Top Ten Reasons you know Lyme and LYMErix were a Lie.
1) Because of what OspA is
2) Because Steere, Garg, Duray, etc said so in 2018 and 1988 (reactivated EBV)
3) Because of the “Occam’s Razor” – you ALWAYS get reactivated EBV and opportunistics in immunosuppression cases, not just with fungal antigens
4) Because the criteria of “The Scientific Method” is met: other fungal antigens do the same thing, cause immunosuppression and not “antibodies”
5) Because “Seronegative Lyme victims are the sickest (SUNY, 1990s)”
6) Because Tolerance and Cross Tolerance (Baumgarth, Harding, Medvedev) to other pathogens and this is not reversible by removing spirochetes, ie, B cell senescence
7) NIH’s & Yale’s MS and Lupus Clinics (which are not “bad knees,” which is the current “Dearborn,” “CDC,” “case definition”)
8) SKB/Yale/Steere did not allow neurologic AEs to be reported (Marks, Dickson)
9) “OspA did not prevent Lyme or disinfect ticks” say the two owners of the two OspA vaccines; due to antigen variation, and because of a fraudulent experiment (Fikrig)
10) Yale could have used its patents Borrelia burgdorferi-specific flagellar DNA method to assess their other patent, LYMErix, since that method was developed before (1991) their OspA patent was applied for (1994).
[This, number 10, is the easiest way to charge this criminally. You can see that Dearborn (falsifying the case definition or serology – 1994) happened AFTER the early Phase I and II trials of the OspA vaccines. In 1993 both Yale’s Durland Fish and Alan Barbour published an article trashing Lyme, LYMErix and ImmuLyme victims and in which they mentioned that the Phase I and II trials were underway. Allen Steere also trashed Lyme and LYMErix victims with his “Overdiagnosis (sic)” article, in which he said these very sick post-sepsis victims had fibromyalgia or chronic fatigue syndrome At that time, Fibro and CFIDS cases were considered psychiatric (vague term) cases and not really sick. This is Deprivation of Rights under Color of Law (discrimination, slander and libel) – denying people access to medical care of any sort. They did that because the OspA vaccines caused the same immunosuppression disease and they wanted to discard those adverse evens as not “Lyme disease. Here we see, in this patent, 5,618,533, Yale had a way to determine if their OspA vaccine really prevented spirochetes. They chose to lie to the FDA and to the public instead.]
Firstly note that all of this and more are recorded in the criminal charge sheets:
Here is the overview (which people should read so they can get the picture that this model is repeated, forwards and backwards with a glut of data and evidence):
Immunosuppression? –> Reactivated latent viruses and tolerance to other pathogens.
Fungal antigens? –> Immunosuppression.
CONTENTS (Chapters or Criminal Charge Sheets):
1. ALDF-CDC “Enterprise” (read “RICO”) Conspires to Defraud USA in Dearborn-Vaccine Scam — charge sheet on patents; the very people who falsified the testing are the ones who own the patents for the bogus vaccines and test kit products. – page 3
2. Lyme Disease Patents owned by the Dearborn scammers, CDC officers, Yale in association with Corixa, Mayo Clinic and Imugen. Leaving OspA and B out of the Dearborn standard was intended to facilitate a monopoly on post-LYMErix approval on blood testing for all vector-borne disease – page 31
3. Lyme Disease Biomarkers, as compared to scientifically invalid psychiatric check lists. These biomarkers were identified by the very people who later said Lyme was not even a disease, and who are the same people who own the vaccine patents and falsified the testing at Dearborn — page 38
4. The Primers (DNA, RNA) Shell Game; the very people who own all the patents and falsified the testing for Lyme in order to falsify the outcomes of those bogus products, use the wrong DNA to not-find Lyme or other spirochetes in humans, while using the correct DNA to patent borrelia-specific DNA; no biofilms. – page 49
5. “Occam’s Razor” — If it quacks like a duck, it must be Epstein-Barr/post-sepsis syndrome (as the REAL “Great Imitator”) — page 105
6. The Common Mechanisms of Fungal-Viral Damage in CFIDS, Vaccines-Autism, and “Chronic Lyme”/ New Great Imitator, per the CDC, NIH and IDSA; This paper reveals the CDC’s own data on what Lyme and CFIDS are, and how immunosuppression-via-fungal contamination also explains the failed childhood vaccines, giving children the very viruses the vaccines are intended to prevent (with resultant encephalitis).—page 150
7. Simon Wessely and the abuse of Gulf War veterans, Justina Pelletier and 21st century witch trials; with scientifically valid evidence for real illness, a vast majority of post-sepsis and vaccine injured are slandered and libeled with invalid psychiatric terminology. – page 197
8. The State of Connecticut and Yale Assaulted Czech Children with a known fake vaccine (OspA or LYMErix) just to see how serious would be the adverse events. – page 204
9. The totally false OspA trials; never prevented Lyme or spirochetes, never disinfected ticks. All false claims and downright crazy – page 205
OspA’s Molecular type = Pam3Cys; 3 acyl groups or fatty acid groups; “TLR2/1 agonist” (look that up on your own). OspA either is, or looks very much like Pam3Cys and is immunologically handled the same way, experimentally, by the mammalian host.
THE FIRST REASON – Because of what OspA is.
Because the Osps or the Vmps or the surface antigens of Borrelia (all spirochetes, really) are fungal or are triacyl lipoproteins, or where they and other TLR2/1 agonists are shed by spirochetes in what’s called “blebbing” or “exported vesicles.”
[Use your Google Images machine to look at that – see it with your eyeballs; see the 3 acyl groups. Acyl groups, especially 3 or more, are bad. The human body knows that’s gonna be a bad bug.]
Radolf: The chemical determination:
Immunogenic integral membrane proteins of Borrelia burgdorferi are lipoproteins.
“Furthermore, most of these immunogenic proteins, including the previously characterized OspA and OspB membrane antigens, could be biosynthetically labeled when B. burgdorferi was incubated in vitro with [3H]palmitate. The OspA and OspB antigens were radioimmunoprecipitated from [3H]palmitate-labeled detergent-phase proteins with monoclonal antibodies, and [3H]palmitate was recovered unaltered from these proteins after sequential alkaline and acid hydrolyses. The combined results provide formal confirmation that the major B. burgdorferi immunogens extracted by Triton X-114 are lipoproteins. The demonstration that B. burgdorferi integral membrane antigens are lipoproteins may explain the basis of their immunogenicity and may help to improve our understanding of the surface topology of B. burgdorferi.”
