Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."

07/25/2016 16:41:51


Predicting all of  Bush's warcrimes, Oct 2000

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151218 Merck's MMR monograph

151127 Predicting Bush's warcrime results, Fawaz Gerges

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CDC/Yale/IDSA: "LYMErix causes  same multisystem disease" as 'Chronic Lyme'"  OspA is a fungal toxin causing immunosuppression



Whoever does not know what LYMErix-disease is does not know what Lyme disease is.  This includes and all of the Lyme non-profits.  One has to know what the antigen is, in order to know what it does.  This is basic science.


Norman Latov on how OspA vaccination caused the same disease as chronic Lyme:

Neuropathy and cognitive impairment following vaccination with the OspA protein of Borrelia burgdorferi.
“Neurological syndromes that follow vaccination or infection are often attributed to autoimmune mechanisms. We report six patients who developed neuropathy or cognitive impairment, within several days to 2 months, following vaccination with the OspA antigen of Borrelia burgdorferi. Two of the patients developed cognitive impairment, one chronic inflammatory demyelinating polyneuropathy (CIDP), one multifocal motor neuropathy, one both cognitive impairment and CIDP, and one cognitive impairment and sensory axonal neuropathy. The patients with cognitive impairment had T2 hyperintense white matter lesions on magnetic resonance imaging. The similarity between the neurological sequelae observed in the OspA-vaccinated patients and those with chronic Lyme disease suggests a possible role for immune mechanisms in some of the manifestations of chronic Lyme disease that are resistant to antibiotic treatment.”


Gary Wormser on OspA causing immunosuppression (which means it was the opposite of a "vaccine"):

Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA).
”… After exposure to either the unaltered vaccine preparation or OspA prepared in saline, normal lymphocyte responses to the mitogens concanavalin A, phytohemagglutinin-M or pokeweed mitogen, or the antigen BCG were consistently reduced. Whole cell extracts of B. burgdorferi also modulated immune responses but required a much greater quantity of protein than needed for theOspA preparation. 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 theOspA molecule responsible for this effect may lead to improved vaccine preparations.”





Donald H. Marks on how LYMErix caused the same disease as chronic Lyme:

Neurological complications of vaccination with outer surface protein A (OspA).
”A wide range of neurological complications have been reported via the medical literature and the VAERS system after vaccination with recombinant outer surface protein A (OspA) of Borrelia. To explore this issue, 24 patients reporting neurological adverse events (AE) after vaccination with Lymerix, out of a group of 94 patients reporting adverse events after Lymerix vaccination, were examined for causation. Five reports of cerebral ischemia, two transient Ischemic attacks, five demyelinating events, two optic neuritis, two reports of transverse myelitis, and one non-specific demyelinating condition are evaluated in this paper. Caution is raised on not actively looking for neurologic AE, and for not considering causation when the incidence rate is too low to raise a calculable difference to natural occurrence.”

It’s not “Autoimmune.”  It’s Subimmune.  This Subimmunity represents the entire class of the DSM's VooDoo Somatoformia – as well as cancer.  Cancer is in the Subimmune class, at the other end of the immunity spectrum from Autoimmunity.   This fact or condition completely flips the entire medical paradigm where you have to have a biomarker that is above-, or more-than- the normal range.  Lyme is not an inflammatory disease.  There are always negative correlations to biomarkers of autoimmunity or illness or infection except when using sophisticated DNA techniques using spinal fluid, in particular in these chronic, waste-basket diseases.  Henceforth, Autoimmunity will be an obsolete word that connotes the previous Medical Establishment where BigPharma is going to “block” something with their drugs.  They are dinosaurs.  You can’t block a mechanism that is already permanently blocked and you can’t unblock it.

It could be that a person has an HLA-linked outcome to one of the secondary infections like Epstein-Barr or HHV-6, reactivated by the AIDS-like Lyme and LYMErix.  Those people would for instance have the official, hypersensitivity outcomes of MS or Lupus or whatever.  But they are not also called Incompetent Incantation-ators and they are not mistreated by the entire universe (family, friends, Social Security, “doctors,” everyone, including ILADS and the non profits).


Ben Luft at the 1998 FDA Vaccine Meeting on LYMErix:

 "The point that I wanted to make in regard to the study is that there is very heavy dependence on serologic confirmation. And when we start thinking about the adverse events, *** it was stated originally when we got the overview of the disease that the disease is really quite protean. And actually the adverse events are very similar to what the disease manifestations are.**** And if you start to, as I think Dr. Hall was eluding to -- if you start to kind of say well how often do you actually become seropositive, you can start to have a different take on when someone has an adverse event or whether it is disease specific or infection specific versus vaccine specific. And I think that that is an important issue that we have to deal with. ..."



