Now that it has been proven (1 , 2, 3), re-proven (4,, 5) and re-re-proven (6,, 7) once again and in recent history, that indeed “Lyme Disease (8, 9)” is a chronic, un-eradicable infection primarily of the central nervous system, formerly, formally serologically known as Relapsing Fever (10, 11, 12), and that long term intravenous antibiotic treatment generally results in relief-but-then-relapse (3, 5), one wonders, “Where do we go from here?”
The first order of business is the clarification of falsified antibody testing for “Lyme Disease.”
In 1992 Allen Steere went to Germany, with, as he claimed,
“The group 1 strain of B. burgdorferi, G39/40, used in this study and in the previous study of US patients was isolated from an Ixodes damini tick in Guilford, Connecticut . The group 2 strain, FRG [Federal Republic of Germany], was isolated from Ixodes ricinus near Cologne . The group 3 strain, IP3, was isolated from Ixodes persulcatus near Leningrad . All three strains used in this study were high passage isolates, which were classified by Richard Marconi (Rocky Mountain Laboratory, Hamilton, MT) using 16S ribosomal RNA sequence determination as described [11, 24]. The recombinant preparations of OspA and OspB used in this study were purified maltose- binding protein-Osp fusion proteins derived from group 1 strain B31 . The fusion proteins contained the full-length OspA or OspB sequence without the lipid moiety or the signal sequence -”
— illegal, plasmid-dropping, antigen-and-antibody dropping, “high passage strains” and OspA and B with no lipids attached (not likely to produce antibodies), resulting in the new, 1994, Centers for Disease Control (CDC), “case definition” of “Lyme Disease (8, 9).”
At the Dearborn, MI, Consensus Conference regarding the “standardization” of Western Blotting for “Lyme Disease,” the invited labs assessed Steere’s scientifically fraudulent proposal for a new diagnostic standard for Lyme from 8% to 28% accurate (detected % of known cases).
As part of their Dearborn submission, New York Medical College (NYMC) assessed the Steere proposal in 1993 as:
“Overall, 51 of 59 (86%) convalescent-phase serum specimens were reactive by IB, 35 of which were interpreted as positive: 26 based on IgM criteria, 8 based on both IgG and IgM criteria, and 1 based on IgG criteria,”
or 9 out of 59 patients were positive for Steere’s Dearborn proposal in IgG. Or, 15% accurate (13).
With this Steere/Germany standard the two OspA vaccines (ImmuLyme and LYMErix) were allegedly assessed for safety and efficacy (14, 15), which meant 85% of known cases would be thrown out of consideration, which, hypothetically, was the game plan all along. Later we found out that the Western Blots in OspA vaccinated people were not readable due to multiple reactive species or generalized darkening of the Western Blot strips, rendering any potential bands that would demonstrate illness/Lyme breakthrough in vaccinated persons, undecipherable (16, 17).
That leaves us with the years 1992 to the present, almost 2011, completely wasted.
In terms of research dollar-years and lives we’re now back at Square One, wondering what is to be done with the testing for “Lyme Disease,” and even more importantly, what do we call a “case” of “Lyme Disease” once the millions of people who were misdiagnosed in the Lyme-OspA scam process have gone on to chronic illness?
We know from scientifically valid biomarkers of illness (scientifically valid in the sense that valid methods were used to assess the markers or signs that a person suffered real illness or health irregularities), the true and correct DNA and RNA methods to determine chronic infections status, and especially of the prominent question of “seronegativity” being associated with the greatest apparent suffering. In 1994 at the meeting of the Food and Drug Administration regarding potential Lyme vaccines, Raymond Dattwyler (SUNY-Stony Brook) noted that “the ones that failed to mount a vigorous immune response tended to do worse, clinically. So, there was an inverse correlation between the degree of serologic response and the outcome.”
In 2005, Mark Klempner (Boston University) and Gary Wormser (NYMC) reported that the arthritis cases and seroposivity tended to be associated with Allen Steere’s alleged haplotypes over which SmithKline was sued in a class action after the Yale-owned LYMErix trial (18): “Patients generally feel well aside from their arthritis symptoms.”
In 1988, Raymond Dattwyler published that he wondered about seronegative “Lyme” and the suppression of NK cells (19), and he wondered enough to come up with a new assay to determine if exposure to Lyme and a lowered immunological response (20). His new assay was called “Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi.” Later, Allen Steere used this same seronegative “Lyme” assay and determined that 4/9 of his lab workers had been exposed to Borrelia (21).
The question was why.
