BACKGROUND OF THE INVENTION:
“Science,” “doctors” and the “journals” all defaulted. They left medicine up to the American Psychiatric Association and the DSM, and look what it got us. In the United States alone, there are 4 million people with fibromyalgia, 8 million with chronic fatigue syndrome, and untold millions with Lyme disease, Gulf War Illness, mitochondrial disorders, and the various explanations that involve voodoo witch magic with self-backfiring incantations, AKA “somatoform.”
That’s right—it’s Halloween—a good time to remind everyone that medical profession believes there are upwards of 30 million real, live witches in the U.S.—terrible witches who can’t cast a proper spell and end up disabling themselves.
Really. We can put a rover on mars, MIT can electromagnetically explain crop circles, yet the only explanation for all these millions of sick and disabled and brain-addled people is that they are so worried about being sick, they are actually making themselves sick.
DSM witchcraft and half the medical journal articles are bogus and no one can find Lyme disease. That’s where we are now.
Richard Horton, editor of The Lancet:
“The case against science is straightforward: much of the scientific literature, perhaps half, may simply be untrue.”
Let’s take Dr. Horton’s assertion at face value. Now consider the “New Great Imitator,” Lyme. What’s it imitating? A whole lot of diseases under one umbrella—multiple sclerosis, fibromyalgia, lupus, chronic fatigue syndrome, dementia, rheumatiod arthritis, stroke, ALS…and Willy Burgdorfer said, “after 30 years we have nothing.” Make that 40 years now. Forty years after the “discovery” of Lyme disease, half the “science” on all the diseases it “imitates” is bogus.
Someone assigned Allen Steere to it. No one knows why. Perhaps someone at the CDC ascertained that he was unhappy with medicine as a profession—after all, it was one he chose to avoid the Vietnam draft—and also because he had a severe case of myopia. At the 1998 FDA meeting on LYMErix, Raymond Dattwyler said of Steere’s Bad Knees Disease:
“I see a lot of patients, and I must say that treatment resistant lyme arthritis in our center is low; it is very rare. We see maybe one case a year. And, you know, that is using very strict criteria, saying that the person had, you know, CDC criteria for seropositivity, good history, and usually is monoarticulate knee arthritis.”
Dattwyler sees about *uno* cases per year. There aren’t very many Dearborn, CDC, 2-tiered positive cases of “Lyme disease.” There never were. It was never about arthritis. Neither the disease nor the OspA vaccine trial results were ever really about arthritis. What “Lyme disease” is really about (and LYMErix too), is much, much worse.
FORTY years down the drain. No one is getting better. Too much research fraud and downright stupidity (definition: willful ignorance). We can’t believe the science. We can’t believe how science is reported. WE can’t believe the FDA never looked at the Dearborn case definition. They told us so. This is the reason Senator Richard Blumenthal and company had to have the Office of Budget and Management ORDER the FDA to assure the Lyme testing is valid according to the FDA’s rules on the validation of an analytical method.
The first criterion in a validation is ACCURACY, or, “Does your method detect 100% of the samples where the analyte in question is known to be present?” (Additionally it should give the range of what % of the known analyte your method found, but the first premise is that it should detect SOME of the analyte if it is known to be there.)
If it can’t be 100% for anti-flagellar antibody cases it should be close. (It is about 95% present in known, erythema migrans sampled, DNA for Borrelia, cases.) And for this reason, to increase SENSITIVITY (or how low in concentration of the analyte in question can your method detect), this problem was addressed in 1992 by the late Lou Magnarelli and the people who own the patent for the only FDA-valid test for Lyme—and who are also the owners of the LYMErix patent, Yale’s Fikrig and Flavell:
“A recombinant protein (p41-G) of an antigenic region of flagellin was used in a standard and amplified enzyme-linked immunosorbent assay (ELISA) to detect antibodies to Borrelia burgdorferi, the causative agent of Lyme borreliosis. Comparable sensitivities (88 to 94%) were noted when sera from 17 persons who had erythema migrans and antibodies to whole-cell B. burgdorferi were tested against the p41-G antigen. In tests of a second study group of 36 persons who had erythema migrans but no detectable antibodies to whole-cell B. burgdorferi, 3 (8%) were positive when the p41-G antigen was used. Assay specificity likewise increased when the p41-G fragment was included in an ELISA with human sera containing treponemal antibodies. Recombinant flagellar proteins of B. burgdorferi, such as the p41-G antigen, can be used in an ELISA and may help confirm Lyme borreliosis during early stages of infection and improve specificity.”
Fikrig, Magnarelli and Flavell basically said, “Here we have made the common anti-flagellar antibody (found in most Lyme patients—and the ONLY specific biomarker for Borrelia burgdorferi, thus meeting TWO FDA validations requirements—accuracy and specificity) not only SPECIFIC (FDA validation criterion – does not detect anything else besides Borrelia burgdorferi flagellin), but even more useful by adding in or spiking it into an ELISA made of borrelia sonicate, BECAUSE … some people don’t even make a lot of anti-flagellar antibodies, the one most people make if they make any at all. And if one wanted to go nanotech, the thing to do is put these sorts of fragments of Borreliae-specific flagellins on nanotubes and look for these specific antibodies in human blood, since antigen itself is less likely to be there. Borreliae like to live in the brain.”
That was 1991 and 1992. Fikrig and Flavell own (patented) that test (US Patent #5,618,533). They own the LYMErix patent…and they own this method, the only FDA-valid test to assess it. But they very clearly did not use a valid test to assess LYMErix. We know why.
At the time, lots of researchers were looking for ways to use the anti-flagellar antibody as the primary means of diagnosis. You can look this up. Use the National Lilbrary of Medicine. That was, you know, back in the day when there was less research fraud—the late 1980s, early 1990s. It was a common idea, and valid, because most people with Lyme are known to at least have the flagellar antibody. Here is the report from 1991 that goes with the Yale flagellin method patent:
The NIH’s Lyme-And-MS Division of NINDS found in 2006, however, that exposure to the shed fungal antigens like OspA, found on spirochetal blebs (more about that below) can also turn off the function of the TLR5 receptor that handles flagellin. This could be the reason some Lyme victims are totally seronegative (no antibodies against Lyme at all). Here are the 2 reports by this MS-Lyme group that say OspA is responsible for causing nearly complete immunosuppression, in the end:
Recall that the bogus Klempner long term “retreatment” study where two-thirds of his victims had never before had IV ceftriaxione (the standard of care at the time), was based on the inclusion/exclusion criteria of the fraudulent Dearborn case definition, rendering the entire study invalid.
Additionally, the study was assessed with the non-scientifically valid Fibromyalgia Impact Questionaire (FIQ). “Questionaires” or “check lists” are a means of using invalid psychiatry as the dominant assessment criteria for a real, valid medical illness. The IDSA/CDC Lyme crooks did this despite also being the authors of all the scientifcally valid physiological biomarkers of brain and CNS destruction. Yet, this Klempner report is the basis of the IDSA 2001 and 2006 “guidelines” on the non-diagnosis and non-treatment of Lyme disease.
Therefore once the fraud of the Dearborn event is prosecuted, out go all of IDSA’s “guidelines.”
http://cid.oxfordjournals.org/content/43/9/1089.long << Go ahead and read that for all the ridiculousness and false statements they make and in which they repeatedly quote their own previous research fraud. Mark Klempner himself found ceftriaxone did not kill all the spirochetes even when there weren’t human cells to hide inside:
Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro. [Full Text: KlempnerFibroblastsCombined]
“The Lyme disease spirochete, Borrelia burgdorferi, can be recovered long after initial infection, even from antibiotic-treated patients, indicating that it resists eradication by host defense mechanisms and antibiotics. Since B. burgdorferi first infects skin, the possible protective effect of skin fibroblastsfrom an antibiotic commonly used to treat Lyme disease, ceftriaxone, was examined. Human foreskin fibroblasts protected B. burgdorferi from the lethal action of a 2-day exposure to ceftriaxone at 1 microgram/mL, 10-20 x MBC. In the absence of fibroblasts, organisms did not survive. Spirochetes were not protected from ceftriaxone by glutaraldehyde-fixed fibroblasts or fibroblast lysate, suggesting that a living cell was required. The ability of the organism to survive in the presence of fibroblasts was not related to its infectivity. Fibroblasts protected B. burgdorferi for at least 14 days of exposure to ceftriaxone. Mouse keratinocytes, HEp-2 cells, and Vero cells but not Caco-2 cells showed the same protective effect. Thus, several eukaryotic cell types provide the Lyme disease spirochete with a protective environment contributing to its long-term survival.” http://www.ncbi.nlm.nih.gov/pubmed/1634816
Occam’s Razor: Nobody in Medicine or Science Can Claim to be the Sharpest Blade
Ever hear of Occam’s Razor? It’s the principle that the simplest explanation is usually the correct one. If you hear hoofbeats, think ‘horses,’ not ‘zebras.’ If it quacks like a duck…etc. Don’t overthink this stuff. It’s all there. You just have to look at the big picture.