Philipp and others who say fungal Osps induce IL-10 which is an immunosuppressive cytokine:
Barbour and Barthold: “Stealth Bomber Spirochetes”:
“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. Explains Barbour: “It’s like a bacterial Star Wars defense program,” in which released surface proteins might intercept incoming host antibodies, keeping the spirochete safe from immunological attack. “
[Actually what these shed blebs with the Osps on them are doing is disabling the immune system. OspA sticks to everything and inhibits apoptosis of infect cells (adheres to organelles). You get B cell zombies and T cells fail to present the antigen when the antigen is fungal. B cells dont mature, you get the “premature collapse of B cell germinal centers in the lymph nodes” (Baumgarth).
J Proteome Res. 2011 Oct 7;10(10):4556-66. doi: 10.1021/pr200395b. Epub 2011 Sep 13.
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.” http://www.ncbi.nlm.nih.gov/pubmed/21875077 ]
The shed blebs have the fungal Osps in them or on them:
Dattwyler, Liegner, & Wormser, 1988, 1994, 2000 [saying it is the fatty acid supernatant that causes the inhibition of Natural Killer Cell Activity, Lyme antigens suppress the general immune response (proliferation/IL-2), OspA “blocks cell cycle progression.”]
Ann N Y Acad Sci. 1988;539:103-11.
Modulation of natural killer cell activity by Borrelia burgdorferi.
“..when lymphocytes are cultured in the presence of growing Bb 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 or or toxicity to endogenous NK since viability studies and monoclonal antibodies demonstrate no significant changes after culture with the organism.
“The inhibition is directly attributable to the organism or its supernatants (data not shown).”
Liegner, et al (1994):
Antigens of Lyme disease of spirochaete Borrelia burgdorferi inhibits antigen or mitogen-induced lymphocyte proliferation.
“Modulation of cellular immune responses by the spirochaete Borrelia burgdorferi, the bacteria that causes Lyme disease, was demonstrated. When cultured in the presence of sonicated Borrelia preparation (Bb), the mitogen- or antigen-stimulated proliferative responses of normal lymphocytes were consistently lowered. Bb caused the greatest reduction in Concanavalin A (ConA) or antigen-stimulated proliferation, where almost 100% reduction in proliferation could be achieved. Bb also reduced phytohemagglutinin-M (PHA) or pokeweed mitogen (PWM)-stimulated peripheral blood lymphocyte (PBL) proliferation, with the PWM proliferation being the least affected. This regulatory activity was not due to toxicity and was determined to be caused by Bb protein antigens. The degree of the proliferation reduction was directly proportional to both Bb quantity and length of exposure to lymphocytes. IL-2 production was significantly reduced from Bb-exposed lymphocytes. The entry of lymphocytes into the proliferating phases of the cell cycle was also shown to be blocked. These results have demonstrated an immune suppressive mechanism of B. burgdorferi. The magnitude of host immune responses may be dependent on the degree of suppression which is related to the spirochaete quantity and their length of presence in the host.” https://www.ncbi.nlm.nih.gov/pubmed/8173554
Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (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 SECOND REASON – Because Steere, Duray in 1988, Baumgarth in 2016 and others, and finally Garg in 2018 said (immunosuppression, EBV, wimpy B cells etc) the same thing, 30 years apart (Think: “Sherman Act,” “fraudulent patent enforcement inhibits discovery.” Lyme is not a bad knee for 85% of us).
Allen Steere said so in 1988 with Yale and US Army Pathologist Paul Duray – who later said so two more times. Between 2016 and 2018, 2018 Garg, Baumgarth, Blum, et al confirmed it. EBV et al are reactivated; “B cells are immature-looking”; “fungal antigens inhibit B cell maturation.” EBV and Bb both hang out in the bone marrow and lymph nodes. Lyme is about incompetent B cells. Where else does that happen? The Second Reason you know Lyme and LYMErix are lies is that it was empirically observed that this was an immunosuppression disease right in the beginning of this ridiculous unscientific clown-driven circus.
Versus …. 2018, Garg: Tick-borne disease is not just Lyme — University of Jyväskylä
“However, the research by Garg et al. argues that prolonged exposure to tick transmitted microbes weakens the human immune system increasing the host’s vulnerability to other common microbes’ labelled “non-tick-borne opportunistic microbes,” such as Chlamydia, Mycoplasma, Epstein–Barr virus and many more. “
1988, Steere & Duray: Ann N Y Acad Sci. 1988;539:65-79.
Clinical pathologic correlations of Lyme disease by stage.
”….Soon after the onset of ECM, the organism disseminates hematogenously, with what appears to be random dispersal throughout the body. The immune response involves virtually all of the organs and structures of the reticuloendothelial system including the bone marrow, and clinical pain and discomfort seems to correlate with hyperplasia of lymph nodes and spleen and bone marrow. Diffuse visceral involvement in this acute stage mimics infectious mononucleosis or disseminated viral syndromes. These include conjuctivitis, pharyngitis, pneumonitis with dry cough and mild pleuritic pain, hepato-splenic tenderness, lymph node swelling of the neck and groin, and orchitis. There is lymphoid hyperplasia of the lymph nodes and spleen consisting of prominent germinal centers and numerous perifollicular lymphocytes, with proliferation of plasma cell precursors and mature plasma cells. …
The plasma cell precursors are large, appear tumor-like, and can resemble Reed-Sternberg cells. Others look like typical immunoblasts (FIG. 1). In one example, cervical lymph nodes show cell degeneration with karyorrhexis and nuclear debris of lymphoid elements. This patient had repeated high fevers and marked discomfort of neck nodes. Large atypical immunoblasts can also be seen in the spleen and bone marrow. The red pulp of the spleen is congested, not unlike that seen in infectious mononucleosis. Spirochetes can be demonstrated in the lymph nodes, spleen and bone marrow and liver. There is a transient hepatitis reflected by elevated liver cell enzymes such as SGOT, SGPT, and GGT. The liver can vary from a mild lymphocytic portal triaditis all the way to liver cell derangement that simulates acute viral hepatitis. The cells at this stage appear swollen with clear cytoplasm and microvesicles of fat (FIG. 2). Numerous leukocytes are seen in the sinusoids, and there is Kupffer cell hyperplasia…”
Obviously Garg et al, and Steere/Duray observed something like, um, reactivated EBV, and after all. EBV is strongly implicated in at least 2 of the “Great Imitator” outcomes of Lyme: MS and Lupus. So, while some people will have autoimmune responses to the reactivated opportunistics (which can show up as Lupus or MS), the 85% of us will not. Our disease is called “crazy” (only sane people call it post-sepsis syndrome, which is what it is).
