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Sunday, June 24, 2018

What is Lyme?





“The case against science is straightforward: much of the scientific literature, perhaps half, may simply be untrue,” Dr. Horton

RJ James s & Kelly Irene

Lyme Borreliosis is a multi-systematic disease that's transmitted primarily through the bite of an infected tick, other insect vectors and maternal–fetal transmission (1). Originally, Borrelia was known as a relapsing fever organism because of it’s ability to undergo constant antigenic variation (modify their different outer surface proteins) (2). Unlike most bacteria, they are their own phylum that sheds it's outer membrane lipoproteins to evade the immune system (3). The shed lipoproteins are known as Outer Surface Proteins (Osps) and Variable Major Proteins (Vmps).  Borrelia modify their Osps (blebbing) as a means of evading a host immune response, making it difficult to detect through standard serology (besides an anti-flagellar (band 41) antibody method that is patented by Yale and no longer used (4)). Only those with HLA -linked hypersensitivity responses (~15%) to Borrelia test positive on current testing methods.

These shed blebs are called OspA (5). OspA is a molecule that stops the typical immunity chain reaction (6). It's a triacylated lipoprotein that's managed by toll-like receptors (TLR) 2 and 1 (TLR2/1) (7).TLR’s play a critical role in the innate immune system as they are first-line of defence against invading pathogens. The TLR’s job is to recognize the distinct molecular structure of pathogens so that they can disable or destroy them. TLR2/1 manages mycobacteria or fungal endotoxins (8). They are the same TLR's that manage mycoplasma, mycobacterium, m. tuberculosis, brucella and other fungal antigens..

In addition to being a major lipoprotein shed by spirochetes, OspA was also the antigen used in the LYMErix vaccine. Since it is a fungal – like endotoxin, it is much more toxic and stealth compared to most typical bacteria (TLR4, lipopolysaccharides). OspA or TLR2/1 agonists are so toxic, that the body shuts down the immune system to avoid a septic cytokine storm (9). OspA has the ability to cause permanent global immunosuppression in those who are infected (10).

OspA tolerizes the immune system making it unable to produce antibodies against pathogens that are managed by TLR 2/1 receptors (11). In addition, TLR’s 7/9 also shut down in a mechanism that is known as cross-tolerance whereby the immune system becomes unable to fight other viral, parasitic and bacterial pathogens. Thus, Epstein-Barr, herpesviruses, cytomegalovirus, coxsackie, zoster, etc.) and secondary infections (candida, fungi, mycoplasma, streptococcus, etc.) become the driving force in this neurological chronic fatiguing disease.

The mechanisms listen above occur within the first week of  infection once the Spirochetes disseminate to the lymph nodes (12). B-cell germinal centers collapse (13) and prevent B-cells from properly maturing (leading to a reduction in detectable antibodies). As a result, the host ends up suffering from global immunosuppression and low-grade inflammation of the brain (14). This resembles Pseudolymphoma and Leukemia (15). Chronic Lyme disease is really a B-cell (non – HIV) AIDS whereby sufferers are left with global immunosuppression and reactivated viruses
Even the NIH and Gary Wormser says OspA alone causes permanent immunosuppression (16,17,18). Since OspA is the main driver of disease, you do not need to be exposed to spirochetes to suffer from “Chronic Lyme” (OspA via tick bite or vaccine). Given this information, why is it that Steere purposely removed OspA from the diagnostics at the same time the vaccine was on trial? Namely because, it would make their vaccine look far more effective.

Firstly, you cannot vaccinate against relapsing fever organisms due to its ability to undergo antigenic variation. Secondly you cannot inject people with fungal - like antigens because they can cause immunosuppression and post-septic shock. All fungal bearing vaccine attempts managed by TLR2/1 (Tuberculosis, Brucella,  HIV etc.). were epic failures because they caused the same outcome that they were "intended" to prevent (19).

Raymond Dattwyler, Professor of Microbiology and Immunology from New York Medical College said that "Individuals with a poor immune response tend to have worse disease" (20). Chronic neuro Lyme produces low to no antibodies. In analytical testing you are supposed to look for the lowest antibody concentration possible. However, researchers at the CDC did the opposite. In Dearborn Michigan, 1994, the “scientists” from the CDC/ALDF/Yale committed research fraud by falsified the testing and case definition to detect only a high antibody concentration. This was intended to make their vaccine look far more effective by excluding all neurological immune suppressed cases from the diagnostics. Making both OspA shed by Spirochetes  and LYMErix victims undetectable with current analytical testing.