We know from the previous history of Relapsing Fever (before the era of Allen Steere, et al), that antigenic variation was the nature of the relapse, and that spirochetes become host- and tissue- adapted. This meant that persons who had missed the opportunity for early diagnosis and treatment would not have the Dearborn “case definition” of “late, OspA-hypersensitivity, specific HLA-linked, Lyme Arthritis” in “early Lyme,” would be left to his/her peril in finding a competent MD who had been exposed in pre-medicine undergraduate study to a course in genetics. These organisms are taxonomically classified by differences in flagellin. The best way to detect Lyme with antibody testing is via all-borrelial-specific anti-flagellin antibody detection, because flagellin is not a variable antigen. The group who perfected and patented the anti-Borrelia- burgdorferi specific flagellin method was Yale’s Erol Fikrig and Richard Flavell in 1991 (22, 23).
Why this test was not used to assess Fikrig and Flavell’s OspA vaccine patent, LYMErix, is anyone’s guess.
Regardless of this State of Nonsense (Connecticut), …
People wonder what to make of the serious illness they suffer as a result of “Lyme” and LYMErix vaccination, which appeared to be similar (24). In 1995, David Persing and Yale’s Robert Schoen patented a method wherein they, the winners, would be in receipt of all the government funding and also a national monopoly on the – as they hoped and intended – post-OspA-vaccinated United States:
“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…. ” (25, 26).
And they, most of all, would have access to all the potentially patentable goodies in the national blood with this monopoly on testing.
Further investigations into the outcomes of other lipoprotein/fungal vaccines revealed a similar outcome to that observed in the un-reported LYMErix adverse events patients, resulting in the January 2001 FDA hearing on the matter and the class action lawsuits. Adverse events were only reported to the FDA by the vaccines trials’ administrators if they were of the arthritis kind, since “arthritis only” had become the new “case definition” at the 1994 Dearborn ”conference.” When Dennis Parenti of SmithKline reported that there were only two neurological adverse events to LYMErix at the 2000 Lyme Disease Foundation Conference in Hartford, CT, several physicians and attendees immediately got up and walked out of the conference room, while the rest groaned.
The functional results of OspA vaccination were, we hypothesize, not dissimilar from the results of structurally similar vaccine antigens that are managed by TLR2:
“These results are consistent with a model in which the presence of the 19-kD protein [of Mycobacteria tuberculosis] has a detrimental effect on the efficacy of vaccination with live mycobacteria.” (27)
“Synthetic analogs of lipopeptides from Treponema pallidum also inhibited Ag [antigen] processing.” (28)
“the immunosuppressive effect is dependent on glycosylated and acylated 19-kDa lipoprotein [of Mycoplasma tuberculosis] 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. (29)
“Thus, tolerance to LPS and mycobacterial components cannot be attributed solely to a decrease in TLR/MD-2 expression levels, suggesting inhibition of expression or function of other signaling intermediates 2002, Induction of bacterial lipoprotein tolerance is associated with suppression of toll-like receptor 2 expression.”(30)
“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.” (31)
And, we know that:
[((2003) Borrelia burgdorferi-induced tolerance as a model of persistence via immunosuppression.]
“If left untreated, infection with Borrelia burgdorferi sensu lato may lead to chronic Lyme borreliosis. It is still unknown how this pathogen manages to persist in the host in the presence of competent immune cells. It was recently reported that Borrelia suppresses the host’s immune response, thus perhaps preventing the elimination of the pathogen (I. Diterich, L. Härter, D. Hassler, A. Wendel, and T. Hartung, Infect. Immun. 69:687-694, 2001). Here, we further characterize Borrelia-induced immunomodulation in order to develop a model of this anergy. We observed that the different Borrelia preparations that we tested, i.e., live, heat-inactivated, and sonicated Borrelia, could desensitize human blood monocytes, as shown by attenuated cytokine release upon restimulation with any of the different preparations. Next, we investigated whether these Borrelia-specific stimuli render monocytes tolerant, i.e. hyporesponsive, towards another Toll-like receptor 2 (TLR2) agonist, such as lipoteichoic acid from gram-positive bacteria, or towards the TLR4 agonist lipopolysaccharide. Cross-tolerance towards all tested stimuli was induced. Furthermore, using primary bone marrow cells from TLR2- deficient mice and from mice with a nonfunctional TLR4 (strain C3H/ HeJ), we demonstrated that the TLR2 was required for tolerance induction by Borrelia, and using neutralizing antibodies, we identified interleukin-10 as the key mediator involved. Although peripheral blood mononuclear cells tolerized by Borrelia exhibited reduced TLR2 and TLR4 mRNA levels, the expression of the respective proteins on monocytes was not decreased, ruling out the possibility that tolerance to Borrelia is attributed to a reduced TLR2 expression. In summary, we characterized tolerance induced by B. burgdorferi, describing a model of desensitization which might mirror the immunosuppression recently attributed to the persistence of Borrelia in immunocompetent hosts”. (32)
AGAIN: “Next, we investigated whether these Borrelia-specific stimuli render monocytes tolerant, i.e. hyporesponsive, towards another Toll-like receptor 2 (TLR2) agonist, such as lipoteichoic acid from gram-positive bacteria, or towards the TLR4 agonist lipopolysaccharide. Cross-tolerance towards all tested stimuli was induced.”