“Dormant viruses re-emerge in patients with lingering sepsis, signaling immune suppression.
”A provocative study links prolonged episodes of sepsis — a life-threatening infection and leading cause of death in hospitals — to the reactivation of otherwise dormant viruses in the body. “
Research Supported by Bay Area Lyme Foundation Shows Lower Immune Response Leads To Persistent Lyme Disease Symptoms
”The data show that patients who did not demonstrate strong B-cell immune responses were more likely to experience post-treatment symptoms. Researchers found that the study participants who fully returned to health following 21 days of doxycycline treatment had significantly higher levels of a type of blood B cells, known as plasmablasts, prior to treatment than the patients who experienced persistent symptoms and met the criteria for diagnosis for post treatment Lyme disease syndrome (PTLDS) for at least 6 months following treatment. Importantly, the study also found that plasmablast levels may be useful in predicting which patients have a higher chance of treatment failure after a short course of antibiotics. These data confirm previous findings in some animal models showing demonstrable immune system suppression after infection and wide variability in the immune response among different animals after infection.
“In addition to an association between plasmablasts and disease resolution, researchers also found that patients with persistent symptoms had a lower antibody response; more specifically, these patients exhibited reduced clonal expansion of B-cells.”
T cells don’t present antigen when the antigen is fungal:
Recombinant Lipoprotein Rv1016c Derived from Mycobacterium tuberculosis Is a TLR-2 Ligand that Induces Macrophages Apoptosis and Inhibits MHC II Antigen Processing.
“TLR2-dependent cellular signaling in Mycobacterium tuberculosis-infected macrophages causes apoptosis and inhibits class II major histocompatibility complex (MHC-II) molecules antigen processing, leading to evasion of surveillance. Mycobacterium tuberculosis (MTB) lipoproteins are an important class of Toll-like receptor (TLR) ligand, and identified as specific components that mediate these effects. In this study, we identified and characterized MTB lipoprotein Rv1016c (lpqT) as a cell wall associated-protein that was exposed on the cell surface and enhanced the survival of recombinants M. smegmatis_Rv1016c under stress conditions. We found that Rv1016c lipoprotein was a novel TLR2 ligand and able to induce macrophage apoptosis in a both dose- and time-dependent manner. Additionally, apoptosis induced by Rv1016c was reserved in THP-1 cells blocked with anti-TLR-2 Abs or in TLR2-/- mouse macrophages, indicating that Rv1016c-induced apoptosis is dependent on TLR2. Moreover, we demonstrated that Rv1016c lipoprotein inhibited IFN-γ-induced MHC-II expression and processing of soluble antigens in a TLR2 dependent manner. Class II transactivator (CIITA) regulates MHC II expression. In this context, Rv1016c lipoprotein diminished IFN-γ-induced expression of CIITA IV through TLR2 and MAPK Signaling. TLR2-dependent apoptosis and inhibition of MHC-II Ag processing induced by Rv1016c during mycobacteria infection may promote the release of residual bacilli from apoptotic cells and decrease recognition by CD4+ T cells. These mechanisms may allow intracellular MTB to evade immune surveillance and maintain chronic infection.”
B cells don’t mature when T cells fail to present antigen:
Role of TLR in B cell development: signaling through TLR4 promotes B cell maturation and is inhibited by TLR2.
“Taken together, our results suggest that TLR4 signaling favors B lymphocyte maturation, whereas TLR2 arrests/retards that process, ascribing new roles for TLRs in B cell physiology.”
B cells don’t respond to TLR2 agonists like Pam3Cys:
Plasmacytoid Dendritic Cells Control TLR7 Sensitivity of Naive B Cells via Type I IFN
“Human B cells did not respond to ligands of other TLRs including TLR2, TLR4 and TLR6 with and without type I IFN.”
Also, you could probably say OspA never could have been a vaccine, based on that (above) concept alone. OspA/fungal antigens don’t produce long term IgG, and these TLR2/1 agonists cause tolerance and cross tolerance to other antigen types. Na. Not a good idea. Here again is the proof in action:
Research Supported by Bay Area Lyme Foundation Shows Lower Immune Response Leads To Persistent Lyme Disease Symptoms
“The data show that patients who did not demonstrate strong B-cell immune responses were more likely to experience post-treatment symptoms. Researchers found that the study participants who fully returned to health following 21 days of doxycycline treatment had significantly higher levels of a type of blood B cells, known as plasmablasts, prior to treatment than the patients who experienced persistent symptoms and met the criteria for diagnosis for post treatment Lyme disease syndrome (PTLDS) for at least 6 months following treatment. Importantly, the study also found that plasmablast levels may be useful in predicting which patients have a higher chance of treatment failure after a short course of antibiotics. These data confirm previous findings in some animal models showing demonstrable immune system suppression after infection and wide variability in the immune response among different animals after infection.” — https://www.prnewswire.com/news-releases/research-supported-by-bay-area-lyme-foundation-shows-lower-immune-response-leads-to-persistent-lyme-disease-symptoms-300701693.html
People with a strong immune response do better. Ray Dattwyler said that to the FDA Vaccine Committee in 1994 (below) and here we are, 24 years later… re-hearing the same thing from Bay Area Lyme, Blum and Aucott. (Great job, CDC; you really are morons)
THE THIRD REASON – “Occam’s Razor” or the model repeats; ALL immunosuppression case types result in the activation of opportunistics.
In all immunosuppression cases, be they from fungal exposures (see Fauci’s patent, see the warnings re Humira, Stelara and similar drugs), transplant patients who have to take immunosuppressive drugs, polymicrobial sepsis (you cant fight off more than one infection at a time), astronauts who are stressed out in space, people who are stressed out 24/7 like medical school students,… you get reactivated latent viruses especially EBV et al.
EBV is the main driver of most diseases: many cancers (throat, breast, stomach, blood cancer, and probably many more) Lupus, MS, possibly even RA, it is implicated in many other autoimmune diseases. If the US Government was smart they would look into why EBV is the Great Initiator but they arent.
”If you hear hoofbeats behind you, think horses not zebras.”