HIV-AIDS destroys T-cells
LYME-AIDS renders B-cells immature and useless
Both are Acquired Immune Deficiencies.


1. Maternal-fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi. https://www.ncbi.nlm.nih.gov/pubmed/4003991

2. Selection of Variant Borrelia burgdorferi Isolates from Mice Immunized with Outer Surface Protein A or B http://www.ncbi.nlm.nih.gov/pmc/articles/PMC173206/pdf/631658.pdf|

3. Characterization of multiprotein complexes of the Borrelia burgdorferi outer membrane vesicles. https://www.ncbi.nlm.nih.gov/pubmed/21875077

4. Antigenic variation in vector-borne pathogens. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627965/?tool=pubmed

5. Action of penicillin on Borrelia hermsii. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC182019/

6. Fungal Recognition by TLR2 and Dectin1 https://www.ncbi.nlm.nih.gov/m/pubmed/18071656/

7. Tripalmitoyl-S-Glyceryl-Cysteine-Dependent OspA Vaccination of Toll-Like Receptor 2-Deficient Mice Results in Effective Protection from Borrelia burgdorferiChallenge http://iai.asm.org/content/71/7/3894.abstract

8. TLR2

9. Endotoxin Tolerance Inhibits Lyn and c-Src Phosphorylation and Association with Toll-Like Receptor 4 but Increases Expression and Activity of Protein Phosphatases.

10. Human Lipopolysaccharide-binding Protein (LBP) and CD14 Independently Deliver Triacylated Lipoproteins to Toll-like Receptor 1 (TLR1) and TLR2 and Enhance Formation of the Ternary Signaling Complex* https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617275/

11. Lyme Diseases Greatest Mystery: Understanding Tolerance and Cross Tolerance in the Immune System Caused by Outer Surface Proteins Shed by Borrelia

12. Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102705/

13. Suppression of Long-Lived Humoral Immunity Following  Borrelia burgdorferi Infection. http://journals.plos.org/plospathogens/articl=10.1371%2Fjournal.ppat.100497

14. Bacterial lipoproteins can disseminate from the periphery to inflame the brain. https://www.ncbi.nlm.nih.gov/pubmed/20431027


16. Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.

17. Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA). https://www.ncbi.nlm.nih.gov/pubmed/1086517

18. The Toll of a TLR1 polymorphism in Lyme disease: A tale of mice and men http://onlinelibrary.wiley.com/doi/10.1002/art.34386/a

19. Fungal Bearing Failed Vaccine Parallel Models - Like LYMErix http://truthbetoldx81.blogspot.com/2017/07/fungal-bearing-failed-vaccine-parallel.html



Friday, May 25, 2018

Tick Bite Sepsis: From Pseudoscience to Evidence-Based Research





By Kelly Irene and RJ James

Even tho there is plenty of science that demonstrates what Lyme Disease and its Outer Surface Proteins (Osps) do inside the human host, there are many evil people trying to keep Lyme and its crimes covered up. For decades, the debate about persistence vs non persistent has completely negated the opportunity for evidence-based activists to help bring justice to ALL Lyme patients (not just those who respond to treatments).
Evidence based activists face two key issues while trying to expose the truth about why Lyme Disease is such a “controversy”. Firstly, there is an abundance of advocates who either profit or at least benefit from the false persistence vs non-persistence dichotomy.
Secondly, the CDC/IDSA/ALDF continue to assert that evidence based activists are merely pseudoscientists who have no idea what they are talking about. In brief, “pseudoscience consists of statements, beliefs, or practices that are claimed to be both scientific and factual, but are incompatible with the scientific method” (Pseudoscience, 2018).  Sadly, that is what most Lyme Disease  activism currently is centered around: pseudoscience.
To avoid any claims that the literature provided in this blog is based of pseudoscience, there will be an abundance of literature from “credible scientists”. The studies used in this blog will be based off of systematic observation, measurement, experiment, formulation, testing, and modification of hypotheses.
Another thing to keep in mind is that the disease mechanisms provided in this blog are also shared by other abused groups such as Fibromyalgia (FM),  Myalgic Encephalomyelitis (ME), Chronic Fatigue Syndrome (CFS), Gulf War Illness (GWI), Autism, etc. (That will be explained in another blog). All that said, the key purpose of this blog is to help show Lyme activists that OspA, Pam3cys, and Post Sepsis Syndrome (PSS) are more than just buzz words in the Lyme community.
In order to properly understand what Lyme Disease does to the body, it is essential for Lyme activists to know that OspA is a key mechanism when it comes to understanding how the disease survive in it’s host. Borellia species undergo constant antigenic variation, whereby they shed Osps (i.e OspA) as a means of evading the immune system.  Because of these Osps, Lyme like diseases are not curable.
Spirochetes are pathologically parasitic, and are a relapsing fever organism. To put it differently, spirochetes are constantly pinching off their Osps to evade the immune response through a mechanism that Alan Barbour calls ‘blebbing’ (Barbour, Todd & Stoenner, 1982). These shed blebs are salso covered in lipoproteins known variable major proteins (Vmps).
                  