Epstein-Barr’s activity regarding TLR2:
(2007) Epstein-Barr virus induces MCP-1 secretion by human monocytes via TLR2.
“Epstein-Barr virus (EBV) is a gammaherpesvirus infecting the majority of the human adult population in the world. TLR2, a member of the Toll-like receptor (TLR) family, has been implicated in the immune responses to different viruses including members of the herpesvirus family, such as human cytomegalovirus, herpes simplex virus type 1, and varicella-zoster virus. In this report, we demonstrate that infectious and UV-inactivated EBV virions lead to the activation of NF-kappaB through TLR2 using HEK293 cells cotransfected with TLR2-expressing vector along with NF-kappaB-Luc reporter plasmid. NF-kappaB activation in HEK293-TLR2 cells (HEK293 cells transfected with TLR2) by EBV was not enhanced by the presence of CD14. The effect of EBV was abrogated by pretreating HEK293-TLR2 cells with blocking anti-TLR2 antibodies or by preincubating viral particles with neutralizing anti-EBV antibodies 72A1. In addition, EBV infection of primary human monocytes induced the release of MCP-1 (monocyte chemotactic protein 1), and the use of small interfering RNA targeting TLR2 significantly reduced such a chemokine response to EBV. Taken together, these results indicate that TLR2 may be an important pattern recognition receptor in the immune response directed against EBV infection.” (33)
And we know that:
“Yale researcher Stephen Barthold, a veterinarian and professor of comparative medicine who developed the first mouse model of Lyme disease, studies the expression of B. burgdorferi surface proteins throughout various stages of the spirochete’s life cycle. He finds that during the early stages of infection, B. burgdorferi avoids immune detection by decreasing its expression of surface proteins or cloaking its expressed surface proteins under a layer of slime. “It’s using some sort of stealth-bomber-type mechanism,” he says. Or, using another diversionary tactic called blebbing, the spirochete can pinch off bits of its membrane in order to release its surface proteins Explains Barbour: “It’s like a bacterial Star Wars defense program,” in which released surface proteins might intercept incoming host antibodies keeping the spirochete safe from immunological attack.” (34)
which is what we call the auto-vaccination with OspA – the immune-suppressing fungal antigen amd TLR2-agomist known also, structurally, as Pam3Cys (35).
In short, “Lyme Disease” is chronic and seronegative because it is chronic, or chronically shedding variable (Relapsing Fever-esque) outer surface lipoproteins like OspA, or, as Alan Barbour states in his US Patent #6,719,983:
“2.1 Methods of Treatment
”An important aspect of the invention is the recognition that Borrelia VMP-like sequences recombine at the vls site, with the result that antigenic variation is virtually limitless. Multiclonal populations therefore can exist in an infected patient so that immunological defenses are severely tested if not totally overwhelmed. Thus there is now the opportunity to develop more effective combinations of immunogens for protection against Borrelia infections or as preventive inoculations such as in the form of cocktails of multiple antigenic variants based on a base series of combinatorial VMP-like antigens.”
“antigenic variation is virtually limitless. Multiclonal populations therefore can exist in an infected patient so that immunological defenses are severely tested if not totally overwhelmed.”
What are the other functional outcomes of the chronic agonism of TLR2 – the one that manages triacyl lipopeptides like OspA or Pam3Cys that render the immune system overwhelmed, not to mention the persons who late in the disease who do not serologically (antibodies) react to antigen from spirochetes fresh out of a tick due to antigen variation,… not to mention the diminution of antibody production due to chronic TLR2 agonism?
Says Paul Duray of the National Cancer Institute and Ft. Detrick (hint, hint):
“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.” (36)
The lymphocytes of these chronic “Lyme” victims look like Epstein-Barr transformed cells.