I. Start with the most compelling data; Yale/CDC Lyme perps did a 180 on everything.
1) The CDC, IDSA and Yale claim that only the HLA linked arthritis cases were allowed to be called “Lyme disease.” This is the Dearborn, implemented-in-1994-but-still-current “case definition.” The 2005 Klempner and Wormser HLA report re-stated that the case definition was HLA-linked and the victims had no other illness signs but arthritis. So, that’s the only “case” of Lyme one is allowed to have. It means you may have arthritis, only—an HLA-linked hypersensitivity response with lots of antibodies, and no fatigue or meningitis or anything else. The other symptom-set people, the non-HLA linked people, well, that’s a mystery, right? Must be psychiatric. Witches.
2) But this definition came after the same people claimed:
a) that Lyme caused everything (MS, lupus, ALS, dementia, stroke, chronic fatigue syndrome, fibromyalgia, etc.),
b) that chronic neurologic Lyme was incurable in half the cases (Dattwyler, Luft, Sigal, Steere, in 1989 IDSA Review special supplement on Lyme and Spirochetal diseases), and
c) that spirochetal diseases were incurable, even with ceftriaxone, even when there were no human cells for the spirochetes to hide in (Klempner, 1992).
3) At that time, in the 1989 IDSA Reviews, a one Paul Duray, pathologist for Yale, the US Army, the National Cancer Institute, etc., found that the immune cells in the spinal fluid of chronic neurologic Lyme victims looked immature and mutated, or neoplastic or EBV-transformed. Look those words up:
“EBV-transformed” or “EBV-immortalized” cells is a known thing and very relevant to the OspA crime.
CAUTION: If the reader is not familiar with what “EBV transformed” means, please study the topic and do not make assumptions based on no background.
4) And the OspA vaccine victims were acquiring the same “multi-system,” (Dave Persing), “protean” (Ben Luft) disease manifestations that the ALDF.com, CDC, Yale and later IDSA threw out of the case definition at Dearborn. The chronic fatigue syndrome, the fibromyalgia, the chronic systemic disease with dementia signs and neurological signs, etc. —were thrown out of the vaccine trial results and described as “Unconfirmed Lyme.” Those cases were not counted as vaccine failures.
5) Never lose track of this statement by U.S. Department of Energy and likely a physician at SUNY-StonyBrook:
“It’s the perfect stealth bacteria,” says one frustrated physician. He’s talking about Borrelia burgdorferi, the bacterium that causes Lyme disease. This illness, which is often mistaken for diseases ranging from multiple sclerosis to Lupus, can inflict excruciating headaches and muscle pain, affect the brain and nervous system, attack major organs, and inflame joints…” —Energy Science News, pnl.gov [full article: BrookhavenStealthBacteria]
MS and Lupus are not “solely a monoarticular arthritis with a high antibody concentration against Borrelia with no other symptoms” —the current CDC, Dearborn “case definition.” Says them ^^^.
II. 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:
It’s Pam3Cys or 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:
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 membrane vesicles 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.”
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.”
The thing you should be doing, now that establishment medicine and all the universities have basically defaulted on the Big Picture (20-30 million people disabled from the incompetent witch phenomenon), is follow up on these reports in PubMed, and “See Related” articles, and “See Cited by” articles and do your own research. Don’t be afraid to take your time to develop the vocabulary; use multiple sources for basic biology and chemistry facts. By using multiple sources, you’ll capture some sources that use a language set you already have. Then you can cross over and back to other sources until the picture is clearer for you. And VERIFY, VERIFY, VERIFY. Don’t be afraid. Remember, there are no experts—only DSM voodoo witch hunters.
III. And now some of the Alphabet, A-L, which all point to, well, LYMErix was never a vaccine and caused the same immunosuppression disease as Chronic Lyme. What are the common opportunistics we see emerge in immunosuppression cases?
A. Here next we see Brucella and its TLR2/1 agonist antigens do the same thing: turning off the immune response and causing immunosuppression, producing no antibodies. MHC II or HLA molecules deliver antigens to the surface of the immune cell against which antibodies will be made. If, along comes a TLR2/1 agonist, in time, this function stops. No more antigen is presented; no more antibodies will be made. There are multiple explanations for this mechanism but we have a “THE LIST” at the end of this report with researchers who present information on mechanisms of TLR2-agonist related immunosuppression.
Use your search feature to look for “MHC” elsewhere in this report.
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.”
B. Now here, let us once and for all, pay attention to the fungal antigen specialist Clifford Harding: “Several studies have shown fungal antigens like LYMErix (TLR2-agonists) decrease antibody production or cause seronegativity.”
Regulation of antigen presentation by Mycobacterium tuberculosis: a role for Toll-like receptors
“Several studies have demonstrated that M. tuberculosis-infected macrophages have decreased MHC class II molecule expression and decreased antigen presentation, reducing CD4+ T cell recognition of infected macrophages20,22–24,30,32–38. Comparison of the T cell responses to model antigens presented by M. tuberculosis-infected macrophages and to antigens presented by uninfected macrophages showed that M. tuberculosis reduced antigen presentation by macrophages 12–18 hours or more after infection32,35.
“Recent studies have provided insights into the molecular mechanisms involved in the inhibition of MHC class II antigen presentation by M. tuberculosis. Viable M. tuberculosis is not required for inhibition of macrophage MHC class II expression and antigen presentation, which can be achieved by exposure of macrophages to M. tuberculosis lysate22,30,33–35,39. Biochemical fractionation was used to identify M. tuberculosis components that inhibited MHC class II molecule expression, and several M. tuberculosis lipoproteins, including LpqH32, LprG40 and LprA41, were found to be key inhibitors. These lipoproteins, as well as PhoS1 (also known as PstS1), are agonists of TLR2 (REFS 23,32,40–43) (TABLE 1), and their inhibition of MHC class II molecule expression and antigen presentation is dependent on TLR2 and its adaptor, myeloid differentiation primary-response protein 88 (MYD88)19,23,32,40. Furthermore, MHC class II inhibition that is mediated by viable M. tuberculosis is itself also largely dependent on TLR2 (REFS23,32) and, to an even greater degree, on MYD88 (REF. 23), although some MHC class II inhibition might be due to non-lipoprotein components of M. tuberculosis and could be MYD88 independent18,19,21.
“Thus, prolonged TLR2 signalling induced by M. tuberculosis lipoproteins (and, potentially, by other TLR2 agonists expressed by M. tuberculosis18) results in inhibition of MHC class II molecule expression and antigen presentation by M. tuberculosis-infected macrophages.”
Fungal antigens cause immunosuppression resulting in no antibodies against Borrelia, particularly not OspA. Not TLR2/1 agonists. Not Pam3Cys. No. It does not result in antibodies. Period. You have this outcome if you have “chronic Lyme.” OspA never could have been a vaccine. Clearly Yale falsified their LYMErix vaccine results. And Dearborn, with the requirement for high antibody production, is research fraud. Lyme Osps, Brucella Omps, and Mycobacteria Lprs…and several studies say so.
Whoever does not know what LYMErix disease is does not know what Lyme disease is. This includes the International Lyme and Associated Diseases Society (ILADS) 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.
C. 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.” http://www.ncbi.nlm.nih.gov/pubmed/15363064
D. 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.” http://www.ncbi.nlm.nih.gov/pubmed/21673416
It’s not “Autoimmune.” It’s Subimmune.
This Subimmunity represents the entire class of the DSM VooDoo Somatoformia—as well as cancer. Cancer is in the Subimmune class, at the other end of the immunity spectrum from Autoimminity. 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. 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).
E. 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 alluding 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…” http://www.fda.gov/ohrms/dockets/ac/98/transcpt/3422t1.rtf
F. 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…”
Oh, you mean LYMErix causes the same disease as Lyme?
REVIEW: Latov, Marks, Luft, Persing and Schoen all say LYMErix produced a disease we know of as Chronic Lyme. We have seen that Lyme arthritis barely exists (Dattwyler), and we actually DO know how to detect Lyme disease with 95% accuracy. We have seen what OspA is, how it gets around, and that it is a fungal toxin. Later we will see who else says LYMErix never could have been a vaccine and acts as the complete opposite. We will see who jumped ship from Lyme research to only MS, and who only specializes, oddly, in Lyme and Epstein-Barr (and similar herpesviruses).
The very disease manifestation left out of the Dearborn case definition—the chronic neurologic, MS, Lupus, etc.—was caused by the vaccine in at least 11% of the LYMErix victims. You can look up those trial results. It turns out CDC officer Alan Barbour and Durland Fish, one of the original founders of the ALDF.com (which later hijacked IDSociety.org), had written a paper together in 1993 trashing the non-arthritis people and incidentally stating that the Phase I and II trials of OspA were underway. You can conclude Dearborn happened so that the most serious cases of Lyme —caused by the vaccine, too—could be excluded.