(Barbour, Todd & Stoenner, 1982).

Since much of the science on Lyme Disease is based off of research fraud committed by Steere et al in 1994, any research used to expose the truth has be based off studies that show it’s true disease mechanisms in parallel with similar types of organisms. When it comes to Lyme Disease (OspA),  it is very similar in structure to Pam3cys.
Pam3cys is a “TLR1/TLR2 agonist” (Pam3Cys, 2018). More specifically, it is a synthetic analog of the triacylated N-terminal part of bacterial lipoproteins” (Pam3Cys, 2018). Simply put, Pam3cys is a molecule that stops the immunity chain reaction in the immune systems Toll Like Receptors.

Toll Like Receptors: TLR2 manages mycobacteria or fungal endotoxins
Toll-like receptors are immune receptors that participate in the first line of defense against invading pathogens. They play a critical role in the innate immune response by recognizing the distinct molecular structure of invading pathogens.
Below is some evidence based literature that explains TLR 2’s mechanisms:
“The innate immune system utilizes multiple receptors to recognize fungal pathogens, and the net inflammatory response is controlled by interactions between these receptors. Many fungi are recognized, at least in part, by Toll-like receptor 2 (TLR2).”(Goodridge & Underhill, 2008).
“The agonists include bacterial lipoproteins (44, 53, 54), Gram-positive bacterial lipoteichoic acids (51, 55), mycobacterial lipomannans and lipoarabinomannans (56), pneumococcal peptidoglycans (57), and Treponema-derived glycolipids (58). Thus, LBP and CD14 may function to disaggregate and deliver a variety of acylated microbial agonists to the TLR2 system.”  (Goodridge & Underhill, 2008). Although this may be jargain to the average person, the chart below can help people understand what antigens are specific to TLR 2 receptors and some of the agonists that affect how it responds to presenting antigens.
(TLR2, 2018)
OspA is Pam3cys, a triacyl lipoprotein (3 fatty acid chains)
Now that we understand how Pam3cys works, it is important to understand that it is similar in structure to OspA.
Scientists from the Immunobiology Research Institute published a study that found “OspA is a 30-kDa membrane-associated lipoprotein with a typical tripalmitoyl-S-glycerylcysteine (Pam3Cys) moiety covalently attached to the N terminus of the protein.”  (Goodridge & Underhill, 2008). Another study done by Heilbrun et al (2003) from the Department of Pathology, University of Utah, in Salt Lake City found that “OspA is one of the tripalmitoyl-S-glyceryl-cysteine (Pam3Cys)-modified lipoproteins abundantly expressed on the surface of B. burgdorferi in the gut of the unfed tick (1122).” (Heilbrun et al, 2003). Finally, in one of their many patents, Dattwyler, Gomes-Solecki & Seegers (2009) found that:
“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)” (p.1).
As you can see, there are several credible studies that show that Pam3cys and OspA are very similar in structure. The lipoproteins are TLR 2/1 agonists (agonists are a substance that initiates a physiological response when combined with a receptor). TLR 2 agonists are fungal-like because they cause permanent immune suppression in the Toll Like Receptors that handle fungal antigens.

OspA/Pam3cys is managed by TLR2

As previously mentioned, OspA and Pam3cys are TLR 2/1 agonists. Heilbrun et al (2003) found that “Toll-like receptor 2 (TLR2) is a transmembrane signal transducer for tripalmitoyl-S-glyceryl-cysteine (Pam3Cys)-modified lipoproteins, including OspA from the Lyme disease spirochete Borrelia burgdorferi.” (p.2).  Furthermore, Pam3Cys-modified proteins, such as OspA, have been reported to act as potent inflammatory stimulants though the toll-like 2 receptor mechanism (TLR2)”  (Dattwyler, Gomes-Solecki & Seegers 2009). As confusing as this may sound to people who have no science backgrounds, what this means is that there is plenty of literature that proves that OspA/Pam3cys are managed by TLR 2.