Dave Persing who together with Yale’s Robert Schoen developed this test in 1994 or 1995 says this about the similarities between Lyme and LYMErix disease:

"Additional uncertainty may arise if the vaccines are not completely protective; vaccinated patients with multisystem complaints characteristic of later presentations of Lyme disease may be difficult to distinguish from patients with vaccine failure....”


 So what exactly is OspA? 

“I did not get the vaccine so this does not concern me.”   Oh, yes, you got the vaccine.  Everyone with Lyme got LYMErix.  Here is what LYMErix is, and how this "vaccine-was-the-disease" works:

This is image is of Pam3Cys or OspA.  What is variable is the protein end "("peptide"), but what is immunogenic (seen as an invader to the immune system) are the fatty acids or acyl groups and the very electronegative cysteine core:


Pam3Cys is 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.)

This thing, Pam3Cys and fungal lipid molecules like it, is shed with the blebs.  In other words, like this:

The likes of OspA is on these blebs.  They go to the brain, inflame it, get eaten up by immune cells - which renders them incompetent-, they go to the kidneys (LUAT), etc. You will find this to be so in an NIH-owned patent (5,217,872) and elsewhere.

So, the fungal antigens are on the shed blebs and they go everywhere and they render the immune cells incompetent, resulting in an AIDS-like disease.  Everyone who has Lyme disease also has LYMErix disease. 

The NIH patent explaining how Lyme causes LYMErix-disease (“stealth bomber”):

"The invention relates to novel antigens associated with Borrelia burgdorferi which are exported (or shed) in vivo and whose detection is a means of diagnosing Lyme disease. The antigens are extracellular membranevesicles and other bioproducts including the major extracellular protein antigen. Another object of the invention is to provide antibodies, monoclonal and/or polyclonal, labeled and/or unlabeled, that are raised against the antigens. A further object of the invention is to provide a method of diagnosing Lyme disease by detecting the antigens in a biological sample taken from a host using the antibodies in conventional immunoassay formats. Another object of the invention is to provide kits, for the diagnosis of Lyme disease, comprising the antibodies and ancillary reagents. The advantage of the antibodies used in the invention is that they react with the antigens from geographically diverse strains of Borrelia burgdorferi, but do not react with antigens from related Borrelia spirochetes.",217,872.PN.&OS=PN/5,217,872&RS=PN/5,217,872

The shed blebs (or exosomes or vesicles) have LYMErix on them (delayed fuse or “time bomb”):

Characterization of multiprotein complexes of the Borrelia burgdorferi outer membrane vesicles.
"Although we uncovered the existence of at least 10 distinct OM complexes harboring several unique subunits, the complexome is dominated by the frequent occurrence of a limited diversity of membrane proteins, most notably P13, outer surface protein (Osp) A, -B, -C, and -D and Lp6.6."


Cadavid and the NIH say these shed vesicles or blebs go to the brain and inflame it:








Who else says OspA alone is responsible for the immunosuppression with brain inflammation that is characteristic of "Chronic Lyme?"


Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression (2006).

The spirochete Borrelia burgdorferi is the agent of Lyme disease, which causes central nervous system manifestations in up to 20% of patients. We investigated the response of human brain microglial cells, glial progenitors, neurons, astrocytes, as well as peripheral blood monocytes to stimulation with B. burgdorferi. We used oligoarrays to detect changes in the expression of genes important for shaping adaptive and innate immune responses. We found that stimulation with B. burgdorferi lysate increased the expression of Toll-like receptors (TLRs) 1 and 2 in all cell types except neurons. However, despite similarities in global gene profiles of monocytes and microglia, only microglial cells responded to the stimulation with a robust increase in HLA-DR, HLA-DQ, and also coexpressed CD11-c, a dendritic cell marker. In contrast, a large number of HLA-related molecules were repressed at both the RNA and the protein levels in stimulated monocytes, whereas secretion of IL-10 and TNF-alpha was strongly induced. These results show that signaling through TLR1/2 in response to B. burgdorferi can elicit opposite immunoregulatory effects in blood and in brain immune cells, which could play a role in the different susceptibility of these compartments to infection. 

In other words, the NIH is saying thanks to exposure to shed blebs with TLR2/1 agonists like OspA on them, the HLA molecules will be downregulated and that you will make no antibodies.  This mechanism is mimicked elsewhere, in other fungal diseases models.  It is also CALLED endotoxin tolerance.


“Endotoxin tolerance [Lyme, LYMErix-Disease, CFIDS, etc] protects the host by limiting excessive 'cytokine storm' during sepsis, but compromises the ability to counteract infections in septic shock survivors."- Medvedev.


Endotoxin Tolerance Inhibits Lyn and c-Src Phosphorylation and Association with Toll-Like Receptor 4 but Increases Expression and Activity of Protein Phosphatases.

“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.


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