In 2003, Hulinska et al report in
“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 or 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.” (37)
One of the characteristics of chronic neurologic “Lyme” is that it is called an “aseptic meningitis” (38, 39, 40). This is, of course, while the German Multiple Sclerosis expert Roland Martin had been recruited by the National Institute of Health to research the association between “Lyme” and Multiple Sclerosis.(41, 42). Martin went home once he found out that OspA-induced immunosuppression was the likelier reason “Lyme” was mistaken for Multiple Sclerosis or vice versa.
DISCLAIMER: We Lyme victims did not dream up this nonsense. We only report it.
Could the co-TLR2 agonists (inducing tolerance and a lack of antibodies) Epstein-Barr and Borreliosis be simply responsible for: “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?”(36) ?
It is common knowledge that 95% of the adult population in Western cultures has been exposed to Epstein-Barr and its common similar herpes viruses. Hypothetically, there is a mouse herpesvirus (gamma2herpes) that to our knowledge has not been investigated regarding transmission to other hosts via ticks. We’re not privileged to know much about what happens on Plum Island. We only know there is a “Plum Island” strain of mycoplasma, and that Yale’s Durland Fish experimented with trying to get African Swine Fever virus to “take” to local hard-bodied ticks at that Not-Bioweapons/Just-Helpin laboratory (43, 44).
However, it’s something that might have been discovered 10 or 15 years sooner had not certain persons associated with Yale and New York Medical College made an agreement with Kaiser-Permanente (45) to sell a vaccine against a disease they suddenly decided doesn’t actually cause any illness (and the world is flat, the moon made of green cheese, and all hospitals are going to become brothels because it’s cheaper and therefore cost-effective to deploy self-alleged MDs who never perform any scientifically valid rule-outs before making theoretical diagnostic assumptions based on “projection,” rather than bog down the likes of the actual laboratories with the fancy machinery that serves no purpose other than to take up space and look shiny, just like the misguided folks at Silly NASA…).
“Epstein-Barr virus (EBV) efficiently drives proliferation of human primary B cells in vitro, a process relevant for human diseases such as infectious mononucleosis and posttransplant lymphoproliferative disease. Human B-cell proliferation is also driven by ligands of Toll-like receptors (TLRs), notably viral or bacterial DNA containing unmethylated CpG dinucleotides, which triggers TLR9. Here we quantitatively investigated how TLR stimuli influence EBV-driven B-cell proliferation and expression of effector molecules. CpG DNA synergistically increased EBV-driven proliferation and transformation, T-cell costimulatory molecules, and early production of interleukin-6. CpG DNA alone activated only memory B cells, but CpG DNA enhanced EBV-mediated transformation of both memory and naive B cells. Ligands for TLR2 or TLR7/8 or whole bacteria had a weaker but still superadditive effect on B-cell transformation. Additionally, CpG DNA facilitated the release of transforming virus by established EBV-infected lymphoblastoid cell lines. These results suggest that the proliferation of EBV-infected B cells and their capability to interact with immune effector cells may be directly influenced by components of bacteria or other microbes present at the site of infection.–
Toll-like receptor agonists synergistically increase proliferation and activation of B cells by epstein-barr virus. (46)
We know that “Lyme” is associated with the production of Amyotrophic Lateral Sclerosis (in 47% of the ALS cases in Lyme-endemic areas) (47) and Multiple Sclerosis. And we know that ALS is associated with mycoplasmal infection (tolerance to TLR2 agonists), and, MS, and apparently “Lyme” is associated with Epstein-Barr virus or something like it (36, 48).
We know that 90% of Chronic Fatigue patients found out they had “Lyme Disease” when finally assessed by a reputable laboratory – one not like Quest Diagnostics, which uses strain B31, the non-neurotropic, non-OspC- bearing, non-band-23-producing strain (49). We hypothesize that since it is known that mycoplasmal infections in the blood disrupt the osmotic potential in erythrocytes (disrupt the transfer of oxygen), and metabolism (these things need to be fed, after all) (50, 51), and since there has been reported a high association to mycoplasmal infections in Chronic Fatigue and Gulf War Illness victims (52, 53), that the tolerance to TLR2 agonists Lyme/LYMErix results in tolerance to mycoplasma in the blood (Chronic Fatigue) with no relative antibody production (28).
“Lyme” also produces a Lupus-like syndrome (54), and recently (and formerly, formally associated with Allen Steere) was linked by the Allen-Steere-Lupus-Lyme group (now known as the biotech spin-off, “L2-Diagnostics”) with Epstein-Barr (55).