Chronic Fatigue Syndrome (CFIDS)/Fibromyalia are also post sepsis syndrome, also. CFIDS is not due to some exotic, as-yet undiscovered virus, as much as Certain People would like to have a Very Special and Unique Disease and not a common one like Epstein-Barr. Nor are these illnesses due to Somatoformia or Conversionosis – imaginary, invented scientifically meaningless terms which are no more than code language for “witch.” The direct scientific and legal translation of these two terms mean “a person can have real, valid biomarkers of real illness,” but, say these-psychiatrists-who are-very-far-from-scientists, “are due to a form of brain magic or apporting of test results. They are real, but not real.”
Nobody asks them how “real” and at the same time “not real” diseases can be, or exist at the same time, yet these psychiatric experts are the alleged experts on crazy. Maybe that is why no one asks. Regular doctors might be afraid Crazy is contagious and that psychiatrists are infected; Regular docs be keeping their Cognitive Distances-ness.
The biggest reason this lie has persisted for so many decades is because of the totally fake medical practice of psychiatry. It is a human flesh dumping ground the failures of doctors to understand basic science or even ask questions.
Fauci’s patent for the immune booster IL-2 as a treatment for fungal immunosuppression diseases:
“….Illustrative of specific disease states in treatment of which the present invention can be applied are HIV infection and *** other diseases characterized by a decrease of T-cell immunity, for example, mycobacterial infections like tuberculosis and fungal infections such as cryptococcal disease. This method also can be used in the treatment of secondary infections that occur in patients with suppressed immune systems, such as the opportunistic infections that occur in AIDS patients.*** …”
Humira/Stelara Commercials basically say: Avoid fungal diseases or you will become too immunosuppressed and then possibly end up with lymphoma from the reactivated EBV.
Fatigue in Medical Residents Leads to Reactivation of Herpes Virus Latency
Here is a good explanation from 1975:
The Results of Testing Out OspA-ish Antigens Elsewhere as Vaccines:
The 3 Tuberculosis vaccine attempts that all failed the same way LYMErix failed, by making people sicker and more susceptible to disease:
Clin Exp Immunol. 2000 May;120(2):274-9.
The 19-kD antigen and protective immunity in a murine model of tuberculosis.
Yeremeev VV1, Lyadova IV, Nikonenko BV, Apt AS, Abou-Zeid C, Inwald J, Young DB. 2017, TruthCures.org 125 125
“The 19-kD antigen is a cell wall-associated lipoprotein present in Mycobacterium tuberculosis and in bacille Calmette-Guérin (BCG) vaccine strains. Expression of the 19-kD antigen as a recombinant protein in two saprophytic mycobacteria-M. vaccae and M. smegmatis-resulted in abrogation of their ability to confer protection against M. tuberculosis in a murine challenge model, and in their ability to prime a DTH response to cross-reactive mycobacterial antigens. Induction of an immune response to the 19-kD antigen by an alternative approach of DNA vaccination had no effect on subsequent M. tuberculosis challenge. These results are consistent with a model in which the presence of the 19-kD protein has a detrimental effect on the efficacy of vaccination with live mycobacteria. Targeted inactivation of genes encoding selected antigens represents a potential route towards development of improved vaccine candidates.”
Infect Immun. 2001 Mar;69(3):1433-9.
Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits Mycobacterium smegmatis-induced cytokine production by human macrophages in vitro.
Post FA1, Manca C, Neyrolles O, Ryffel B, Young DB, Kaplan G.
“Vaccination of mice with Mycobacterium vaccae or M. smegmatis induces some protection against M. tuberculosis challenge. The 19-kDa lipoprotein of M. tuberculosis, expressed in M. vaccae or M. smegmatis (M. smeg19kDa), abrogates this protective immunity. To investigate the mechanism of this suppression of immunity, human monocyte-derived macrophages (MDM) were infected with M. smeg19kDa. Infection resulted in reduced production of tumor necrosis factor alpha (TNF-alpha) (P < 0.01), interleukin-12 (IL-12) (P < 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared to infection with M. smegmatis vector (M. smegV). Infection with M. smeg19kDa and with M. smegV had no differential effect on expression of costimulatory molecules on MDM, nor did it affect the proliferation of presensitized T cells cocultured with infected MDM. When MDM were infected with M. smegmatis expressing mutated forms of the 19-kDa lipoprotein, including non-O-glycosylated (M. smeg19NOG), nonsecreted (M. smeg19NS), and nonacylated (M. smeg19NA) variants, the reduced production of TNF-alpha or IL-12 was not observed. When the purified 19-kDa lipoprotein was added directly to cultures of infected monocytes, there was little effect on either induction of cytokine production or its inhibition. Thus, the immunosuppressive effect is dependent on glycosylated and acylated 19- kDa lipoprotein present in the phagosome containing the mycobacterium. These results suggest that the diminished protection against challenge with M. tuberculosis seen in mice vaccinated with M. smegmatis expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha and IL-12 production, possibly leading to reduced induction of T-cell activation.” http://www.ncbi.nlm.nih.gov/pubmed/11179309
Infect Immun. 2003 Jun;71(6):3146-54.
The Mycobacterium tuberculosis recombinant 27-kilodalton lipoprotein induces a strong Th1- typeimmune response deleterious to protection.
Hovav AH1, Mullerad J, Davidovitch L, Fishman Y, Bigi F, Cataldi A, Bercovier H.
”Th1 immune response is essential in the protection against mycobacterial intracellular pathogens. Lipoproteins trigger both humoral and cellular immune responses and may be candidate protective antigens. We studied in BALB/c mice the immunogenicity and the protection offered by the recombinant 27-kDa Mycobacterium tuberculosis lipoprotein and the corresponding DNA vaccine. Immunization with the 27-kDa antigen resulted in high titers of immunoglobulin G1 (IgG1) and IgG2a with a typical Th1 profile and a strong delayed hypersensitivity response. A strong proliferation response was observed in splenocytes, and significant nitric oxide production and gamma interferon secretion but not interleukin 10 secretion were measured. Based on these criteria, the 27-kDa antigen induced a typical Th1-type immune response thought to be necessary for protection. Surprisingly, in 27-kDa-vaccinated mice (protein or DNA vaccines) challenged by M. tuberculosis H37Rv or BCG strains, there was a significant increase in the numbers of CFU in the spleen compared to that for control groups. Furthermore, the protection provided by BCG or other mycobacterial antigens was completely abolished once the 27-kDa antigen was added to the vaccine preparations. This study indicates that the 27-kDa antigen has an adverse effect on the protection afforded by recognized vaccines. We are currently studying how the 27-kDa antigen modulates the mouse immune response.” https://www.ncbi.nlm.nih.gov/pubmed/12761093 http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12761093
“A deleterious effect on immunity,”
“an adverse effect on the protection,”
“the immunosuppressive effect,”
“reduced T cell activation,…”
THEY DON’T WORK; lipoproteins are the opposite of vaccines.