The kind of Lyme detected by the Dearborn case definition? Barely exists. Good way to have a vaccine trial. Design a fake disease serology that no one has, then have a fake vaccine trial. No one has the disease. Voila, your vaccine is amazing. Still no one has that disease. Oh, and deploy the DSM because no one is really looking at the DSM and psychiatry’s inconsistent perceptions and attitudes towards the paranormal, not to mention their kaleidoscopic cornucopia of interchangeable “disorders” and drugs. The evanescent Chronic Fatigue Syndrome and Fibromyalgia—they’re a totally handy thing. Twelve million of us have “it” and not a nickel towards research on the cause. Because the cause is actually known, and no one cares, since nearly everyone already has most of the herpesviruses, and especially Epstein-Barr.
The CDC themselves held the Dearborn conference, being owners of several useless vaccine candidates, including Alan Barbour who owned one of the OspA vaccine patents (ImmuLyme), which threw out the most serious LYMErix adverse events, which were identical to the case definition thrown out at Dearborn. In other words, Dearborn was constructed to falsify the OspA vaccines outcomes and they clearly knew these adverse events/neurologic, chronic cases were being caused by the vaccine.
Dearborn excludes 85% of all cases (the ones that are NOT HLA-linked arthritis-lots of antibodies-hypersensitivity cases), and 100% of all the neurologic Great Imitator outcomes. You now may only have a disease if you have no disease. Just a bad knee. We are not making this up. Here is exactly what Klempner and Wormser said about the HLA-link to the Dearborn case definition, 11 years later:
G. A Case-Control Study to Examine HLA Haplotype Associations in Patients with Posttreatment Chronic Lyme Disease
“…There appear to be at least 2 distinct syndromes in patients with persistent symptoms after antibiotic treatment. One syndrome has localized symptoms that are similar to pretreatment symptoms. Patients with this syndrome often have recurrent episodes of arthritis/synovitis. Results of synovial fluid cultures and polymerase chain reaction (PCR) for B. burgdorferi are negative . Patients generally feel well aside from their arthritis symptoms. Specific HLA haplogroups (i.e., HLA-DR4 and HLA-DR2) have been associated with the failure to respond to antibiotics in this group of patients, and their arthritis may be due to molecular mimicry between a dominant epitope of outer surface protein A (OspA) of B. burgdorferi and lymphocyte function–associated antigen–1 (LFA-1) . A much more common syndrome of persistent symptoms is a systemic illness that is characterized by profound fatigue, myalgias, polyarthralgias without arthritis, paresthesias, and mood and memory disturbances. This syndrome has been variously referred to as “chronic Lyme disease,” “post–Lyme disease syndrome,” and “posttreatment chronic Lyme disease” (PTCLD). The cause of the persistent systemic symptoms in these patients is unknown. However, we have reported elsewhere that the impact that PTCLD has on health-related quality of life was highly significant and that treatment with placebo or 90 days of additional antibiotics did not differentially affect patients’ health-related quality of life . We also did not find evidence of persistent infection with B. burgdorferi or exposure to other tickborne infectious agents that could explain the persistent systemic symptoms.”
So, there are 2 distinct diseases: Arthritis (“one case a year”—Dattwyler), and the other thing —the chronic neurologic. The first thing, where people do not feel sick, is a Dearborn “case” of Lyme. But, these criminals claim, those chronic neurologic cases are not sick from B. burgdorferi.
No, it’s much much worse. The OspA, Pam3Cys, LYMErix and ImmuLyme vaccines caused it, too. And then there’s those irksome “Epstein-Barr like mutated B cells in the spinal fluid of chronic neurologic Lyme victims…”
H. And there’s the venom, the slander, the libel, the trashing, the Salem Witch Trials dealt to chronic neurologic Lyme victims all these years, started by the ALDF.com [Durland Fish, Gary Wormser, Barbara Johnson (CDC), Alan Barbour (CDC), Dave Persing, Robert Schoen, John Nowakowski, Mark Klempner, Edward McSweegan, Allen Steere, Stanley Plotkin, a guy named Sood, Vijay Sikand, Eugene Shapiro, Henry Feder, Larry Zemel, Lenny Sigal, Dave Dennis, Phil Baker, etc.]. …Suttins up.
ILADS was there.
ILADS did not exist in its present form at the time of the vaccines scandals, in the late 1990s and early 2000s. They were merely an e-list called MMI. But they did exist in the middle of 2001. Kathleen Dickson wrote their original Klempner rebuttal in June 2001; it was a simple list of proofs that the whole report was invalid, starting with Dearborn being invalid, since Dickson had already shown that to the FDA in Jan 2001. (Analytical Methods development and validations is what she did for a living at Pfizer.)
ILADS knew what went down with that vaccine and how Dearborn was falsified, as Dickson was on their e-list and also testified at the FDA hearing on LYMErix in January 2001. Yet, ILADS say nothing about it, because they’re treating “Lyme disease.” “Spirochetes.”
Meanwhile the OspA vaccines alone caused the same disease ILADS alleges to be treating. It’s no wonder people get second and third mortgages and end up with no house in addition to not being any better from their chronic Lyme. ILADS and the Lyme non-profits clearly do not care. It is obvious no one is getting better. Look at all the celebrities who have all kinds of money. We all know if Lyme is not caught early, it is incurable. But is it incurable? Perhaps not if the Cause is Known.
You’ve Heard this Before:
We will get to this in more detail in this report, but basically the disease is this: When your immune system is turned off by constantly shed “vesicles” or “exosomes” or “blebs,” or blobs of protoplasm, some of which contain DNA, latently ubiquitous herpes viruses can be reactivated—HSV, CMV, HHV-6, Zoster, and especially EBV. It very much appears—and we are not the only ones saying so—that these viruses are the true culprits behind what we know as chronic Lyme disease. Little else explains the variety show of MS, Lupus, Chronic Fatigue, or an AIDS like outcome. That this happens is claimed by many: Washington University in St Louis, MO, and even the NIH. They refer to it as post-sepsis and you have heard us remark about this phenomenon before (all roads pointing to OspA-induced or fungal antigen-induced AIDS-like disease):
This phenomenon of blebbing or shedding vesicles or microbial sharing of DNA goes for nearly all organisms, not just spirochetes. In particular the Borrelia blebs have OspA-ish or fungal antigens on them. And these shed blebs go all around the body, into the brain and into the kidneys as we have shown, and so says the NIH in one of their patents from 1995. Igenex tried to capture them in the old days with their urine antigen capture method called the LUAT. SUNY Stony Brook also had an antigen-antibody de-complexing method for spinal fluid analyses. But blebs, and OspA antigen on them, is what they were looking for to show active infection regardless of a patient’s antibiotic history. There are many more of them than there are spirochetes. Immune cells pick them up, and then… they’re stuck. Literally.
I. Back Up, “beep beep beep…” Has anyone ever tried to make fungal antigens into vaccines before?
Let’s look at some other fungal-type, lipoprotein (managed by TLR2/1 as a pair, together, meaning it is such and such type of antigen, in this case, highly lipidated, tri-acyl or higher) vaccine attempts to see if the same outcome LYMErix gave happened in parallel? That should be a good researcher’s first thought. Apparently neither ILADS nor IDSA nor even the entire U.S. Department of Health and Human Services (under which are all the National Institutes, OMG) had any such first thoughts:
The 19-kD antigen and protective immunity in a murine model of tuberculosis.
“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.”
Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits Mycobacterium smegmatis-induced cytokine production by human macrophages in vitro.
“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.”
The Mycobacterium tuberculosis recombinant 27-kilodalton lipoprotein induces a strong Th1-type immune response deleterious to protection.
“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.”
“A deleterious effect on immunity,” “an adverse effect on the protection,” “the immunosuppressive effect,” “diminished protection,” “reduced T cell activation…”
THEY DON’T WORK. Lipoproteins are the opposite of vaccines.
J. Raymond Dattwyler, 1988. Not surprisingly, that data on the failed Tuberculosis (Tb) fungal vaccines is all quite reminiscent of what Ray Dattwyler said about Borrelial supernatant—the stuff that floats on the top, the oil of the oil and vinegar, yeah, the oil, the lipids, the lipoproteins, the Osps…
From: 1988, Modulation of natural killer cell activity by Borrelia burgdorferi. Golightly M, Thomas J, Volkman D, Dattwyler R.
“Effect of B burgdorferi Culture on Normal PBL
“..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).”
K. Lipoproteins BLUNT immunity. Here is what Gary Wormser said about OspA vaccines for dogs in July 2000, while LYMErix was still on the market:
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.”