We hypothesize that due to the induction of tolerance to TLR2 agonists like fungal or mycoplasmal antigens (Pam3Cys or OspA blebbing or vaccination) interrupting Epstein-Barr latency,
“Chronic infection or colonization by mycoplasma(s) could gradually and significantly alter many biologic properties of mammalian host cells in culture, including induction of malignant transformation. We examined effects of Mycoplasma fermentans infection on the continuing survival and immortality of human peripheral blood mononuclear cells (PBMCs) from healthy blood donors. Without specific supplemental growth factors, human PBMCs normally die rapidly, with few cells other than macrophages/monocytes surviving after 2 weeks in cultures. Only occasional Epstein-Barr virus (EBV)-positive B lymphocytes would continue to proliferate and undergo spontaneous immortalization. Our present study revealed that infection of human PBMCs in culture with the incognitus and PG18 strains of M fermentans, but surprisingly not with some other strains tested in parallel, markedly enhanced the rate of EBV-positive B lymphocytes to undergo immortalization (74% vs 17%). Compared with spontaneously immortalized PBMCs, the PBMCs immortalized in cultures infected with the mycoplasmas often had prominent karyotype changes with chromosomal loss, gain, or translocations. Furthermore, many of these immortalized B lymphocytes were found to be monoclonal in nature. The in vitro findings would be of relevance to lymphoproliferative disorders that occurred in patients with immune suppression. The mycoplasma-mediated promotional effect in cell immortalization and its potential clinical implications warrant further study. –2004; Blood; Mycoplasma fermentans infection promotes immortalization of human peripheral blood mononuclear cells in culture. (56)
the induction of chronic Lyme results in the un-latency of Epstein-Barr. Says one researcher,
Regulation and dysregulation of Epstein-Barr virus latency: implications for the development of autoimmune diseases.
“Epstein-Barr virus (EBV) is a human herpesvirus hiding in a latent form in memory B cells in the majority of the world population. Although, primary EBV infection is asymptomatic or causes a self-limiting disease, infectious mononucleosis, the virus is associated with a wide variety of neoplasms developing in immunosuppressed or immunodeficient individuals, but also in patients with an apparently intact immune system. In memory B cells, tumor cells, and lymphoblastoid cell lines (LCLs, transformed by EBV in vitro) the expression of the viral genes is highly restricted. There is no virus production (lytic viral replication associated with the expression of all viral genes) in tight latency. The expression of latent viral oncogenes and RNAs is under a strict epigenetic control via DNA methylation and histone modifications that results either in a complete silencing of the EBV genome in memory B cells, or in a cell-type dependent usage of latent promoters in tumor cells, germinal center B cells, and LCLs. Both the latent and lytic EBV proteins are potent immunogens and elicit vigorous B- and T-cell responses. In immunosuppressed and immunodeficient patients, or in individuals with a functional defect of EBV-specific T cells, lytic EBV replication is regularly activated and an increased viral load can be detected in the blood. Enhanced lytic replication results in new infection events and EBV-associated transformation events, and seems to be a risk factor both for malignant transformation and the development of autoimmune diseases. One may speculate that an increased load or altered presentation of a limited set of lytic or latent EBV proteins that cross-react with cellular antigens triggers and perpetuates the pathogenic processes that result in multiple sclerosis, systemic lupus erythematosus (SLE), and rheumatoid arthritis. In addition, in SLE patients EBV may cause defects of B-cell tolerance checkpoints because latent membrane protein 1, an EBV-encoded viral oncoprotein can induce BAFF, a B-cell activating factor that rescues self-reactive B cells and induces a lupus-like autoimmune disease in transgenic mice.”(57)
Down-regulation of MHC class II expression through inhibition of CIITA transcription by lytic transactivator Zta during Epstein-Barr virus reactivation.