OspA/TLR2 agonists are much more toxic and stealth than typical bacteria
One thing that important for activists to understand is that unlike sepsis caused by regular bacteria (managed by TLR 4 and is generally reversible), sepsis caused by TLR 2 agonists can cause permanent and irreversible damage.
More specifically,”TLR2 mediates inflammatory responses to a wide variety of lipidated microbial components, including bacterial lipoproteins, atypical lipopolysaccharides, and lipomannans (26–28). Among these microbial agonists, bacterial lipoproteins are by far the most potent  (Kelley, Ranoa & Tapping, 2013).  Moreover, “it became apparent that specific TLRs such as TLR2 and TLR4 play differential roles in the activation of the various arms of the innate immune response” (Kullberg, Meer & Netea, 2007). In the Journal of Immunology,   Akira, Hayashi, & Nobrega (2005) published a study whereby “experiments with TLR2-knockout mice confirmed that the inhibitory effects of Pam3Cys depend on the expression of TLR2” (p.6640).  Furthermore, their study concluded that “Pam3Cys keeps the precursors on a more immature stage” (Akira, Hayashi, & Nobrega, 2005). Taken together, the study done by Akira, Hayashi, & Nobrega (2005) “suggest that TLR4 signaling favors B lymphocyte maturation, whereas TLR2 arrests/retards that process, ascribing new roles for TLRs in B cell physiology.” (p. 6645).  In sum, there is plenty of research that shows that OspA/Pam3cys are TLR 2 agonists (fungal like) and cause irreversible/permanent immunosuppression.

OspA is the key mechanism to understand when it comes to Lyme Disease .
Now that we understand how OspA affects the host, the next part of this blog will use published evidence based literature that proves that OspA is the main driver of disease in Lyme patients.


Norman Latov - OspA vaccination caused the same chronic neurological disease as Lyme:  Neuropathy and cognitive impairment following vaccination with the OspA protein of Borrelia burgdorferi.
"Neurological syndromes that follow vaccination or infection are often attributed to autoimmune mechanisms. We report six patients who developed neuropathy or cognitive impairment, within several days to 2 months, following vaccination with the OspA antigen of Borrelia burgdorferi. Two of the patients developed cognitive impairment, one chronic inflammatory demyelinating polyneuropathy (CIDP), one multifocal motor neuropathy, one both cognitive impairment and CIDP, and one cognitive impairment and sensory axonal neuropathy. The patients with cognitive impairment had T2 hyperintense white matter lesions on magnetic resonance imaging. The similarity between the neurological sequelae observed in the OspA-vaccinated patients and those with chronic Lyme disease suggests a possible role for immune mechanisms in some of the manifestations of chronic Lyme disease that are resistant to antibiotic treatment."


Gary Wormser - OspA causes immunosuppression
(which means it was the opposite of a “vaccine”):  
"The modulation of human lymphocyte proliferative responses was demonstrated with a recombinant outer surface protein A (OspA) vaccine preparation for the prevention of Borrelia burgdorferi infection. After exposure to either the unaltered vaccine preparation or OspA prepared in saline, normal lymphocyte responses to the mitogens concanavalin A, phytohemagglutinin-M or pokeweed mitogen, or the antigen BCG were consistently reduced. Whole cell extracts of B. burgdorferi also modulated immune responses but required a much greater quantity of protein than needed for the OspA preparation. The magnitude of modulation was directly dependent on the quantity of OspA. OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression. Future studies designed to delete the particular region or component of the OspA molecule responsible for this effect may lead to improved vaccine preparations."               



Donald H. Marks – an OspA vaccine trial administrator – LYMErix caused the same disease as chronic Lyme: 
"A wide range of neurological complications have been reported via the medical literature and the VAERS system after vaccination with recombinant outer surface protein A (OspA) of Borrelia. To explore this issue, 24 patients reporting neurological adverse events (AE) after vaccination with Lymerix, out of a group of 94 patients reporting adverse events after Lymerix vaccination, were examined for causation. Five reports of cerebral ischemia, two transient Ischemic attacks, five demyelinating events, two optic neuritis, two reports of transverse myelitis, and one non-specific demyelinating condition are evaluated in this paper. Caution is raised on not actively looking for neurologic AE, and for not considering causation when the incidence rate is too low to raise a calculable difference to natural occurence."  https://www.ncbi.nlm.nih.gov/pubmed/21673416


