme disease vaccine is based on the outer-surface lipoprotein (OspA) of the pathogen Borrelia burgdorferi, and 95% of vaccine recipients develop substantial titers of antibodies against OspA. Here, we identified seven individuals with very low antibody titers after vaccination (low responders). The macrophages of low responders produced less tumor necrosis factor-alpha and interleukin-6 after OspA stimulation and had lower cell-surface expression of Toll-like receptor (TLR) 1 as compared to normal cells, but normal expression of TLR2. TLRs activate innate responses to pathogens, and TLR2 recognizes lipoproteins and peptidoglycan (PGN). After OspAimmunization, mice genetically deficient in either TLR2 (TLR2(-/-)) or TLR1 (TLR1(-/-)) produced low titers of antibodies against OspA. Notably, macrophages from TLR2(-/-) mice were unresponsive to OspA and PGN, whereas those from TLR1(-/-) mice responded normally to PGN but not to OspA. These data indicate that TLR1 and TLR2 are required for lipoprotein recognition and that defects in the TLR1/2 signaling pathway may account for human hyporesponsiveness to OspA vaccination.”

So there Fikrig is saying in 2002 that OspA causes immune suppression.  Which is ironic given that Valneva, a French company, is starting a new trial for a Lyme vaccine THIS YEAR.  Clinical trials are starting in only a few short months here in the United States and Belgium.  Guess what the vaccine antigen is?



Nebraskans, get on your phones and tell your Representatives to stop this immediately.

Here are links with more information:

That vaccine worked by injecting people with an outer surface protein of Borrelia, called OspA. This taught the body’s immune system to recognize the bacteria — and launch an attack if they showed up after a bite from an infected tick.

But the protein in US Borrelia isn’t the same as it is in European species of the bacteria, or even from one region to another. There are six different types. That’s something LYMErix didn’t address, so Valneva-funded researchers based their vaccine on all different kinds of OspA to cover US and European strains of Borrelia.

Business Insider Article- Lyme Vaccine OspA


Lastly, here is one of the many reports that exist telling us the same thing that TruthCures has been this whole time.  Most of the information pertaining to the content of this particular post are in the Occam’s Razor Report:

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

“Toll-like receptors (TLRs) trigger innate immune responses via the recognition of conserved pathogen-associated molecular patterns. Lipoproteins from Borrelia burgdorferi, the agent of Lyme disease, activate inflammatory cells through TLR2 and TLR1. We show that stimulation of human monocytes with B. burgdorferi lysate, lipidated outer surface protein A, and triacylated lipopeptide Pam3CysSerLys4 results in the up-regulation of both TLR2 and TLR1 but the down-regulation of TLR5, the receptor for bacterial flagellin, and that this effect is mediated via TLR2. TLR4 stimulation had no effect on TLR2, TLR1, and TLR5 expression. Human monocytes stimulated with TLR5 ligands (including p37 or flaA, the minor protein from B. burgdorferi flagella) up-regulated TLR5. In addition, TLR2 stimulation rendered cells hyporesponsive to a TLR5 agonist. These results indicate that diverse stimuli can cause differential TLR expression, and we hypothesize that these changes may be useful for either the pathogen and/or the host.”


So there you have it.  They knew that “Lyme disease” was a Relapsing Fever germ capable of antigenic variation that sheds fungal lipoproteins and wrecks humans, therefore it could never have been a vaccine.  It seems that they also know that the disease was largely about immune suppression and that you can’t kill spirochetes.  They knew that patients could be seronegative and Dattwyler is the one who says that these are the sickest patients.

Just for fun- Mark Klempner on HLA and differences in outcomes from “Lyme disease”.  Right now the only type of the disease that is allowed to be diagnosed and treated is the HLA linked hypersensitivity response that accounts for only 15% of cases.  The other 85% are the chronic neurologic cases and this type of the disease has been ruled out of the case definition for one reason- stupid criminals wanted to commercialize tick borne diseases for financial gain.  The cryme is the disease, the disease is the cryme:

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