“The presentation of peptides to T cells by MHC class II molecules is of critical importance in specific recognition to a pathogen by the immune system. The level of MHC class II directly influences T lymphocyte activation. The aim of this study was to identify the possible mechanisms of the down-regulation of MHC class II expression by Zta during EBV lytic cycle. The data in the present study demonstrated that ectopic expression of Zta can strongly inhibit the constitutive expression of MHC class II and CIITA in Raji cells. The negative effect of Zta on the CIITA promoter activity was also observed. Scrutiny of the DNA sequence of CIITA promoter III revealed the presence of two Zta-response element (ZRE) motifs that have complete homology to ZREs in the DR and left-hand side duplicated sequence promoters of EBV. By chromatin immunoprecipitation assays, the binding of Zta to the ZRE(221) in the CIITA promoter was verified. Site-directed mutagenesis of three conserved nucleotides of the ZRE(221) substantially disrupted Zta-mediated inhibition of the CIITA promoter activity. Oligonucleotide pull-down assay showed that mutation of the ZRE(221) dramatically abolished Zta binding. Analysis of the Zta mutant lacking DNA binding domain revealed that the DNA-binding activity of Zta is required for the trans repression of CIITA. The expression of HLA-DRalpha and CIITA was restored by Zta gene silencing. The data indicate that Zta may act as an inhibitor of the MHC class II pathway, suppressing CIITA transcription and thus interfering with the expression of MHC class II molecules.” (58)
It could be that it’s actually OspA-induced Epstein-Barr that is the “New Great Imitator.”
And that the Yale-Plum-Permanentes are the Greatest Great-Imitators.
Of either physicians or scientists.
Still, where do we go from here?
“We don’t know.” First, we have to deal with the sugarplum fairy-dancing cocoanut-heads, masquerading as “MDs” and “scientists,” doing perpetual, eternal lapses and re-lapses between the green cheese moon and the flat earth on the dot guv dime because they haven’t the plain old regular nuts to admit that they knew all along – and from the beginning, 1992, when Allen Steere went to Europe with his “high passage” plasmid-dropping spirochete strains and “recombinant OspA-B with the no-lipid attached” to come up with a “diagnostic standard” for “Lyme” that ended up with none of the two “primary immunodominant antigens” represented – that OspA was not a vaccine.
— — — — —
“To be most effective, advances in regulatory science must be fully integrated into the entire product development process,” says the new FDA chief, Margaret Hamburg.
The Biomarkers if Illness, developed by the ALDF.com or IDSociety.org
And the End of the Almighty Checklist – a sign of the auto-detonation of the adherents to Psychiatry:
What do the Biomarkers, published by the same gang who now says “Lyme is a consequence of inadequate sexual release,” say “Chronic Lyme/LYMErix Disease” is?.
1) Using Dark Field to study the modified erythrocytes, modified via the tolerance induced from chronic stimulation of TLR2 by spirochetal blebbing of the likes of TLR2 agonist OspA, and subsequent colonization by mycoplasma [recall that many sufferers of “Chronic Fatigue Syndrome” have been found to own a colony of Candida (a fungus)].
Brazil makes fun of US “Lyme” “scientists” mycoplasma-like and spiroplasma-like organisms in the blood of Lyme-like illness
See Erythrocytes of RBC in Biomarkers page. Crooks don’t want anyone using Dark Field to look at the blood. Sweeg went after Lisa Masterson for making this proposal.
2) The “We Don’t Know What You Have” Negative Data Rule re the DNA/RNA testing for all the mycoplasma and activated viral infections that won’t be producing antibodies (because some are also TLR2 agonists like Epstein-Barr, and chronic TLR2 agonism results in no-antibodies (Justin Radolf: ,” 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 may be the main reason the crooks don’t want us treated with antibiotics- we will create antibiotic resistant Tuberculosis (because we will likely have seronegative TB oand other primarily TKR2 agonising infections like Staph aureus), not to mention, changing the RNA of the likes of mycoplasma as the Chinese did:
J Clin Microbiol. 2010 Sep 22. [Epub ahead of print]
Nested PCR-Linked Capillary Electrophoresis and Single-Strand Conformation Polymorphisms for Detection of Macrolide-Resistant Mycoplasma pneumoniae in Beijing.
3) QEEG or Fibro-Lenny Sigal’s (who we’ll now refer to as Lenny Squiggy) findings that persons with chronic Lyme have changes to electroencephalograms.
http://www.ncbi.nlm.nih.gov/pubmed/7554300 “Abnormal QEEG and/or EPs were found in 75% of the active Lyme disease patients and in 54% of the post CNS Lyme disease patients.”
4) modified cytokine profile suggested by Lenny Sqiggy in the Cold Spring Harbor Conference book (1992, Schutzer:) mentioned above, to which Paul Duray attended and re-iterated his “EBV-modified lymphocytes” findings:
Says Sigal: “Since cytokines can alter endothelial cell function and increase the entry of inflammatory cells to the organ whose vasculature has been modified, the presence of cytokines in the Lyme synovium may have an important indirect effect on local inflammation [Yednock et al. 1992]. The presences of circulating levels of these cytokines may be the cause of the certain clinical features of Lyme disease; eg., sleep disorder due to elevated levels of IL-1 (Opp and Krueger 1991) may be part f the cause of fibromyalgia seen during and after active Lyme disease (Sigal 1990)
1991, Steve Schutzer.