Ben Luft at the 1998 FDA Vaccine Meeting on LYMErix – You can't tell the difference between chronic neurological Lyme and LYMErix victims
  “The point that I wanted to make in regard to the study is that there is very heavy dependence on serologic confirmation. And when we start thinking about the adverse events, *** it was stated originally when we got the overview of the disease that the disease is really quite protean. And actually the adverse events are very similar to what the disease manifestations are.**** And if you start to, as I think Dr. Hall was eluding to — if you start to kind of say well how often do you actually become seropositive, you can start to have a different take on when someone has an adverse event or whether it is disease specific or infection specific versus vaccine specific. And I think that that is an important issue that we have to deal with.”  
http://www.fda.gov/ohrms/dockets/ac/98/transcpt/3422t1.rtf

OspA Patent: Dave Persing 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….”           


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.”  


Based on published NIH research studies, it appears that OspA tolerizes immune cells and impairs the immune system from responding to any antigens that are managed by TLR 2. In addition, OspA also causes cross-tollerance whereby the immune system is no longer able to recognize and fight off other viral, parasitic, and bacterial pathogens

Additional resoruces on Toll Like Receptors affected by Lyme Disease (OspA)
TLR4 agonists – lipopolysaccharides, known as the more typical bacteria.    https://www.ncbi.nlm.nih.gov/pubmed/23695305http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714565/
TLR5 agonists – Flagellins             https://www.ncbi.nlm.nih.gov/pubmed/16479520
TLR7/9 agonists – Herpesviruses, Epstein-Barr and all other viral infections.           https://www.ncbi.nlm.nih.gov/pubmed/22227568
As a result of counter transference, both viral and opportunistic infections reactivate and take over the human host.
OspA or TLR2/1 agonists are so toxic, that the body shuts down the immune system to avoid a septic cytokine storm. Xiong et al (2015) from the Department of Microbiology and Immunology at the University of Maryland School of Medicine found that “Endotoxin tolerance protects the host by limiting excessive ‘cytokine storm’ during sepsis, but compromises the ability to counteract infections in septic shock survivors” (p. 172). Further more, “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” (Xiong et al, 2015).  In another study, researchers found that the “development of endotoxin tolerance following the initial cytokine storm phase of sepsis is thought to protect the host from an over exuberant immune response and tissue damage but at the same time, may render the host immunocompromised and more susceptible to secondary infection” (Medvedev, Pennini, Vogel, & Xiong, 2013). As you can see, the complexities of Lyme Disease go far beyond what mainstream activists let on.

Discussion/recap
Based of the research studies provided in previous paragraphs, it’s easy to see that spirochetes  are constantly undergoing antigenic variation by shedding their outer surface to avoid immune detection.
In addition, these shed blebs are covered in fungal-like Osps that have the ability to inhibit apoptosis and cause Post-Sepsis Syndrome in its victims.
Spirochetes travel to the lymph nodes, bone marrow, and the brain within the first week of infection where they shed these OspA “blebs” that get eaten up by immune cells.
As a result,  B-cell germinal centers are wrecked permanently and prevents B-cells from properly maturing (Leading to a reduction in detectable antibodies).
This leads to global immunosuppression in the blood and an immune system that is tolerized to opportunistic infections and reactivated viruses (Epstein-barr, HHV-6, cytomegalovirus, coxsackie, zoster, candida, mycoplasma, streptococcus, etc). All while also causing  inflammation in the brain.
In at least half the cases, Lyme Disease causes post sepsis and permanent B-cell immune disorders (Firbo, ME, CFS, GWI, etc.). Think of the spirochetes as just the detinator of this immunosuppressive neurologic nightmare.
Therefore spirochete persistence is not the main driver of disease in Lyme patients, it’s the exposure to fungal-like antigens (Osps/Pam3cys) that wreaks havoc in the human body.
In addition to OspA being shed by spirochetes, it was also used in the failed LYMErix vaccine. As mentioned before, you cannot vaccinate against relapsing fever organisms due to antigenic variation. Keep this in mind for the new vaccine that they are currently attempting to push through without it going through phase three of the trials.
Researchers concluded in the first vaccine trials, that the vaccine caused “defects in the TLR1/2 signaling pathway are associated with an impaired ability to generate antibodies following immunization with OspA lipoprotein” (Fikrig & Thomas, 2002). If you are an activist and want to see changes, you need to take this information seriously and protest this vaccine and attempt to stop it before it finishes phase 2 trials.
Being that OspA is the driving force behind Lyme Disease,  how convenient is it that the criminals left out OspA from the “case definition” at the same time the vaccine was on trial?
From the multitude of evidence based studies used to source this blog, it is clear that you cannot inject people with TLR 2/1 agonists because they cause immunosuppression and Post Sepsis Syndrome (B-cell immune disorders).
All fungal bearing vaccine attempts managed by TLR2/1 were epic failures causing the same outcome in which they “intended” to prevent (Tuberculosis, Brucella, HIV, Borrelia are parallel models in fungal-like vaccines).
OspA is Pam3cys = Permanent Immunosuppression = Oppurtunistic Infections = Tick Bite Sepsis
If OspA alone causes the same multi-system disease, what is the disease?