It is the LIPIDS that are all the trouble. The protein end is not immunogenic.
You can find this is true, abundantly, now, on pubmed. Repeat injections of fungal endotoxins cause immunosuppression. We really dont need to go on and on to prove it. All we need to do is convince everyone to go take a look for themselves, show them what The Scientific Method means, and what an Occam’s Razor is. You get the same result (reactivated latent opportunistics) regardless of what is the source of the immunosuppression (= a Razor), and you are supposed to show if your model repeats independently (or IS TRUE, per How Science is Done).
Both OspA (and antigens like it) and EBV inhibit apoptosis.
THE FOURTH REASON – “The Scientific Method”; Experiments with triacyl lipoproteins other than from Borrelia give the same immunosuppression/tolerance result.
All similar, independent experiments with repeat injections of the fungal triacyl lipoprotein like pam3cys – a mimic if not exactly OspA, in form or molecular type – a TLR2/1 agonist (with CD14) or similar … produced the same immunosuppression results, regardless of from whence these triacyl lipoproteins or TLR2/1 agonists came. That is, The Scientific Method was satisfied in that the model was verified independently (Mycobacteria, Brucella, mycoplasma, etc). as happening other than in Lyme/Borrelia. The reader may have heard of the “Replication Crisis” in science. That refers to the failure to show the model repeats or is reproducible.
Example 1: Mycobacteria tuberculosis lipoproteins:
The 19-kD antigen and protective immunity in a murine model of tuberculosis.
”These results are consistent with a model in which the presence of the 19-kD protein has a detrimental effect on the efficacy of vaccination with live mycobacteria. Targeted inactivation of genes encoding selected antigens represents a potential route towards development of improved vaccine candidates.” http://www.ncbi.nlm.nih.gov/pubmed/10792376
Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits Mycobacterium smegmatis-induced cytokine production by human macrophages in vitro.
“Thus, the immunosuppressive effect is dependent on glycosylated and acylated 19- kDa lipoprotein present in the phagosome containing the mycobacterium. These results suggest that the diminished protection against challenge with M. tuberculosis seen in mice vaccinated with M. smegmatis expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha and IL-12 production, possibly leading to reduced induction of T-cell activation.”
The Mycobacterium tuberculosis recombinant 27-kilodalton lipoprotein induces a strong Th1- typeimmune response deleterious to protection.
”This study indicates that the 27-kDa antigen has an adverse effect on the protection afforded by recognized vaccines.”
Example 2: Brucella
Outer Membrane Vesicles from Brucella abortus Promote Bacterial Internalization by Human Monocytes and Modulate Their Innate Immune Response
“Previous studies have shown that smooth and rough strains of Brucella spontaneously release OMVs that contain outer membrane proteins, LPS and other bacterial components , . While these OMVs were initially characterized by chemical and immunochemical methods, a proteomic analysis performed more recently  revealed that such vesicles contain several factors known or presumed to be related to the virulence of the bacterium, including the outer membrane proteins Omp16, Omp19, Omp25 and Omp31. It has been shown that Omp16 and Omp19 are lipoproteins that modulate MHC II expression in monocytes. On the other hand, Omp25 has been linked to the ability of Brucella to modulate TNF-α secretion in human macrophages . Therefore, it can be speculated that OMVs from Brucella may mediate the transfer of virulence factors to the host cell to generate immunomodulation or other effects that may favor the survival of the pathogen within cells. To our knowledge, the interaction of Brucella OMVs with mammalian cells and the potential immunological consequences of such interaction have not been studied. The evaluation of these phenomena was the goal of the present study.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3506553/
Brucella abortus inhibits IFN-γ-induced FcγRI expression and FcγRI-restricted phagocytosis via toll-like receptor 2 on human monocytes/macrophages.
“The strategies that allow Brucella abortus to persist for years inside macrophages subverting host immune responses are not completely understood. Immunity against this bacterium relies on the capacity of IFN-γ to activate macrophages, endowing them with the ability to destroy intracellular bacteria. We report here that infection with B. abortus down-modulates the expression of the type I receptor for the Fc portion of IgG (FcγRI, CD64) and FcγRI-restricted phagocytosis regulated by IFN-γ in human monocytes/macrophages. Both phenomena were not dependent on bacterial viability, since they were also induced by heat-killed B. abortus (HKBA), suggesting that they were elicited by a structural bacterial component. Accordingly, a prototypical B. abortus lipoprotein (L-Omp19), but not its unlipidated form, inhibited both CD64 expression and FcγRI-restricted phagocytosis regulated by IFN-γ. Moreover, a synthetic lipohexapeptide that mimics the structure of the protein lipid moiety also inhibited CD64 expression, indicating that any Brucella lipoprotein could down-modulate CD64 expression and FcγRI-restricted phagocytosis. Pre-incubation of monocytes/macrophages with anti-TLR2 mAb blocked the inhibition of the CD64 expression mediated by HKBA and L-Omp19. These results, together with our previous observations establish that B. abortus utilizes its lipoproteins to inhibit the monocytes/macrophages activation mediated by IFN-γ and to subvert host immunonological responses”.
Example 3: MRSA
Staphylococcus aureus PSM Peptides Modulate Human Monocyte-Derived Dendritic Cells to Prime Regulatory T Cells.
“Staphylococcus aureus (Sa), as one of the major human pathogens, has very effective strategies to subvert the human immune system. Virulence of the emerging community-associated methicillin-resistant Sa (CA-MRSA) depends on the secretion of phenol-soluble modulin (PSM) peptide toxins e.g., by binding to and modulation of innate immune cells. Previously, by using mouse bone marrow-derived dendritic cells we demonstrated that PSMs in combination with various Toll-like receptor (TLR) ligands induce a tolerogenic DC phenotype (tDC) characterized by the production of IL-10 and impaired secretion of pro-inflammatory cytokines. “
Pretreatment of Pam3CSK4 attenuates inflammatory responses caused by systemic infection of methicillin-resistant Staphylococcus aureus in mice.
