OspA alleen is verantwoordelijk voor Chronische Neuro-Lyme

Buitenoppervlakte-eiwit A (OspA) is alleen verantwoordelijk voor chronische neuro-Lyme door tekenbeet of vaccinatie, zelfs de NIH (National Institutes of Health) is het eens met het ziektemodel. Door een ultimatum van de FDA werd LYMErix in 2001-2002 van de markt gehaald omdat het de oorzaak was van dezelfde ziekte die het vaccin zou moeten voorkomen. Als het vaccin dezelfde ziekte veroorzaakt zonder spirocheten, wat is chronische neuro-Lyme?

OspA was het antigeen dat werd gebruikt in het LYMErix-vaccin en het belangrijkste lipoproteïne op de Borrelia spirocheet. OspA wordt herkend door Toll-like receptoren 2/1 (TLR2/1). TLR’s spelen een cruciale rol in de vroege immuunrespons door herkenning en verdediging tegen binnenvallende pathogenen. TLR2/1 herkent mycobacteriën of schimmelachtige endotoxinen. OspA of TLR2/1-agonisten zijn schimmelachtig en zo toxisch dat het lichaam het immuunsysteem afsluit om een septische cytokine-storm te voorkomen en veroorzaakt zo een permanente immunosuppressie. TLR2-agonisten zijn veel meer stealth (niet zichtbaar) dan typische bacteriën omdat er geen tot weinig antilichamen worden gedetecteerd.

Je kan OspA (Pam3Cys) online kopen en men is heel duidelijk hoe gevaarlijk alle vormen van blootstelling aan OspA zijn, maar de CDC-patenthouders op het vaccin en frauduleuze testkits beweren dat het injecteren van OspA, en het een vaccin noemen, veilig is. “Do not take internally. Wear gloves and mask when handling the product. Avoid contact by all modes of exposure.”

De OspA vaccinatie veroorzaakte dezelfde ziekte als chronische 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.”

OspA veroorzaakt immunosuppressie (wat betekent dat het het tegenovergestelde was van een “vaccin”):

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.”

De ziekte is te wijten aan de schimmelachtige “supernatanten” (bovendrijvende vloeistof) of lipiden (zoals LymeRix) van de Osp’s. Met andere woorden, OspA veroorzaakt immunosuppressie.

“……[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).”

Een OspA vaccin onderzoek administrator – LYMErix veroorzaakte dezelfde ziekte als chronische Lyme:

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 over LYMErix – De bijwerkingen van Lymerix zijn zeer vergelijkbaar met de werkelijke “protean” (multi-systematische) ziekteverschijnselen.

“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. …”

In dat patent stelt Persing dat je het verschil tussen late, “multi-systeem” Lyme en LYMErix letsel niet kunt zien.

“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-agonisten) is verantwoordelijk voor de gegeneraliseerde immunosuppressie of geen antilichamen in het bloed maar chronische encefalitis die we kennen als chronische 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.”

OspA veroorzaakt niet alleen immunosuppressie, OspA alleen veroorzaakt tolerantie, wat betekent dat het de immuunrespons en detectie van deze ziekteverwekker uitschakelt.

– En –

OspA veroorzaakt kruistolerantie door de immuunrespons en detectie van TLR7/9 agonisten zoals herpesvirussen, Epstein-Barr en alle andere virale infecties uit te schakelen.

”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.” 

– En –

OspA schakelt de immuunrespons uit op TLR4 agonisten lipopolysachariden, bekend als de meer typische bacteriën.

“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.”

– En –

OspA veroorzaakt opnieuw kruistoleranties en schakelt de immuunrespons op TLR5-agonisten of flagellinen uit.

“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 schimmelachtig en zo giftig dat het immuunsysteem wordt uitgeschakeld om een ​​septische cytokinestorm te voorkomen, anders zou je sterven. Vervolgens sluit het de immuniteit af voor alle andere virale, schimmel, parasitaire en bacteriële ziekteverwekkers.

“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. “

Dus zoals je ziet veroorzaakt OspA alleen dezelfde multisysteemziekte als chronische Lyme-ziekte zonder spirocheten. en tolereert het immuunsysteem dit of andere binnendringende pathogenen waarbij secundaire opportunistische virale, schimmelachtige-, parasitaire en bacteriële infecties ontstaan. Wat is chronische neuro-Lyme en LYMErix-ziekte? Post-sepsis of een verworven immuundeficiëntie.

Uiteindelijk is het de perfecte stealth-ziekteverwekker die geen tot weinig antilichamen produceert, resulterend in “De Grote Imitator”. De CDC/ALDF/Yale-patenthouders hebben de Lyme-test en -definitie in 1994 vervalst. Door chronische neurologische slachtoffers niet-detecteerbaar te maken, kon een nep-immunosuppressief vaccin goedgekeurd worden en een monopolie gecreëerd worden op alle toekomstige testen van tekenziekten zodra een OspA-vaccin op de markt kwam.

Tot op heden kan geen enkel slachtoffer een diagnose, validatie, bewijs van ziekte of juiste behandeling krijgen. We moeten de OspA-misdaden tegen de menselijkheid vervolgen om een eind te maken aan deze wereldwijde medische holocaust. Miljoenen levens worden verwoest voor winst, hebzucht en macht.