POST-SEPSIS SYNDROME
It’s important to note that these disease mechanisms are shared by many other abused groups (FM, ME, CFS, GWI, etc), and not all are caused by Lyme Disease.
They are caused by TLR 2/1 agonists that cause a fungal like sepsis that leads to permanent immunosuppression. There is nothing pseudoscientific about anything in this blog, as all the sources used are from ‘credible scientists’ from all over the world (many of which deny the severity of Lyme Disease).  In the end, we all need to unite to fight against the B-cell disorder (post sepsis) epidemic that is plaguing the world.
References
Dattwyler, R., Gomes-Solecki, M., & Seegers, J. (2009, December 31). 20090324638 LIVE BACTERIAL VACCINE. Retrieved May 25, 2018, from https://patentscope.wipo.int/search/en/detail.jsf?docId=US42934470&recNum=9&maxRec=30&office&prevFilter&sortOption=Pub Date Desc&queryString=tripalmitoyl cysteine or Pam3Cys and Epstein-Barr&tab=NationalBiblio
Akasaka, K., Tamura, A., Nakagawa, T., Koide, S., Huang, X., Link, K., & Koide, A. (1999). Multistep denaturation of Outer surface protein A (OspA). Seibutsu Butsuri, 39, 89-96. doi:10.2142/biophys.39.s163_1
Akira, S. A., Hayashi, E., & Nobrega, A. (2005). Role of TLR in B Cell Development: Signaling through TLR4 Promotes B Cell Maturation and Is Inhibited by TLR2. The Journal of Immunology, 174(11), 6639-6647. doi:10.4049/jimmunol.174.11.6639
Barbour, A. G., Todd, W. J., & Stoenner, H. G. (1982). Action of penicillin on Borrelia hermsii. Antimicrobial Agents and Chemotherapy, 21(5), 823-829. doi:10.1128/aac.21.5.823
Fikrig, E., & Thomas, V. (2002). The Lyme Disease Vaccine Takes Its Toll. Vector-Borne and Zoonotic Diseases, 2(4), 217-222. doi:10.1089/153036602321653798
Goodridge, H. S., & Underhill, D. M. (2008). Fungal Recognition by TLR2 and Dectin-1. Retrieved May 25, 2018, from https://www.ncbi.nlm.nih.gov/pubmed/18071656
Heilbrun, M., Wang, X., Ma, Y., Philipp, M. T., Yoder, A., Weis, J. H., . . . Weis, J. J. (2003). Tripalmitoyl-S-Glyceryl-Cysteine-Dependent OspA Vaccination of Toll-Like Receptor 2-Deficient Mice Results in Effective Protection from Borrelia burgdorferi Challenge. Infection and Immunity,71(7), 3894-3900. doi:10.1128/iai.71.7.3894-3900.2003
Kelley, S. .., Ranoa, D., & Tapping, R. (2013). Human Lipopolysaccharide-binding Protein (LBP) and CD14 Independently Deliver Triacylated Lipoproteins to Toll-like Receptor 1 (TLR1) and TLR2 and Enhance Formation of the Ternary Signaling Complex. Journal of Biological Chemistry,288(14), 9729-9741. doi:10.1074/jbc.m113.453266
Kullberg, B. G., Meer, J. W., & Netea, M. J. (2007). Recognition of fungal pathogens by Toll-like receptors. Immunology of Fungal Infections, 23(9), 259-272. doi:10.1007/1-4020-5492-0_11
Medvedev, A., Pennini, M., Vogel, S. N., & Xiong, Y. E. (2013). IRAK4 kinase activity is not required for induction of endotoxin tolerance but contributes to TLR2-mediated tolerance. Journal of Leukocyte Biology, 94(2), 291-300. doi:10.1189/jlb.0812401
Pam3Cys-Ser-(Lys)4 (ab142085). (2018, May 21). Retrieved from http://www.abcam.com/pam3cys-ser-lys4-ab142085.html
Pseudoscience. (2018, May 25). Retrieved from https://en.wikipedia.org/wiki/Pseudoscience
TLR2. (2018, May 23). Retrieved May 25, 2018, from https://en.m.wikipedia.org/wiki/TLR2