“Pam3CSK4 is a synthetic tripalmitoylated lipopeptide that acts as a ligand of TLR1/TLR2 by mimicking the acetylated amino terminus of bacterial lipoproteins. Here we found that pretreatment of Pam3CSK4 protected mice from systemic infection of methicillin-resistant Staphylococcus aureus (MRSA), and enhanced the bacterial clearance in bacteremia model. Pro-inflammatory cytokines, such as TNF-α, IL-6, MCP-1 and IFN-γ were significantly decreased in serum from Pam3CSK4-treated mice. Besides, upon PamCSK4 treatment, the TLR2expression was down-regulated, IRAK1 phosphorylation was inhibited, and the expression of IRAK-M and Tollip, two negative regulators of NF-κB pathway, was up-regulated. All of these indicated that Pam3CSK4 attenuated inflammation via inhibiting TLR1/TLR2 and the downstream NF-κB pathways, and suggested that Pam3CSK4 could be a potential immune modulator for MRSA systemic infection.”
There are lots more. You can find more. LYMErix never could have been a human vaccine, and probably not a dog or other animal vaccine in that it causes immunosuppression. And as we will later see, just forces the next antigenic variant (“selection pressure,” ahem).
THE FIFTH REASON – Seronegative Patients are the Neuro Patients are “the SICKEST,” and this 85% were left out of the Dearborn case definition
You have seen the Dattwyler 1994 quote previously in this report, above.
Dattwyler, Luft, Coyle, Schutzer and Volkman at Stony Brook all reported that seronegative Lyme cases were the neurologic cases and “the sickest (see the 1994 FDA meeting minutes).”
Coyle and Steve Schutzer developed a seronegative Lyme antigen capture method (used on spinal fluid) since these neuroLyme cases are not antibody-positive. Lyme is therefore an immunosuppression disease.
Oh, and Schutzer said at the 2000 or 2001 Lyme.org conference in Hartford, when assigned as part of a 4 person roundtable on testing, which included Donta and Nick Harris (and I forgot the 4th person), and when Donta suggested we use only 2 bands to diagnose Lyme, 23 and 41, said, “We cant because people with Chronic Fatigue Syndrome often have a few Lyme bands.”
So, that very creepy statement by Schutzer means he knows seronegative neurologic Lyme is not about spirochetes, but that is causes immunosuppression. On top of that, Coyle quit Lyme and went into MS, since MS is,… well… you know.
You may wonder why Dattwyler, Schutzer, Luft, Volkman, and Coyle say nothing now about the fake IDSA “guidelines” based on the fake Dearborn “case definition,” which was invented to pass off the fake “vaccine,” OspA, but it’s just cowardice. It is just cowardice, all around. The ALDF.com are all dingbats and IDSA does not look at the science at all. Double dingbats.
Fear and brain disablement ?? = one of those chicken and egg questions, but we know it was the egg that came first. See “Evolution and the development of hard shells in formerly aquatic amphiboreptiles.” Also, fear is learned and the genuinely or genetically or neurodevelopmentally brain-disabled would never make it to college much less medical school. Therefore, fear shrunk their brains and that is why IDSA and most “MDs” are stupid. Cowardice.
Netflix ought to make a 30+ episode series on the subject of why/how doctors are stupid because they are cowards. One episode for every year since we knew Lyme was like post-sepsis syndrome, apparently, with the reactivated EBV according to Allen Steere, and yet we have never seen anyone from IDSA, the CDC, the NIH, or the AMA ask “why” not only that outcome, but why Lyme’s just a bad knee, now.
I wish cowardice was despicable again, but no. Shame is not even a thing in America.
Coyle, Schutzer & Seronegative Lyme antibody or antigen capture
Borrelia burgdorferi-specific immune complexes in acute Lyme disease.
Detection of Borrelia burgdorferi-specific antigen in antibody-negative cerebrospinal fluid in neurologic Lyme disease.
Sequestration of antibody to Borrelia burgdorferi in immune complexes in seronegative Lymedisease.
The Fraud in the Case Definition (happened around 1992-1993, after the early Phase I and II trials of LYMErix and ImmuLyme were underway), with Steere’s, “Antigens in Europe,” raising the cutoff with bogus non-science to exclude neuroLyme and IgM cases. What he did was average the responses between the highly reactive hypersensitivity cases (acrodermatitis and arthritis) with the low neuro Lyme (“sickest”) and EM responders. Anyone who is a scientist knows you dont average the responses to get a cutoff. You’re supposed to show the “lowest limit of quantitation” and we can go nano these days. No need for an eyeballing Western Blot test.
Steere’s basic fraud article that is NOT in the Dearborn booklet – only the twin prospective “study” with that fraud criteria is.
One not in Dearborn booklet:
Antibody responses to the three genomic groups of Borrelia burgdorferi in European Lyme borreliosis.
Falsely raising the ELISA cutoff (from this same report, linked above by Steere)
1994, Oct, Dearborn Booklet (not a consensus; no one knows how we got this standard, regardless): http://www.actionlyme.org/1994_Dearborn_Conference.pdf
The labs on average said that Dearborn method (2 tiered case definition with the outrageous cutoffs) was 8 – 28% accurate, which means it detects 8 to 28 out of 100 known cases (known by other means such as DNA sampling of EM rash or xenodiagnosis) or, on average, 15% accurate.
Gary Wormser himself, said the Dearborn Western Blot IgM and IgG criteria only detected 15% of the cases. It was designed that way, as you can see from Steere’s research fraud report above.
Aguero-Rosenfeld ME, Nowakowski J, McKenna DF, Carbonaro CA, Wormser GP.
J Clin Microbiol. 1993 Dec;31(12):3090-5. Erratum in: J Clin Microbiol 1994 Mar;32(3):860.PMID: 8308100 Free PMC Article
Late in the disease, only 8 plus 1 (9) were positive to the Dearborn IgG criteria of 5 of 10 bands or 15%. Wormser said only 15% of people who were tested for Lyme not knowing about a tick bite but finally not well enough to go to a doctor (who goes to the doctor for a summer flu- no one) and get tested for Lyme, were positive to the Dearborn criteria. This was by-design so that the ALDF.com RICO cabal could pass off a bogus vaccine with an 85% failure rate. Which they did.
If you cant detect Lyme, you cant detect whether or not an OspA vaccine prevented it.
THE SIXTH REASON – Tolerance, Cross-Tolerance, and Thimerosal – well known parallel models.
Thimerosal was invented to prevent fungal diseases or fungal disease contamination in vaccine vials, because if you inject a live viruses that is contaminated ESPECIALLY with TLR2/1 agonist slymy fungal multi-acyl peptides, you are going to not have the classic endotoxin shock response, but something worse that is not reversible. LPS is not as toxic as 3-acyl lipoproteins.