Once more (you’ve just seen 5 examples), lipoproteins and lipoprotein vaccines suppress immunity, even in animals, which are known to have more broad natural immunity than humans (making animal diseases very good sources of human disease bioweapons). Three Tb vaccines based on lipoproteins, Dattwyler, et al, claiming Borrelia oily lipoproteins blunt immunity, and Gary Wormser himself said lipoproteins do that mysterious thing… “blocking of cell cycle phase progression.” Later we will learn OspA inhibits apoptosis, which is the same thing EBV does. That is what “EBV-immortalized” means. The infected cell does not kill itself, or undergo apoptosis as a way of keeping the pathogens from reproducing themselves.
BCL2 CLASS MOLECULES AND OSPA INHIBIT APOPTOSIS; NO “BIOFILMS” IN VIVO
BCL2-class molecules do the same thing, they inhibit apoptosis or they block the auto-kill or apoptosis kinases (enzymes). BCL means B Cell Lymphoma (clue). If you have too many copies of a BCL2 class gene, as is the case with “nerve overgrowth syndromes” such as Neurofibromatosis or/and Autism (the Einstein, Tesla, Newton, Grandin kind), their over-expression leads to inhibition of apoptosis. This is thought to be the case with the genetic, large-brain kind of Autism; a “lack of normal synaptic pruning.” A BCL2 class gene happens to co-confer with other copies in the case of reversed duplication, as shown here:
Organisation of the pericentromeric region of chromosome 15: at least four partial gene copies are amplified in patients with a proximal duplication of 15q.
“We identified a fourth pseudogene, BCL8, which maps to the pericentromeric region and is coamplified along with the NF1 sequences. Interphase FISH ordering experiments show that IgH D lies closest to the centromere, while BCL8A is the most distal locus in this pseudogene array;”
OspA-like lipoproteins act like extra BCL2 molecules, inhibiting apoptosis. This is shown in numerous examples of the literature with mycoplasmal and mycobacterial lipoproteins, as well as Brucella lipoproteins. One can use PubMed or the National Library of Medicine. Anyone can find out OspA is the basic Pam3Cys molecule. It occurs naturally and is synthetic (Braun lipoprotein). Epstein-Barr has its own human homolog (similar gene copy), of BCL2.
The first step in dysimmunity, one could claim, is the inhibition of apoptosis. Fungal lipoproteins, of the TLR2/1 type, highly lipidated, with 3 or more acyl (fatty acid, like palmitic acid or linoleic acid, etc) groups, gum up immunity. They inhibit apoptosis. In particular, OspA is sticky and even sticks to itself. This may be the reason spirochetes appear to cluster in vitro. However they don’t cluster or grow in colonies in humans; biofilms are not the reason antibiotic treatment fails. This data summary and explanation of the science abundantly shows spirochetes and “biofilms” are not what makes Chronic Lyme chronic. Especially not if the vaccine caused the same chronic neurologic disease.
Morphology of Borrelia burgdorferi: structural patterns of cultured borreliae in relation to staining methods.
“The microscopic recognition of Borrelia burgdorferi in biologic fluids and tissues is difficult and challenging because of low numbers of organisms occurring as single isolated spirochetes, the apparent lack of colony formation in tissues, and differing lengths and structural morphologies.”
Anyone who has a science background, which includes anyone with an ‘MD” after their names, has for 15 years been able to discover what exactly OspA is and why it caused systemic disease and why it failed—but they didn’t. They took the lazy way out with DSM somatoform witchery victim-blaming.
Continuing with the Alphabet of data points that point to Lyme being like AIDS with reactivated viral infections due to immunosuppression: These next 9 we’ll call the “L” group because we are going to run out of letters.
L1. Adriana Marques formerly of NINDS’ MS-Lyme group and who now works for NIAID, and specializes only in Lyme and MS and herpesviruses (clue):
“Complicating the picture is the fact that some people with PTLDS symptoms apparently never had Lyme disease in the first place,” Dr. Marques said in an interview. “There are other infectious organisms—Epstein-Barr virus, for example—that can produce similar symptoms and may be the real culprits.”
“When Lyme Disease Lasts and Lasts,” by Jane Brody in the New York Times.
L2. Says another NIH employee of post sepsis-herpes-AIDS:
“Surviving Sepsis: Detection and Treatment Advances” by Carolyn Beans for the National Institutes of Health, August 18, 2014
“…Some people who survive sepsis can develop secondary infections days or even months later. A research team that included Richard Hotchkiss, Jonathan Green and Gregory Storch of Washington University School of Medicine in St. Louis suspected that this is because sepsis might cause lasting damage to the immune system…The researchers looked for viruses like Epstein-Barr and herpes simplex that are often dormant in healthy people but can reactivate in those with suppressed immune systems.”
L3. Paul Auwaerter, specializes in only Lyme and herpesviruses: http://www.hopkinsmedicine.org/profiles/results/directory/profile/0000525/paul-auwaerter
L4. Brigitte Huber of Tufts, former partner with Allen Steere in “Lyme is Only a Bad Knee Theatre,” who now specializes in ONLY herpesviruses (actually, claiming EBV could be reactivating a human endogenous retrovirus or a HERV):
L5. If pathologist Paul Duray (NCI, Yale, US Army Ft. Detrick) were still alive, you could ask him why he said, “these look like Epstein-Barr transformed cells” in the spinal fluid of chronic neurologic Lyme victims in 1989, in IDSA’s journal.
Clinical pathologic correlations of Lyme disease.
“Immature B cells can also be seen in the spinal fluid. These cells can appear quite atypical- not unlike those of transformed or neoplastic lymphocytes.”
Or why he said it again, in 1992: “In Chronic Lyme victims’ cerebrospinal fluid, I see what look like Epstein-Barr transformed lymphocytes.”
“On occasion, these atypical-appearing large lymphocytes have been misinterpreted in biopsy by several laboratories as cells of a malignant lymphoma or leukemia. Bb antigens, then, may stimulate growth of immature lymphocytic suibsets in some target organs, as well as in the cerebrospinal fluid (Szyfelbein and Ross 1988). Usual bacterial infections do not produce such lymphocytic infiltrates in tissue. These immunoblastoid cells in Bb infections at times resemble those found in Epstein-Barr virus infections. Does Bb reactivate latent virus infections in tissues? Do some tick inocula harbor simultaneous infectious agents (ixodid ticks can harbor Rickettsiae, Babesia microti, and Ehrlichia bacteria, in addition to Bb), producing multi-agent infections in some hosts? Further studies can clarify these issues by mans of tissue-based molecular probe analysis.”
—Paul Duray, NCI, NIH, Ft. Detrick, at the 1992 Cold Spring Harbor ALDF.com Conference, published in Steve Schutzer’s Lyme Disease: Molecular and Immunologic Approaches.
L6. Patricia K. Coyle, SUNY-SB. Coyle, who was the author of several reports and even methods to detect borrelia antigens in the central nervous system because of the absence of antibodies, now only specializes in Multiple Sclerosis???
L7. Martin and Marques at the NINDS MS and Lyme Division. Martin quit and went home to Germany once he found out LYMErix was responsible for the immunosuppression-come-New Great Imitator (in other words, that LYMErix or OspA-ish antigens were responsible for the MS outcome of Lyme:
Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression (2006).
“…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.”
L8. Anthony FAUCI on immunosuppression and common opportunistics:
NIAID director Anthony Fauci says this in his patent for IL-2 as an immune booster. He lists fungi and stuff like common opportunistics, you know like…
“FIELD OF THE INVENTION
“The present invention pertains to a method for activating the immune system of a patient by intermittently administering interleukin-2 (IL-2) to that patient. Such administration of IL-2 can optionally be combined with other therapies, such as anti-retroviral, anti-bacterial or anti-fungal therapies, suitable for treatment of the patient’s condition. This invention also relates to an approach to gene therapy that entails administering IL-2 to a patient so as to facilitate in situ lymphocyte transduction by a retroviral vector also administered to the patient.
“BACKGROUND OF THE INVENTION
“….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. …”
“…Opportunistic infections may also be treated using the present invention. For example, AIDS related opportunistic infections are described in Mills et. al. (1990) Scientific American 263:51-57, which is hereby incorporated by reference in its entirety. Mills show that common opportunistic infections are caused by, for example, Cytomegalovirus, Pneumocystis carnii, Candida albicans, Varicella-Zoster virus, Epstein-Barr virus, Toxoplasma gondii, Mycobacterium avium, Cryptococcus neoformans. It is envisioned that IL-2 may be administered along with other compounds used to treat infectious diseases or other diseases. Examples of other agents include antifungal, antiviral, or antibacterial drugs. Additionally, IL-2 may be administered in combination with other efficacious cytokines. For example, combination therapy may include IL-2 with GM-CSF, G-CSF, M-CSF, IL-3, IL-12, IL-15, a-, b-, or g-interferons.”
“Diseases of immunosuppression like fungal diseases.” “Opportunistic infections like the herpesviruses and other fungal infections which now have a free ride due to TLR2-agonist tolerance and cross tolerance.”