5) MMP-130 and GFAp in the CSF of Mark Klempner’s Neuroborreliosis (which is not “Lyme Disease,” BTW, because Lyme Disease became “only the HLA-linked knee-presentation” at Dearborn),
6) Allen Steere’s Nitric Oxide in the CSF of Lyme victims (we now know that the exposure to these reactive oxygen species/byproducts are downregulators of TLR2)
J Infect Dis. 1994 May;169(5):1014-22.
Borrelia burgdorferi and Escherichia coli lipopolysaccharides induce nitric oxide and interleukin-6 production in cultured rat brain cells.
Tatro JB, Romero LI, Beasley D, Steere AC, Reichlin S.
Division of Endocrinology, New England Medical Center Hospitals, Boston, MA 02111.
7) CORRECT Borrelia (all species) DNA/RNA primers and not the OspA gene, because that changes according to Alan Barbour; we can throw out all “studies” in which the OspA gene was the determinant for infection with the “Lyme” spirochete [~10 citations]
8) Quinolinic acid and the degradants of monoamines in the CSF of borreliosis victims (JJ Halperin),
9) brain SPECT and PET imaging (we now know that the metabolism of erythrocytes are hijacked by the mycoplasma in the blood – infections we can’t fight off because they have OspA or TLR2 agonizing lipoproteins in them), NOTE: psychiatry likes to suggest that changes to the brain perfusion seen in chronic Lyme/Fatigue victims is a result of Bipolar, when not ever once was anyone who was diagnosed with Bipolar have shown hyper- or hypo- perfusion as a result of any of the “poles” without other true, real, scientific valid biomarkers of real illness first performed as a rule out. Secondarily, when studies have been performed in which there are brain structural changes to the likes of 17 year olds who are determined to be psychopathic or sociopathic, have these conditions studied a contribution by trauma. As a third outstanding parameter, why, we wonder, are lawyers undable to view anything from a scientific standpoint? Why do they score so low on the visual-spatial scale of cognitive abilities? Why are lawyers so left-brain dominant and why do they have no understanding of vocabulary as a simple means to draw a picture in the mind of another.
Most of all, why is this seen in both lawyers and psychiatrists? Why are the best scientists and engineers known to be visual-spatial or right-brain dominant? Is this nature or nurture? The victims of their chronic fraud crime are not entitled to know why self-alleged scholars as these are clearly unable to think. We are not entitled to see their own cognitive differentials and potentials.
10) Allen Steere’s anti-phospholipid antibodies (now known to be caused by activated Epstein-Barr, as reported by Allen Steere’s own Lyme/Lupus reporting team member, Joe Craft at Yale), (54)
11) the auto-reactive band 41 [specific to borrelia or not; scientists seem to think an antibody against flagellin cross reacts with nerve and other tissues, such as skin and intestine (H. pylori and Campylobacter, producing autoimmune hives, thyroid disease, GERD…)], [Refs, Barbour patent, Lenny Sigal]
Biochim Biophys Acta. 1993 Mar 24;1181(1):97-100.
Molecular mimicry in Lyme disease: monoclonal antibody H9724 to B. burgdorferi flagellin specifically detects chaperonin-HSP60.
Dai Z, Lackland H, Stein S, Li Q, Radziewicz R, Williams S, Sigal LH.
Center for Advanced Biotechnology and Medicine, Piscataway, NJ.
12) anti-heat shock proteins (a sign of MS), (others besides Sigal) Bands 60, 74, etc.
13) anti-gangliosides, Benach, Steere
1989; Total, anti-viral, and anti-myelin IgG subclass reactivity in inflammatory diseases of the central nervous system.
Total IgG subclass levels, anti-viral, anti-myelin basic protein (anti-MBP), and anti-ganglioside 1 (anti-GM1) IgG subclass levels were measured in 6 patients with herpes simplex virus encephalitis (HSVE), 16 with borreliosis, 8 with other bacterial infections, 12 with multiple sclerosis (MS), 13 with subacute sclerosing panencephalitis (SSPE), 5 with glioblastoma and 12 controls. Total IgG1 levels were elevated in cerebrospinal fluid (CSF) from all patient groups (but not in the controls), IgG2 in bacterial infections, IgG3 in HSVE and borreliosis and IgG4 in some SSPE patients. The anti-viral (anti-measles, varicella zoster virus and rubella) IgG antibodies in MS were restricted to IgG1, anti-measles IgG to IgG1 and sometimes IgG4 in SSPE, anti-borrelia IgG to IgG1, IgG2 and IgG3. In contrast to anti-viral antibodies, anti-MBP and GM1 antibodies belonged to IgG1, IgG3 or IgG4 in MS. The nature of the immunological activation appears to be reflected in the subclass patterns elicited in the central nervous system. Different IgG subclass patterns in infectious diseases and MS suggest a difference between antigen-specific and non-specific B-cell activation.