Xiong, Y., Murphy, M., Manavalan, T. T., Pattabiraman, G., Qiu, F., Chang, H., . . . Medvedev, A. E. (2015). Endotoxin Tolerance Inhibits Lyn and c-Src Phosphorylation and Association with Toll-Like Receptor 4 but Increases Expression and Activity of Protein Phosphatases. Journal of Innate Immunity,8(2), 171-184. doi:10.1159/000440838



Thursday, May 10, 2018

A Shift in Lyme Disease Activism: Exposing the Crimes Commited at Dearborn, Michigan in 1994





By: Kelly Irene & RJ James

Long-term Antibiotics vs. No Antibiotics 
ILADS vs IDSA
Since 1994, Lyme activism has fundamentally been based off a false dichotomy.  In the early 90’s, Allen Steere described Lyme Disease as a disease that affects the brain causes a mass amount of systemic issues.
Then, when the CDC decided to make a vaccine for Lyme Disease, in 1992 Allen Steere decided to go to Europe and change the entire definition of Lyme Disease. In order to promote the new Lyme vaccine, Steere committed research fraud where he purposely added the Elisa test to omit 85% of the sickest Lyme sufferers by falsifying the Lyme Disease case definition to only detect high antibody HLA linked arthritic knee Lyme Disease which only accounts to 15% of all Lyme sufferers. The whole fraud was done to qualify Yale's immune suppressing LYMErix vaccine and create an enterprise off of tick borne diseases; DNA products, test kits and vaccines. CDC officers, Yale, Corixa and Imugen own patents and received grants and are who own the  license to use the new fraudulent testing that has been designed to omit  chronic neurological Lyme.


Here we are, over twenty years later, and we are still arguing over a case definition that was designed to miss the sickest Lyme patients as means of making a vaccine look more effective. http://www.actionlyme.org/CRYMEDISEASE_CHP3_B.htm
Since then, the entire Lyme Debate on long-term antibiotic therapy vs no antibiotics has been based of this fraudulent case definition. Prior to changing the case definition at the Dearborn conference in 1994, Steere and is mob claimed that “that the treatment(antibiotics) failed because it did not wipe out the bacteria completely or because the patient's' nervous systems were irreversibly damaged”. Suddenly, they decided that Chronic Lyme no longer exists so that they could push a vaccine that contained OspA which they knew caused immune suppression.  Even in his patent,  David Persing’s admits that “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."
At this point, it should be clear to Lyme activists the reason Steere et al work so hard to suppress and ignore the root problem and real Lyme Disease  mechanisms.  Since 1994, the truth has been completely silenced and suppressed by those claiming to be on the victim’s side. Truth is, Lyme Disease is far more serious than a bacterial infection. Lyme disease is post sepsis syndrome or an acquired immune deficiency where antibiotic therapy fails in 50% of all victims.
In order for activists to properly understand Lyme Disease, they must understand how spirochetes and their outer surface proteins (Osps) operate. Spirochetes are their own phylum. They are a relapsing fever germ that continuously shed their Osps known as blebbing. Those Osps and Vmps are themselves variable undergoing constant antigenic variation. Within 24 hours of being infected, spirochetes travel to the lymph nodes and shed these OspA “blebs" that can permanently prevent B-cells from properly maturing (Leading to a reduction in detectable antibodies). That is because OspA forces the immune system to shut itself off to avoid the host from a potentially fatal septic cytokine storm. For Lyme activists, it is essential to understand that OspA is a highly toxic permanent immune suppressing TLR2/1 fungal antigen (remarkably similar to LYMErix/Pam3cys).


Not only do the CDC crooks say Lyme looks like cancer (Lymphoma and Leukemia), they also published studied that show Lyme/Ospa is  AIDS- like. Once OspA does its damage, the immune system is then tolerized. Meaning it no longer can recognize pathogens that are managed by the toll like receptors that have been affected. Making it a breeding ground for opportunistic infections such as EBV, coxsackie, herpes viruses, cytomegalovirus, candida, streptococcus, mycoplasma, etc.