L9. CDC’s Suzanne Vernon explaining how Epstein-Barr contributes to fatigue; How she committed research fraud to try to say fungal antigens are not involved in fatigue; How we know fungal antigens adhere to erythrocyte membranes (causing hypoxic fatigue), stick to internal cell components, depolarizing membranes, etc.
a) (Vernon) Preliminary evidence of mitochondrial dysfunction associated with post-infective fatigue after acute infection with Epstein Barr virus.
“Those who developed post-infective fatigue had gene expression profiles indicative of an altered host response during acute mononucleosis compared to those who recovered uneventfully. Several genes including ISG20 (interferon stimulated gene), DNAJB2 (DnaJ [Hsp40] homolog and CD99), CDK8 (cyclin-dependent kinase 8), E2F2 (E2F transcription factor 2), CDK8 (cyclin-dependent kinase 8), and ACTN2 (actinin, alpha 2), known to be regulated during EBV infection, were differentially expressed in post-infective fatigue cases. Several of the differentially expressed genes affect mitochondrial functions including fatty acid metabolism and the cell cycle.”
“CONCLUSION: These preliminary data provide insights into alterations in gene transcripts associated with the varied clinical outcomes from acute infectious mononucleosis.”
b) Vernon commits research fraud by throwing out the mycoplasma before she even starts to allegedly look for mycoplasmal DNA:
2003; Absence of Mycoplasma species DNA in chronic fatigue syndrome
“Blood was collected in sodium citrate Vacutainer tubes (Beckton Dickinson) and shipped by overnight courier to the Centers for Disease Control (CDC), where plasma was collected by separation on lymphocyte separation medium (LSM; ICN Biomedicals). Plasma (1 ml) was concentrated to approximately 250 μl in a Centricon centrifugal filter unit YM-100 (Millipore). Cell-free plasma DNA was extracted by using a QIAamp DNA Mini kit (Qiagen) according to the manufacturer’s instructions and quantified by using a DyNA Quant 200 fluorometer (Amersham Biosciences).”
CDC’s Suzanne Vernon ↑ committed research fraud by centrifuging out the very cells to which mycoplasma adhere and then said, “How Amazing, there is no mycoplasma here!!”
c) Mycoplasma adhere to erythrocytes (red blood cells) interfering with membrane potential and therefore the potential for oxygen to cross the erythrocyte membrane (causing fatigue):
[The effect of Eperythrozoon suis infection on the osmotic fragility of erythrocytes]
“Osmotic fragility of erythrocytes was tested in weaned pigs experimentally infected with Eperythrozoon (E.) suis. Acute eperythrozoonosis of splenectomized pigs led to an increase of osmotic fragility. It is supposed that E. suis infection causes a structural change in erythrocyte membrane. Possible mechanisms of this cell membrane injury are discussed.”
d) Mycoplasma—remember now, thrown out by the CDC, fraudulently and deliberately, as a contributor to FATIGUE—mess with mitochondrial membrane potential—as a way of inhibiting apoptosis (consider the possible synergy here with Epstein-Barr, which does the same thing):
Mycoplasma fermentans inhibits tumor necrosis factor alpha-induced apoptosis in the human myelomonocytic U937 cell line.
“Loss of mitochondrial inner transmembrane potential induced by TNFα is reduced in U937 cells infected with M. fermentans…
”In many apoptosis scenarios, including TNF-mediated apoptosis, the mitochondrial inner transmembrane potential (m) collapses.19, 20 To investigate whether the antiapoptotic effect of M. fermentans in TNF-induced apoptosis is upstream or downstream of the mitochondria, we measured the loss in Delta-Sigmam, induced by TNF (20 ng/ml), in infected and noninfected cells. At 24 h post infection, the cultures were stimulated with TNF (20 ng/ml) for 2 h, and each culture was stained with 3,3′-dihexyloxacarbocyanine iodide (DiOC6 (3)) and analyzed by FACS (a typical experiment is shown in Figure 6a).
IF Epstein-Barr alone were responsible for chronic fatigue syndrome, then one can see their idiot point of view that “stress” causes the reactivation of Epstein-Barr (“somatiformical” = reactivating EBV) and that de-stressing solves the problem. Maybe that is the case with the somatoformical medical students and astronauts and the like, who are so well known to have stress-reactivated Epstein-barr or mono. But here we see something much more sinister at work. The CDC does not want anyone to know how fungal antigens cause fatigue and how tolerance to fungi causes irreversible fatigue and how that spreads to other infections (“common, now, opportunistics”).
We think the reason has to do with childhood vaccines being contaminated with fungal antigens, which is the reason for thimerosal in the first place. We think the reason for this fraud on the part of the CDC is that they do not want us to be aware of the common mechanisms at work in vaccines-virus-acquired Autism (brain damage is the more correct term).
We think the 20-30 million witches and warlocks in the country are the price the CDC pays to continue to brain damage around 1:60 children for life. It’s a great bargain for the CDC. They even say “it is a calculated risk,” this vaccines-enforcement and the brain damaged for life outcome. CDC does the calculating. You know who all the real monsters are.
People should follow up on these reports; here is one from 2008:
Staying alive: bacterial inhibition of apoptosis during infection.
“The ability of bacterial pathogens to inhibit apoptosis in eukaryotic cells during infection is an emerging theme in the study of bacterial pathogenesis. Prevention of apoptosis provides a survival advantage because it enables the bacteria to replicate inside host cells. Bacterial pathogens have evolved several ways to prevent apoptosis by protecting the mitochondria and preventing cytochrome c release, by activating cell survival pathways, or by preventing caspase activation. This review summarizes the most recent work on bacterial anti-apoptotic strategies and suggests new research that is necessary to advance the field.”
TOLERANCE and CROSS TOLERANCE
One of the most important mechanisms of synergy between fungal antigens and viruses—and we have mentioned this many times in our reports and criminal charge sheets against IDSA and the CDC (see http://www.ohioactionlyme.org et al), has to do with tolerance and cross tolerance and we have explained what this means in the past. Tolerance means your body no longer sees the invading pathogen’s components are a threat and stops responding to them immunologically. Cross-tolerance is when an infection with one pathogen or antigen type renders the immune system incompetent to other types.
“Endotoxin Tolerance” is a known thing, known for decades. Endotoxin is considered mainly to be LPS or lipopolysaccharide (feel free to google the structure or the image) which are TLR4 agonists. TLR4 agonists are not as toxic as the fungal TLR2/1 agonists of say spirochetes, mycoplasma, Brucella, or mycobacteria. You have seen some of this with Clifford Harding (in “P.” below), and others have proposed or observed the mechanics or function of other intracellular compounds (“in the mileux”) being inhibited.
One of the best sources (also in “THE LIST” below):
New, October 13, 2015
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.
© 2015 S. Karger AG, Basel.
A person who knows how to use the National Library of Medicine can follow up on all this. The NIH endorses it, as you have seen.
AND WE’RE BACK TO THE ALPHABET
M. Multiple Sclerosis and EBV? Let’s look:
Some say yes, some say no, some say Cytomegalovirus, some say HHV-6, some say an EBV reactivated HERV, some say it’s more than one herpes, and some say VOILA! What do you know, immunosuppression from malaria seems to be associated with EBV-associated Burkitt’s Lymphoma. Synergy. Another kind of parallelism to our model. One infection invites the other, such as when in the old days it was known a cold virus could result in a dual bacterial infection and they gave children antibiotics to prevent a secondary ear infection. Or when in 1918 we had Spanish Flumonia, wherein one infection invited the other. Regardless, it seems to be unsettled as to which common virus or which two or which three, but it does seem to be a consensus that the herpesviruses are associated with MS.
N. Where do spirochetes and the herpesviruses live, by the way? (Oh, and the famous B cell depleter.)
Well, Lyme and EBV hang out in the lymph nodes and both live in B cells. Varicella zoster lives in the nerve root ganglia. And spirochetes also travel along nerves, as was proposed long ago and recently, when we heard from a dental group about the frequency of oral spirochetes found in Alzheimer’s brains (1999)
What is Bell’s Palsy caused by?
Some say EBV, some say Varicella, some say Simplex… Maybe it’s not spirochetes, maybe it is spirochetes, maybe it is a herpesvirus, maybe it is a combination of herpesviruses, maybe it is herpesviruses and spirochetes. But given that more than one kind of spirochete is associated with Alzheimer’s, and given that immunosuppression diseases are reactivation of COMMON VIRUSES, well, maybe that is the reason ILADS can’t cure anyone. They don’t know what they’re doing and willfully do not look at the big picture.
Lyme spirochetes and EBV live in B cells (use PubMed). And it just so happens, Rituximab, a bad-B-cell-depleter works for Chronic Fatigue Syndrome:
Benefit from B-lymphocyte depletion using the anti-CD20 antibody rituximab in chronic fatigue syndrome. A double-blind and placebo-controlled study.
B-Lymphocyte Depletion in Myalgic Encephalopathy/ Chronic Fatigue Syndrome. An Open-Label Phase II Study with Rituximab Maintenance Treatment.