Vaccine Rule is Said to Hurt Health Efforts
”But a proposal that the ban include thimerosal, which has been used since the 1930s to prevent bacterial and fungal contamination in multidose vials of vaccines, has drawn strong criticism from pediatricians.
“They say that the ethyl-mercury compound is critical for vaccine use in the developing world, where multidose vials are a mainstay.
“Banning it would require switching to single-dose vials for vaccines, which would cost far more and require new networks of cold storage facilities and additional capacity for waste disposal, the authors of the articles said.
^^^ It is pretty clear from that report that mercury inhibits bad bad fungal growth, which is bad to co-inject with live viruses, especially. But that is hardly the only evidence that scientifically, you don’t inject 2 infections at the same time, especially when one bears fungal antigens and the other is a virus. “Fatal outcome,” is the phrase you will see in the literature.
IRAK4 kinase activity is not required for induction of endotoxin tolerance but contributes to TLR2-mediated tolerance.
“Prior exposure to LPS induces “endotoxin tolerance” that reprograms TLR4 responses to subsequent LPS challenge by altering expression of inflammatory mediators. Endotoxin tolerance is thought to limit the excessive cytokine storm and prevent tissue damage during sepsis but renders the host immunocompromised and susceptible to secondary infections. Tolerance initiated via one TLR can affect cellular responses to challenge via the same TLR (“homotolerance”) or through different TLRs (“heterotolerance”).”
https://www.ncbi.nlm.nih.gov/pubmed/23695305 <<< And you get the cross tolerance which is a bitch. Now you cant fight off viral diseases or LPS driven diseases, either.
Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection.
“Furthermore, influenza immunization administered at the time of Borrelia infection also failed to induce robust antibody responses, dramatically reducing the protective antiviral capacity of the humoral response. Collectively, these studies show that B. burgdorferi-infection results in targeted and temporary immunosuppression of the host and bring new insight into the mechanisms underlying the failure to develop long-term immunity to this emerging disease threat.”
TLR2 signaling depletes IRAK1 and inhibits induction of type I IFN by TLR7/9.
“IL-1R-associated kinase 1 (IRAK1) was depleted rapidly (within 10 min) by TLR2 agonist, but not until later (e.g., 2 h) by TLR9 agonist. 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. “
THE SEVENTH REASON – The NIH and Yale have said Lyme causes MS and Lupus, which are not the case definition (arthritis in a single joint). They said these were about immunosuppression and EBV.
The NIH had a “Lyme and MS division” in the NINDs.gov run by Roland Martin, a scientist recruited from Germany because he thought he had found a molecular mimic in borrelia that caused an autoimmune reaction, resulting in the well known MS outcome of Lyme.
Yale had a “Lyme and Lupus Clinic” which after they realized there was a problem with their OspA vaccine, closed up shop and opened “L2” (for Lyme and Lupud) Diagnostics, which was funded by Yale’s Endowment Fund, run by Robert Schoen, and which was part of the Rico within the RICO with Corixa and Imugen. The 3 companies had rights to a Mayo Clinic patents spirochete with no OspA and B plasmid which they intended to use to test people after the OspA vaccine was on the market. This is fraud and racketeering at its finest. Exclude OspA-B from the case definition after saying it they were so specific to Lyme they could be vaccines, have a fake vaccine trial, lie about the results and [
Borrelia burgdorferi–specific and autoreactive T-cell lines from cerebrospinal fluid in Lyme radiculomyelitis.
Martin and Marques of the NIH now saying Borrelia causes disease via immunosuppression, but with chronic inflammation in the brain, and that these are caused by the triacyl, fungal Osps.
Martin and Marques; the NIH:
Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.
“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.
Martin and Marques – the NIH:
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.”
Likewise, Yale had a “Lyme and Lupus Clinic” which later became “L2 Diagnostics,” part of the “Little Rico within the RICO” enterprise consisting of Corixa, L2 Diagnostics, and Imugen. Lupus is not an autoimmune arthritis, which is now the case definition of Lyme, Lupus is considered an autoimmune neurologic disease, and there is much evidence that it too is run by chronic active Epstein-Barr. Even Joe Craft (buddy of Steere’s) at Yale thinks so… Lupus and MS are well known to be outcomes of Lyme.
Lyme is not really a bad knee but something that activates latent viruses that result in an HLA-linked autoimmune hypersensitivity response to one of more of the secondary opportunistics or latent viruses or other pathogens reactivated by Lyme’s classic endotoxin tolerance and cross tolerance – slash – post-sepsis – slash – immunosuppression – slash – is AIDS-ish :
Dormant viruses re-emerge in patients with lingering sepsis, signaling immune suppression. A provocative study links prolonged episodes of sepsis — a life-threatening infection and leading cause of death in hospitals — to the reactivation of otherwise dormant viruses in the body.
Yale’s Joe Craft and Lupus as reactivated EBV:
J Immunol. 2004 Jan 15;172(2):1287-94.
Defective control of latent Epstein-Barr virus infection in systemic lupus erythematosus.
1Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06520, USA.
“EBV infection is more common in patients with systemic lupus erythematosus (SLE) than in control subjects, suggesting that this virus plays an etiologic role in disease and/or that patients with lupus have impaired EBV-specific immune responses. In the current report we assessed immune responsiveness to EBV in patients with SLE and healthy controls, determining virus-specific T cell responses and EBV viral loads using whole blood recall assays, HLA-A2 tetramers, and real-time quantitative PCR. Patients with SLE had an approximately 40-fold increase in EBV viral loads compared with controls, a finding not explained by disease activity or immunosuppressive medications. The frequency of EBV-specific CD69+ CD4+ T cells producing IFN-gamma was higher in patients with SLE than in controls. By contrast, the frequency of EBV-specific CD69+ CD8+ T cells producing IFN-gamma in patients with SLE appeared lower than that in healthy controls, although this difference was not statistically significant. These findings suggest a role for CD4+ T cells in controlling, and a possible defect in CD8+ T cells in regulating, increased viral loads in lupus. These ideas were supported by correlations between viral loads and EBV-specific T cell responses in lupus patients. EBV viral loads were inversely correlated with the frequency of EBV-specific CD69+ CD4+ T cells producing IFN-gamma and were positively correlated with the frequencies of CD69+ CD8+ T cells producing IFN-gamma and with EBV-specific, HLA-A2 tetramer-positive CD8+ T cells. These results demonstrate that patients with SLE have defective control of latent EBV infection that probably stems from altered T cell responses against EBV.”