14) GFAp or glial fribrillary acidic protein in the CSF – signs of gliosis mentioned by Yale’s Robert Schoen when he mentioned reasons why we need a Lyme vaccine, http://www.annals.org/content/132/8/661.full.pdf+html (gliosis would be a sign of multiple CNS degenerative diseases),
“Other peripheral neuropathies and Lyme meningitis are also seen at this stage. In late-stage disease, the central nervous system may be involved. A new diagnostic test measuring glial fibrillary acidic protein in cerebrospinal fluid may prove to be a useful tool for measuring such involvement (20).” — Yale’s Robert Schoen talking about how serious Lyme is, and that we need a vaccine for this disease that goes away and has no illness signs and is psychiatric and the result of not-enough-sex or self-poisoning.
15) Gadolinium-Contrast MRI – performed in monkeys with Lyme but never Lyme-MS Victims which show Lyme is an active meningitis, and now performed by the Japanese when deciphering the cause of meningitis in a patient who was mistakenly diagnosed with MS when they had Large B-cell Lymphoma of the CNS:
Primary central nervous system large B-cell lymphoma with prolific, mixed T-cell and macrophage infiltrates, mimicking multiple sclerosis.
16) EMG Allen Steere:
I think we should fund an EMG study where we try to find out whether or not Lyme victims suffer “hysteria” or the electrification of our hysters. I think this most of all would be a fun study: Could we find out via EMG that not-enough-sex really causes Lyme-ALS, or Lyme-MS or Lyme-Lupus, or Lyme-stroke, or bad knees, or Guillain-Barre? Who wants to volunteer for that study? And what about men with Low-T? Can that study be performed? Can we women watch?
We’ll rate their manliness while this EMG study of their genitals to determine if not-enough sex is “The Reason for Low T or the Inability of Psychiatrists and Lawyers to Think like Scientists or Engineers” is performed with our own Checklist.
17) T cell proliferation:
Steere references Dattwyler’s report here:
None of these biomarkers were applied by Mark Klempner from 1997 to 2001 when he determined that “there is no such thing as Chronic Lyme,” despite being the author of two of the main signs that it is. The first was Klempner’s MMP-130 only found in the spinal fluid of chronic Lyme victims and his other two studies from 1992 where he determined and published the reasons he believed ceftriaxone failed to eradicate all spirochetes [REF]
Now, back to Reason: What we do know about such emotionalisms over science is that aggression comes from cowardice or the fear of being less-than another person. We call it jealousy, we call is envy and we call it pride, hubris and arrogance. Or we fear not being believed that we suffer a terrible illness – one not detectable by antibodies, such as those fungal like stealth infections as Relapsing Fever or Relapsing Fever plus the synthetic antigen Pam3Cys.
Common sense tells us that you can’t see Multiple Sclerosis or Lupus, but sometimes medical schools attract and even accept people who have studied only the likes of English literature or psychology or philosophy in undergraduate study. These are the toughest nuts to crack. You can’t teach an old dog new tricks.
7″You hypocrites, rightly did Isaiah prophesy of you:
8′(F)THIS PEOPLE HONORS ME WITH THEIR LIPS,
BUT THEIR HEART IS FAR AWAY FROM ME.
9’BUT IN VAIN DO THEY WORSHIP ME,
TEACHING AS (G)DOCTRINES THE PRECEPTS OF MEN.'”
Or, they purport self-flattering, unscientific concepts as medical doctrine because it is too frightening to see and accept the reality that they’re truly addicted (repetitious cognitive loops or mental frameworks) in a medical sense to some philosophical (psychiatric) Kool Aid, dreamed up by some pervert and drug addict (Freud).
The biggest of the guns in our arsenal – besides all of the published applications of the science that says Pam3Cys or OspA or LYMErix or the HIV antigens gp120 and 41 – are TLR2 agonists and result in the downregulation of the immune response and the inhibition B cell apoptosis… is the RNA/DNA Shell Game, we know to be criminal in anyone’s mind.
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