Could be about bad B cells, since the treatment fits the model. Ya think?
Remember now, Lyme causes Chronic Fatigue Syndrome and Fibromyalgia, say the ALDF.com and Yale Lyme cabal. And 12 million people in the United States alone have those…things. So it can’t be anything too mysterious if it also causes Lupus and MS.
O. The Yale Lupus and Lyme Clinic
The NIH used to have an MS-Lyme section of the NINDS, and Yale used to have a “Lyme and Lupus Clinic” before that became the criminal entity “L2 Diagnostics,” led by none other than Robert Schoen of “we can’t tell LYMErix apart from “multisystem late Lyme” infamy.
Steere (formerly at Yale) on Lyme and Lupus:
1993, Reactivity of neuroborreliosis patients (Lyme disease) to cardiolipin and gangliosides.
“A subset of patients (50%) with neuroborreliosis (Lyme disease) showed IgG reactivity to cardiolipin in solid phase ELISA. In addition, a subset of patients with neuroborreliosis (29%) and syphilis (59%) had IgM reactivity to gangliosides with a Gal(beta 1-3) GalNac terminal sequence (GM1, GD1b, and asialo GM1). Anti-ganglioside IgM antibodies were significantly more frequent in these two groups of patients compared to patients with cutaneous and articular Lyme disease, primary antiphospholipid syndrome, systemic lupus erythematosus and normal controls. Correlative evidence and adsorption experiments indicated that antibodies to cardiolipin had separate specificities from those directed against the gangliosides. IgM antibodies to Gal(beta 1-3) GalNac gangliosides appeared to have similar specificities since these were positively correlated and inhibitable by cross adsorption assays. Given the clinical associations of patients with neuroborreliosis and syphilis with IgM reactivity to gangliosides sharing the Gal(beta 1-3) GalNac terminus, we suggest that these antibodies could represent a response to injury in neurological disease or a cross reactive event caused by spirochetes.”
Do you like the way Steere says there is such a thing as neuroborreliosis? Now, of course, there is no such disease. In 2001 Mark Klempner gave a talk about <whatever> at a hospital in Rhode Island in which he was RECORDED as saying this about the Dearborn case definition:
Questioner8: I just have one more question for Dr. Klempner. Um, being that there are inadequacies, inaccuracies in the testing methods, seropositivity, etc., and the surveillance criteria that you used were just that, surveillance. And the CDC recognizes that there are so many more people that have Lyme disease who do not meet the CDC criteria. What’s your feeling on what percentage of patients who have Lyme disease because they have not met the criteria for diagnosis?
Klempner: I, um, I think there are a number of inaccuracies in what you just said. The CDC does not recognize that there are patients who have, um, that are seropositive that don’t meet seropositive criteria. What they say, is that these are the criteria.…
CDC does not recognize anything that is not the Dearborn criteria. Dattwyler sees only one patient a year with only bad knees. And there used to be a thing called Neuroborreliosis, but no more.
Now the Yale Lyme and Lupus gang say this about Lupus (and EBV):
2004: Defective control of latent Epstein-Barr virus infection in systemic lupus erythematosus.
“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…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…These results demonstrate that patients with SLE have defective control of latent EBV infection that probably stems from altered T cell responses against EBV.”
P. Hotchkiss, Washington University, Saint Louis, MO:
WUSTL discovers that sepsis is like Chronic Lyme, in that the survivors of it are likely to have survived via the immunosuppression (TLR2-agonist tolerance/Endotoxin tolerance), but the result is the reactivation of latent viruses:
Dormant viruses re-emerge in patients with lingering sepsis, signaling immune suppression
“Patients with lingering sepsis had markedly higher levels of viruses detectable in the blood, compared with the healthy controls and critically ill patients without sepsis. Among the sepsis patients, for example, the researchers found that 53 percent had Epstein-Barr virus, 24 percent had cytomegalovirus, 14 percent had herpes-simplex virus, and 10 percent had human herpes simplex virus-7.
“These viruses generally don’t lead to significant illness in people who are healthy but can cause problems in patients who are immune-suppressed. “
FULL JOURNAL REPORT, snippet: Reactivation of Multiple Viruses in Patients with Sepsis
“Sepsis is the host’s non-resolving inflammatory response to infection that leads to organ dysfunction , . A current controversial hypothesis postulates that if sepsis pursues a protracted course, it progresses from an initial primarily hyper-inflammatory phase to a predominantly immunosuppressive state –. Experimental therapeutic approaches in sepsis have almost exclusively focused on blocking early inflammation or host-pathogen interaction and failed –. Recently, immuno-adjuvant therapies that boost host immunity, e.g., GM-CSF and interferon-γ, have been successful in small clinical trials thereby supporting the concept that reversing immunosuppression in sepsis is a plausible strategy to improve outcome , . However, several issues have limited this approach including lack of consensus that immunosuppression is a clinically important phenomenon , , . Also, difficulty in identifying patients with impaired immunity as well as determining optimal timing for administration pose significant challenges to pursuing this approach . While immuno-adjuvant therapies might improve sepsis survival if administered during the later immunosuppressive phase, these agents might worsen outcome if given during the early hyper-inflammatory phase , . Thus, a means to distinguish these two contrasting phases of sepsis is needed not only to verify the hypothesis that sepsis progresses to an immunosuppressive state but also to guide use of potential agents which boost immunity.
“Latent viruses such as cytomegalovirus are normally held in abeyance by cellular and immune surveillance mechanisms which if impaired, for example by immunosuppressive medications, often result in viral reactivation, replication, and virally-mediated tissue injury –. Sepsis impairs innate and adaptive immunity by multiple mechanisms including apoptosis-induced depletion of immune effector cells and induction of T-cell exhaustion thereby possibly predisposing to viral reactivation and dissemination –. …”
Q. Medvedev and Cross-Tolerance; Medvedev talking about Immunosuppression from Post-Lyme and Post-LYMErix Sepsis (TLR2-agonists or Pam3Cys is OspA or shed borrelial antigens)
IRAK4 kinase activity is not required for induction of endotoxin tolerance but contributes to TLR2-mediated tolerance
“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]. …
“Reprogramming  of TLR4 signaling in endotoxin-tolerant monocytes and macrophages does not occur as a result of decreased TLR4 expression but involves altered recruitment, tyrosine phosphorylation, and K63-linked polyubiquitination of proximal receptor-adapter-kinase complexes [22,–27] and induction of negative regulators IRAK-M, SHIP1, and A20 [24, 25, 28]. Although a few studies have sought to dissociate kinase and adapter functions of IRAK4 in IL-1R/TLR signaling, albeit with conflicting results [13,–16, 29,–31], it is unclear how IRAK4 kinase activity affects induction of TLR2 and TLR4 homo- and heterotolerance. To address these questions, we used IRAK4KDKI mice to determine the impact of kinase deficiency of IRAK4 on the induction of TLR tolerance. Our data showed comparable induction of endotoxin tolerance in WT or IRAK4KDKI PMs and BMDMs, as judged by attenuated MAPK phosphorylation, inhibited expression of proinflammatory cytokines and chemokines, and up-regulation of negative TLR regulators, A20 and IRAK-M. 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.”
R. Remember Pam3Cys is the basic molecule of LYMErix or OspA and others shed by Borrelia:
A20 is critical for the induction of Pam3CSK4-tolerance in monocytic THP-1 cells.
“A20 functions to terminate Toll-like receptor (TLR)-induced immune response, and play important roles in the induction of lipopolysacchride (LPS)-tolerance. However, the molecular mechanism for Pam3CSK4-tolerance is uncertain. Here we report that TLR1/2 ligand Pam3CSK4 induced tolerance in monocytic THP-1 cells. The pre-treatment of THP-1 cells with Pam3CSK4 down-regulated the induction of pro-inflammatory cytokines induced by Pam3CSK4 re-stimulation. Pam3CSK4 pre-treatment also down-regulated the signaling transduction of JNK, p38 and NF-κB induced by Pam3CSK4 re-stimulation. The activation of TLR1/2 induced a rapid and robust up-regulation of A20, suggesting that A20 may contribute to the induction of Pam3CSK4-tolerance. This hypothesis was proved by the observation that the over-expression of A20 by gene transfer down-regulated Pam3CSK4-induced inflammatory responses, and the down-regulation of A20 by RNA interference inhibited the induction of tolerance. Moreover, LPS induced a significant up-regulation of A20, which contributed to the induction of cross-tolerance between LPS and Pam3CSK4. A20 was also induced by the treatment of THP-1 cells with TNF-α and IL-1β. The pre-treatment with TNF-α and IL-1β partly down-regulated Pam3CSK4-induced activation of MAPKs.
Furthermore, pharmacologic inhibition of GSK3 signaling down-regulated Pam3CSK4-induced A20 expression, up-regulated Pam3CSK4-induced inflammatory responses, and partly reversed Pam3CSK4 pre-treatment-induced tolerance, suggesting that GSK3 is involved in TLR1/2-induced tolerance by up-regulation of A20 expression. Taken together, these results indicated that A20 is a critical regulator for TLR1/2-induced pro-inflammatory responses.”
