OspA Alone is Responsible for Chronic Neuro-Lyme





Outer surface protein A (OspA) is alone responsible for chronic neuro-Lyme via tick bite or vaccination, even the NIH agrees with the model. In 2001-2002 the FDA finally ordered LYMErix off the market via ultimatum because it was causing the very same disease that was marketed to prevent. If the vaccine caused the same disease without spirochetes, what is chronic neuro-Lyme?


OspA was the antigen used in the LYMErix vaccine and the major lipoprotein on the Borrelia Spirochete. OspA is managed by toll-like receptors 2/1 (TLR2/1). TLRs play a critical role in the early immune response by recognizing and defending against invading pathogens. TLR2/1 manages mycobacteria or fungal endotoxins. OspA or TLR2/1 agonists are fungal and so toxic the body shuts down the immune system to avoid a septic cytokine storm causing permanent immunosuppression. TLR2 agonists are much more stealth than typical bacteria as no to little antibodies are detected.


You can buy OspA (Pam3Cys) online and they are very clear how dangerous all modes of exposure to OspA are but the same CDC patent holders on the vaccine and fraudulent test kits claim injecting it and calling it a vaccine is safe.




Norman Latov
The 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 
OspA causes immunosuppression (which means it was the opposite of a “vaccine”): Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant OspA        

“The modulation of human lymphocyte proliferative responses was demonstrated with a recombinant outer surface protein A (OspA) vaccine preparation for the prevention of Borrelia burgdorferi infection. 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 the OspA 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 the OspA molecule responsible for this effect may lead to improved vaccine preparations.”                   

The disease is attributable to the fungal "supernatants" or lipids (like LymeRix) from the Osps. In other words, OspA causes immunosuppression

“……[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).”
An OspA vaccine trial administrator –  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 occurence.”

1998 FDA Vaccine Meeting on LYMErix - The Lymerix adverse events are very similar to the actual "protean" (multi-systematic) disease manifestations are.

“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. …”



USPTO # 6,045,804 Mayo Clinic’s David Persing 
In that patent, Persing states that you can’t tell the difference between late, “multi-system” Lyme and LYMErix injury.

“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….”             
OspA (TLR2/1 agonists) is responsible for the generalized immunosuppression or no antibodies in the blood but chronic encephalitis we know of as chronic Neuro-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.  

Not only does OspA cause immunosuppression, OspA alone causes tolerance meaning it turns off the immune response and detection to this pathogen.


-  And  -


OspA causes cross tolerance by turning off the immune response and detection to TLR7/9 agonists like Herpesviruses, Epstein-Barr and all other viral infections.

”Because IRAK1 is required for TLR7/9-induced IFN-I production, 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.”  


-  And  -

OspA turns off the immune response to
TLR4 agonists lipopolysaccharides, known as the
more typical bacteria.

"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].....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.”


-  And  -


OspA once again causes cross tolerizes and turns off the immune response to TLR5 agonists or flagellins.
“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

OspA is fungal and so toxic the
shuts down the immune system to avoid a septic cytokine storm, otherwise, you would die. In turn, it shuts off immunity to all other pathogens including viral, fungal, parasitic and bacterial

“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. “


So as you see OspA alone causes the same multi-system disease as chronic Lyme disease without spirochetes and tolerizes the immune system to no longer detect this or other invading pathogens where secondary opportunistic viral, fungal, parasitic and bacterial infections become a free for all. What is chronic neuro-Lyme and LYMErix disease?
Post-sepsis or an aquired immune deficiency.


Ultimately its the perfect stealth pathogen producing no to little antibodies resulting in "The Great Imitator". The CDC/ALDF/Yale patent holders falsified the Lyme testing and case definition in 1994 to make all chronic neurological victims undetectable to pass off a bogus immunosuppressive vaccine and create a monopoly on all future TBD's testing in USA and Canada once an OspA vaccine was on the market.


Til this date, not a single victim can get a diagnosis, validation, vindication or proper treatment. We must OCCUPY the USDOJ to prosecute OspA crimes against humanity to end this global Medical Holocaust inflicting humanity. Millions of lives are ripped to shreds for profit, greed and power.

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