THE EIGHT REASON: The crooks did not allow adverse events to LYMErix to be reported during the trial, so we went to the FDA ourselves in 2001 to reveal that LYMErix resulted in what we call “chronic neuro Lyme,” and we were not the only ones. DONALD MARKS
It Being Empirically Observed by a LYMErix Trial Administrator. Donald Marks, too.
“HOW SMITHKLINE BEECHAM (GLAXO SMITHKLINE) USED CONFUSING LANGUAGE, KEEPING FDA AND PHYSICIANS IN THE DARK:
“The Company dismissed the significance of adverse events reported since marketing by stating the vaccine’s profile had not changed “except as described below…” The description referred to, rendered with numbers but given no contextual explanation, in fact implied a huge change in safety. The company’s confusing language made it sound as if the adverse events, many of them severe, had no particular significance at all.
“As proof of safety, the company inoculated arthritis-prone mice with Osp-A. But since the mice did not possess the HLA marker known to interact with Osp-A in humans, the experiment was, in fact, meaningless.
“The company has masked serious causally-related adverse events behind qualifiers, such as “…and which may have no causal relationship with the vaccine” and “…cannot be distinguished from the natural history of the underlying disease,” all the while knowing these are confusing the issues.
“The company tries to shift the blame from the vaccine to the patient with statements such as “the possibility of a severe rheumatologic, neurologic, autoimmune adverse event is inherent in Lyme disease.” The company does not inform physicians that the adverse events can result from Lymerix, completely apart from the disease.
“As a result of these actions, GPs in the US were kept in the dark about the life-threatening side effects of Lymerix. …”
It being observed, and the Lyme crooks actually admitted that you cant tell the difference between Lyme and LYMErix disease. That is, the neurologic seronegative kind. Latov:
Neuropathy and cognitive impairment following vaccination with the OspA protein of Borrelia burgdorferi.
Dave Persing (of Corixa, with Robert Schoen of Yale and Imugen, the Little Ricosketeers):
Method for detecting B. burgdorferi infection
“…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.”
Finally, me, as a support group leader finding out from the victims LYMErix was causing “Lyme, again,” telling the FDA about Dearborn – how no one approved among the invited labs – and how OspA caused immunosuppression:
That was Jan 31, 2001.
THE NINTH REASON — Disinfecting Ticks with Human Blood ?? (allegedly how LYMErix “worked”). Yeah, that was a fraud or false claim too;
Okay, so that was a ridiculous enough claim, especially coming from the very people who own the 2 OspA vaccine patents, ImmuLyme and LYMErix and who said you cant have vaccines for Borreliae spirochetes due to antigenic variation or selection pressure. But WHY couldnt you use your Bb speciific Fla-DNA method to see if OspA disinfected ticks? Because OspA then, wont be expressed (selected against) and flagellin is not surface exposed. This is Fikrig now (graphic below):
Watch. You cant make this up… Both vaccine patent holders, Fikrig/Flavell (Yale, LYMErix) and Alan Barbour (owns most TBD related patents in the world, owns the ImmuLyme OspA patent), say OspA wont work as a vaccine due to selection pressure or antigenic variation.
“This report describes the ability of OspA and OspB antibodies to cause the in vivo selection of B. burgdorferi organisms with subtle genetic alterations that result in the expression of OspA or OspB which do not bind to, or weakly bind with, antibodies that are protective in nature. These data suggest a potential reason for the lack of complete efficacy of an Ospbased Lyme disease vaccine. Over extended periods of time, the administration of an OspA- or OspB-based vaccine to hosts that are involved in the natural life cycle of the spirochete may result in the expansion of variant B. burgdorferi isolates within ticks at a higher frequency than would normally be found in the general population. If this selection pressure was to be maintained, the number of variant spirochetes could rise to a significant level, such that the efficacy of a monovalent OspA- or OspB-based vaccine could be impaired in the future.”
Alan Barbour, owner of the ImmuLyme OspA patent, talking about how it would not work due to OspA undergoing antigenic variation in
Antibody-resistant mutants of Borrelia burgdorferi: in vitro selection and characterization.
OspA is not expressed at 37 C, that is why these criminals made up a story about the OspA vaccination works by human blood disinfecting ticks.
J Infect Dis. 1998 Oct;178(4):1198-201.
Differential expression of Borrelia burgdorferi genes during erythema migrans and Lyme arthritis.
“ospA was investigated because OspA is down-regulated by B. burgdorferi in ticks during engorgement and is a vaccine candidate in phase III clinical trials.”
“OspA is not present in the salivary glands of feeding ticks…and OspA antibodies are not in the sera of mice infected with tick transmitted spirochetes.”
“In general, OspA is thought to be down-regulated in engorging ticks and in early stages of infection.”
“When ticks engorge, OspA is downrregulated and OspC is up-regulated [1–3].,”
So, what they should have done was feed DIRTY, Lyme-infected ticks to an OspA vaccinated mammal, and then put the ticks for a second feeding on some other mammal to see if that second mammal was infected. Because the trouble is not OspA, it is OspC, the brain invasion antigen, according to Alan Barbour (use pubmed and find that out for yourselves).
The Tenth Reason
Here is the patent/development report for the 1991 Yale flagellin DNA method that is SPECIFIC to Lyme borrelia:
“The earliest humoral response in patients infected with Borrelia burgdorferi, the agent of Lyme disease, is directed against the spirochete’s 41-kDa flagellar antigen. In order to map the epitopes recognized on this antigen, 11 overlapping fragments spanning the flagellin gene were cloned by polymerase chain reaction and inserted into an Escherichia coli expression vector which directed their expression as fusion proteins containing glutathione S-transferase at the N terminus and a flagellin fragment at the C terminus. Affinity-purified fusion proteins were assayed for reactivity on Western blots (immunoblots) with sera from patients with late-stage Lyme disease. The same immunodominant domain was bound by sera from 17 of 18 patients. This domain (comprising amino acids 197 to 241) does not share significant homology with other bacterial flagellins and therefore may be useful in serological testing for Lyme disease. “
Here is the patent for that (US 5,618,533, 1991):
Here is the patent for Yale’s OspA vaccine (applied for in 1994):
That is the easiest way to prosecute this. Obviously Fikrig/Flavell knew LYMErix would not prevent Lyme, only force antigenic variation. And obvious OspA would not be a vaccine if it caused immunosuppression, instead -, and is the reason Lyme is a Great Imitator. It is the opportunistics that cause all the trouble. This is why Lyme is not curable with antibiotics.