TLR2/1-induced tolerance or LYMErix or Lyme tolerance is a thing, like Endotoxin Tolerance, only worse, since so far it is not reversible. In other words, IDSA and the CDC have no idea what they are talking about, and this concerns every major disease, if not every disease.
S. Poland, 2013, The influence of toll-like receptor stimulation on expression of EBV lytic genes.
“Epstein-Barr virus (EBV) establishes latency in the resting memory B-cell compartment. It has been recently suggested that maintenance of chronic infection is dependent on periodic reactivation. Although the stimuli for EBV reactivation in vivo during natural infections are largely unknown, there is evidence indicating that heterologous infections could trigger herpesviruses reactivation. The purpose of this work was to identify the influence of Toll-like receptors stimulation on EBV replication in EBV latently infected Burkitt lymphoma cells (P3HR-1, Raji and Namalwa). The cells were stimulated with Pam3CSK4 (synthetic triacylated lipoprotein), PolyI:C (synthetic analog of dsRNA), LPS (lipopolysaccharide from E.coli), measles virus (MeV) and PMA (phorbol myristate acetate). Non-stimulated cells (NS) served as control. EBV expression was investigated at mRNA level for three viral lytic genes: BZLF1 (immediate early, ZEBRA), BALF2 (early, EA) and BcLF1 (late, VCA). Additionally, the effect of stimulation on NF-kBp65 and inflammatory cytokines (IL-lb, IL-6, IL-8, IL-10, IL-12p70, and TNF) was investigated. Stimulation of TLRs led to limited changes in EBV expression manifesting as increase of ZEBRA at mRNA level in cells treated with PolyI:C and Pam3CSK4. Stimulation with PolyI:C, Pam3CSK4 and LPS also lead to considerable increase of NF-kBp65, while increased levels of inflammatory cytokines were observed for IL-8, TNF and IL-6 in cells treated with PMA and MeV. In conclusion, the results of our experiments support the suggestion that TLRs stimulation with microbial ligands influences EBV virus replication.”
T. Clifford Harding and Justin Radolf on the downregulation of MHC or HLA molecules, resulting in immunosuppression or lack of antibodies from exposure to the likes of OspA covered blebs:
Toll-like receptor 2-dependent inhibition of macrophage class II MHC expression and antigen processing by 19-kDa lipoprotein of Mycobacterium tuberculosis.
“Mycobacterium tuberculosis (MTB) induces vigorous immune responses, yet persists inside macrophages, evading host immunity. MTB bacilli or lysate was found to inhibit macrophage expression of class II MHC (MHC-II) molecules and MHC-II Ag processing. This report characterizes and identifies a specific component of MTB that mediates these inhibitory effects. The inhibitor was extracted from MTB lysate with Triton X-114, isolated by gel electroelution, and identified with Abs to be MTB 19-kDa lipoprotein. Electroelution- or immunoaffinity-purified MTB 19-kDa lipoprotein inhibited MHC-II expression and processing of both soluble Ags and Ag 85B from intact MTB bacilli. Inhibition of MHC-II Ag processing by either MTB bacilli or purified MTB 19-kDa lipoprotein was dependent on Toll-like receptor (TLR) 2 and independent of TLR 4. Synthetic analogs of lipopeptides from Treponema pallidum also inhibited Ag processing. Despite the ability of MTB 19-kDa lipoprotein to activate microbicidal and innate immune functions early in infection, TLR 2-dependent inhibition of MHC-II expression and Ag processing by MTB 19-kDa lipoprotein during later phases of macrophage infection may prevent presentation of MTB Ags and decrease recognition by T cells. This mechanism may allow intracellular MTB to evade immune surveillance and maintain chronic infection.”
Here are 4 examples from the literature of how Epstein-Barr also can be seronegative via the same mechanism of downregulation of antigen-presenting molecules or downregulation of HLA molecules (shows antigen so that B cells can make antibodies) or the MHC or “Major Histocompatibility Class” of cell components (all the same thing):
Down-regulation of MHC class II expression through inhibition of CIITA transcription by lytic transactivator Zta during Epstein-Barr virus reactivation.
Innate immune modulation in EBV infection
“Dysregulation of EBV-specific immune responses is also characteristic of EBV-associated autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). CTL response to EBV infection has been well documented since the discovery of EBV . However, significant progresses in characterizing individual viral proteins involved in evasion of the T cell-mediated adaptive immune response have only been made in the last decade [12-16]. For example, the functional homologue of human IL10, BCRF1, elicits CD8+ T cell responses, and can be processed and presented to CD8+ CTLs through a TAP-independent pathway .”
The lytic cycle of Epstein-Barr virus is associated with decreased expression of cell surface major histocompatibility complex class I and class II molecules.
Epstein-Barr virus evasion of CD8(+) and CD4(+) T cell immunity via concerted actions of multiple gene products.
“Evidence is accumulating that this paradoxical situation is the result of actions of multiple viral gene products, inhibiting discrete stages of the MHC class I and class II antigen presentation pathways. Immediately after initiation of the lytic cycle, BNLF2a prevents peptide-loading of MHC class I molecules through inhibition of the Transporter associated with Antigen Processing, TAP. This will reduce presentation of viral antigens by the large ER-resident pool of MHC class I molecules. Synthesis of new MHC class I molecules is blocked by BGLF5. Viral-IL10 causes a reduction in mRNA levels of TAP1 and bli/LMP2, a subunit of the immunoproteasome. MHC class I molecules present at the cell surface are downregulated by BILF1. Also the antigen presenting capacity of MHC class II molecules is severely compromised by multiple EBV lytic gene products, including gp42/gH/gL, BGLF5, and vIL-10. In this review, we discuss how concerted actions of these EBV lytic proteins result in highly effective interference with CD8(+) and CD4(+) T cell surveillance, thereby providing the virus with a window for undisturbed generation of viral progeny.” http://www.ncbi.nlm.nih.gov/pubmed/18977445
Therefore, never use antibody testing to show an association between an illness and an infectious disease.
Harding says the chronic agonism of TLR2/1 by these lipoproteins also inhibit TLR7/9 function (manages the viruses like EBV); people want to know how Lyme and LYMErix activate EBV, besides that being about what happens commonly, in all general immunosuppression such as Humira and Stelara and post-transplant patients who acquired EBV-induced lymphoma, which we will get to:
TLR2 signaling depletes IRAK1 and inhibits induction of type I IFN by TLR7/9.
“Pathogens may signal through multiple TLRs with synergistic or antagonistic effects on the induction of cytokines, including type I IFN (IFN-I). IFN-I is typically induced by TLR9, but not TLR2. Moreover, we previously reported that TLR2 signaling by Mycobacterium tuberculosis or other TLR2 agonists inhibited TLR9 induction of IFN-I and IFN-I-dependent MHC-I Ag cross processing. The current studies revealed that lipopeptide-induced TLR2 signaling inhibited induction of first-wave IFN-α and IFN-β mRNA by TLR9, whereas induction of second-wave IFN-I mRNA was not inhibited. TLR2 also inhibited induction of IFN-I by TLR7, another MyD88-dependent IFN-I-inducing receptor, but did not inhibit IFN-I induction by TLR3 or TLR4 (both Toll/IL-1R domain-containing adapter-inducing IFN-β dependent, MyD88 independent). The inhibitory effect of TLR2 was not dependent on new protein synthesis or intercellular signaling. 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.”
U. The Stelara and Humira and other mab (monoclonal antibody) commercials:
We’ve all seen them. They warn particularly against fungal infections, against taking immune suppressing drugs like steroids, and that there is a risk of Lymphoma. Well, what causes Lymphoma?
More than 600 articles. Could be a thing. A thing like, you know the chronic fatigue syndrome patients who ended up with cancer, and who were then treated with Rituximab and to-everyone’s-surprise-except-us…
V. Raymond Dattwyler is so convinced LYMErix causes immunosuppression he proposes to use it in combination with a virus for an inhalation form—something we proposed years ago, given the pandemic flu of 1918 killed people due to the secondary infection, the mycobacteria, or flumonia. It only killed healthy people, remember, people with strong immune responses. Therefore, he thinks it could be an inoculum or a tolerizer against the serious septic shock event (but in the lungs) that results in death or near death for the post-sepsis survivors of Lyme and LYMErix:
“A lipidation/processing reaction has been described for the intact OspA gene of B. burgdorferi. The primary translation product of the full-length B. burgdorferi OspA gene contains a hydrophobic N-terminal sequence, of 16 amino acids, which is a substrate for the attachment of a diacyl glyceryl to the sulflhydryl side chain of the adjacent cysteine (Cys) residue (at position 17). Following this attachment, cleavage by signal peptidase II and the attachment of a third fatty acid to the N-terminus occurs. The completed lipid moiety, a tripalmitoyl-S-glycerylcysteine modification, is termed Pam3Cys (or is sometimes referred to herein as Pam(3)Cys or Pam3Cys). It has been suggested that the lipid modification allows membrane localization of proteins, with polypeptide portions exposed as immune targets. In addition to serving as targets for the immune response, Pam3Cys-modified proteins, such as OspA, have been reported to act as potent inflammatory stimulants though the toll-like 2 receptor mechanism (TLR2).”
Dattwyler says OspA is Pam3Cys and is a TLR2 agonist. So far, he is the only one who has openly admitted LYMErix never could have been an injectable vaccine. Or said what it was. HHS.gov claims to not know. Yale says they do not know what OspA is (it was their vaccine, LYMErix), the CDC said they do not know what OspA is, Paul Auwaerter said he does not know what OspA is, NIH Director Francis Collins did not know, NIAID director Anthony Fauci did not know, and IDSA refused to reply to our emails or phone calls.
“Here, take this here vaccine. We don’t know what it is and just about no one has this disease it prevents, and when they do, like Wormser and Klemper said, the people only have arthritis and no other symptoms.
Thanks and have a nice day.”
—CDC, IDSA, Yale, et al.
W. It being empirically observed that Lyme helps activate EBV:
Interaction of Borrelia burgdorferi sensu lato with Epstein-Barr virus in lymphoblastoid cells.
“Since the possibility of interruption of latent EBV infection has been suggested by the induction of the lytic virus cycle with chemical substances, other viruses, and by immunosuppression, we hypothesized that the same effect might happen in B. burgdorferi sensu lato infection as happens in Lyme disease patients with positive serology for both agents. We have observed EBV replication in lymphoblastoid cells after superinfection with B. garinii and B. afzelii strains after 1 and 4 h of their interaction. We found that viral and borrelial antigens persisted in the lymphoblasts for 3 and 4 days. Morphological and functional transformation of both agents facilitate their transfer to daughter cells. Association with lymphoblasts and internalization of B. garinii by tube phagocytosis increased replication of viruses more successfully than B. afzelii and chemical inductors. Demonstration of such findings must be interpreted cautiously, but may prove a mixed borrelial and viral cause of severe neurological disease.”
X. It being empirically observed that the Lyme Criminals observed that Lyme causes immunosuppression:
Borrelia burgdorferi-induced tolerance as a model of persistence via immunosuppression
Here they are citing it: http://www.ncbi.nlm.nih.gov/pubmed?linkname=pubmed_pubmed_citedin&from_uid=12819085 (Auwaerter, Fish, Krause, Radolf)
Y. Mario Philipp (Tulane) has for years said OspA was associated with the production of the immunosuppressive cytokine, IL-10 (this was mentioned to the FDA by Dickson, Jan 31, 2001)
The latest one is this:
It has been established that interleukin-10 (IL-10) inhibits inflammatory cytokines produced by macrophages in response to Borrelia burgdorferi or its lipoproteins. The mechanism by which IL-10 exerts this anti-inflammatory effect is still unknown. Recent findings indicate that suppressors of cytokine signaling (SOCS) proteins are induced by cytokines and Toll-like receptor (TLR)-mediated stimuli, and in turn they can down-regulate cytokine and TLR signaling in macrophages. Because it is known that SOCS are induced by IL-10 and that B. burgdorferi and its lipoproteins most likely interact via TLR2 or the heterodimers TLR2/1 and/or TLR2/6, we hypothesized that SOCS are induced by IL-10 and B. burgdorferi and its lipoproteins in macrophages and that SOCS may mediate the inhibition by IL-10 of concomitantly elicited cytokines. We report here that mouse J774 macrophages incubated with IL-10 and added B. burgdorferi spirochetes (freeze-thawed, live, or sonicated) or lipidated outer surface protein A (L-OspA) augmented their SOCS1/SOCS3 mRNA and protein expression, with SOCS3 being more abundant. Pam(3)Cys, a synthetic lipopeptide, also induced SOCS1/SOCS3 expression under these conditions, but unlipidated OspA was ineffective. Neither endogenous IL-10 nor the translation inhibitor cycloheximide blocked SOCS1/SOCS3 induction by B. burgdorferi and its lipoproteins, indicating that the expression of other genes is not required. This temporally correlated with the IL-10-mediated inhibition of the inflammatory cytokines IL-1beta, IL-6, IL-12p40, IL-18, and tumor necrosis factor alpha. Our data are evidence to suggest that expression of SOCS is part of the mechanism of IL-10-mediated inhibition of inflammatory cytokines elicited by B. burgdorferi and its lipoproteins.”
At the same time, Epstein-Barr is known to have a human homolog of IL-10. To review, EBV has a mimic of the human BCL2, anti-apoptosis gene, a human homolog of human interleuken 10, and as you have seen in this report, Epstein-Barr downregulates the MHC or antigen-presenting cells and may be antibody-negative or seronegative in active disease. These could be three reasons EBV contributes to so many cancers—in the Subimmune Class of diseases—as well as its well-known association to Autoimmune diseases (Great Imitator ones, like MS and Lupus and even some evidence that EBV is associated with Rheumatoid arthritis —search PubMed using RA and DNA and EBV and not antibodies).
Since this is such an important topic, how fungal antigens activate IL-10 and the role does such a phenomenon has in causing disease should be studied:
In the next topic, THE LIST, several of those authors show mechanisms by which fungal antigens suppress the immune response, such as Harding and Medvedev. We, ActionLyme and the Society for Advancement of Scientific Hermeneutics (SASH), have been reporting this phenomenon since early 2004, when we discovered lipoproteins like LYMErix inhibit apoptosis—making it reminiscent of what BCL2 class molecules do, and that “EBV-immortalized B cells” is basically the same thing Duray saw in the cerebral spinal fluid of chronic neurologic Lyme victims.
Since the whistle was blown at the FDA (mentioning Philipp and IL-10 and Dattwyler and his “Inhibition of NK cell activity” as shown above, from exposure to borrelial lipids) in January 2001
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf, the question has been for us, what causes this synergy? We know from Baumgarth and Barthold (THE LIST) and others, that Borrelia live in B cells and so does Epstein-Barr, and they both prefer the lymph nodes. We know that the sticky Pam3Cys molecules adhere to intracellular components membranes, including mitochondria (CDC even says so, as you have seen in this report).
Z. THE LIST: Here we have compiled a list of researchers who say and show that something like OspA never could have been a vaccine, as a TLR2/1-agonist, causing immunosuppression (observed and mechanisms):
It can’t be about spirochetes and biofilms and co-infections if LYMErix vaccination caused the exact same systemic and neurologic disease as Lyme. These are scientists who know what they are talking about regarding Lyme/spirochetes and OspA as immunosuppressive. Notice that none of the Lyme “non-profits” tell you what Lyme and Lyme cryme is all about. They do not want anything to change. They are happy about all the people who die from Lyme disease as long as their “CEOs” make several hundred thousand dollars a year for doing nothing but being blowhard self-promoters.
We will be attacked for this report as we always are; people will say this is “So-and-So’s science,” when it is no science the ActionLyme and SASH groups have themselves discovered in a lab and reported in the journals. We welcome all such comments on the science to be directed towards the authors of all of these reports. We have even provided a form letter for the self-alleged Lyme activists who “help people” to send to those researchers at the end of this summary of the science.
NIH’s Martin and Marques
http://www.ncbi.nlm.nih.gov/pubmed/?term=Martin+and+Marques+and+tlr2 (<<The NIH’s “Lyme and MS” Division find that OspA-ish lipopropteins shed by borrelia all the time cause humoral immunosuppression with brain inflammation)
Justin Radolf on what else has OspA-sorta in it:
Radolf saying OspA causes immunosuppression:
Ray Dattwyler, et al (SUNY-SB)
Here is the form letter for the anti-science rebuttal-ists associated with ILADS.org and the fake non-profits like lymedisease.org, NatCapLyme, “MayDay,” etc.
We the undersigned take issue with your racist, bully, “science” and find it offensive. Rather than using our tax dollars for your fancy big-word-saying (we have read this hundreds of times and we still don’t get it, which means you are a bully), kindly say words like “awareness” and “support,” and talk about how famous you are for giving referrals to LLMDs.
How in the world can we advance our causes and raise money for Lyme research, cars, travel expenses, hairdos, and travel to protest events and for signs that say, “IDSA you’re bad, do your homework,” etc., when you are sowing all this confusion with words no one understands.
Everyone is entitled to their opinion. Ours is equal to yours. To Wit: NASA has asked us to advise on rocket propulsion, and General Motors consults with us on many other important matters regarding how cars can move apparently by themselves on the roads and this is well-known.
We have spoken in front of Congress about how we speak in front of Congress, many times. You may frame a copy of this if you like since it contains our autographs.
Oh, and you need a translator.