In sum, Lyme victims are left with a permanently destroyed immune system and a cesspool of opportunistic infections which is the force behind this neurological chronic fatiguing massacre what we call, "chronic Lyme disease". An incurable stealth pathogen where nobody can get a diagnosis, disability, assistance, validation or treatment while the crooks say their victims are psych patients.
A Shift in Lyme Disease Activism
Once you understand how Lyme/OspA works, it makes you wonder why the main discussion in LymeLand still focuses on long-term antibiotic therapy as a universal solution for all Tick Bite Sepsis sufferers. If ILADS is on our side, why have they never tried to figure out why antibiotics fail in half the cases. Why have they not ever addressed the fact that spirochetes/OspA can collapse b-cell germinal centers and permanently damage the immune system? If ILADS really wants to help Lyme victims, they should be training their doctors to address the permanent B-cell AIDS outcomes instead of leaving those who don’t respond to antibiotics to die. If ILADS continues to ignore those who do not respond to antibiotics, 50% of all Lyme victims will be left alone and disabled without any treatment.
Because of this false dichotomy, Lyme Disease activism continues to center on whether or not Chronic Lyme Disease exists. Prior to 1994, Steere et al had an accurate and tested diagnostic criteria for Lyme Disease. Instead of fighting about unproven treatments, Lyme activism should be focusing on changing the definition of Lyme Disease back to what it was before the criminals decided to commit perjury to make their vaccine appear more effective:
"The typical response of our patients to antibiotic therapy supports the role of spirochetal infection in the pathogenesis of each of the syndromes described here. However, our results were not as good as those in previous reports.6 , 7 Six months after treatment, more than one third of the patients either had relapsed or were no better. In addition, more than half had previously received antibiotic therapy thought to be appropriate for their stage of disease and still had progression of the illness. The likely reason for relapse is failure to eradicate the spirochete completely with a two-week course of intravenous ceftriaxone therapy. On the other hand, the patients whose conditions did not improve may have had irreversible damage to the nervous system, particularly since the response to therapy tended to be worse in patients with longer durations of disease. This is reminiscent of far-advanced neurosyphilis, in which the response to penicillin may be minimal

Not only does the Lyme Crime affect Lyme patients, the CDCs research fraud stunt in 1994 ultimately threw all immunosuppressive diseases under the bus (i.e Lyme, ME, CFS, GWI, Fibro and Autism). According the NIH, In the USA alone, there are over 8 million people who have Fibromyalgia, 4 million who have Chronic Chronic Fatigue Syndrome and 1 in 36 children who have autism, not counting the millions with Lyme. They know what these diseases are, however, the real disease mechanisms ultimately expose the source of the Autism pandemic.
It’s important for Lyme activists to understand that what is happening is intentional, and the entire case definition is fraud. It’s not some conspiracy theory, the CDC themselves have published multiple studies on how Lyme Disease/OspA is a disease of immunosuppression. Therefore, any activism about antibiotics vs non antibiotics only benefits the 50% who are lucky enough to respond. Our best chance of winning the Lyme wars are to unite and occupy the United States Department of Justice (USDOJ) to press them to do their job and prosecute the Lyme Crime. In addition, once you understand the Lyme Crime, it essential that we reach out to the other abused groups to show them how prosecuting the Lyme crime will also bring Fibro, CFS, ME, Autism, GWI, along with many other groups justice as well.


In the end, activists need to come together and press the USDOJ so that they can prosecute the CDC/ALDF/Yale criminals who have kept an entire class of immunosuppressive diseases. The criminal charges proposed are; research fraud, falsification of the case definition/testing, racketeering, human rights abuses under color of law, and slander of their victims that's left millions without hope, disabled or worse, dead.
Additional Resources
Treatment fails in 50% of cases due to pathological changes prior to antibiotic therapy and, the OspA vaccine caused the same systemic disease. 
IDSA: The reviews of Infectious Diseases  
"Clinical studies have documented the efficacy of antibiotics, but therapy has failed in as many as 50% of cases of chronic infection."  


Norman Latov ~ it's much more serious than just persistent infection and many are resistant to antibiotic therapy due to immune suppression from TLR2/1 antagonism via vaccine or tick bite.  
  https://www.ncbi.nlm.nih.gov/pubmed/15363064 
"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."    



Raymond Dattwyler ~ Borrelia and its fungal lipoproteins inhibits natural killer cell activity, or immunosuppression. 50% of all patients do not respond to any treatment. 


1994: FDA meeting. Dattwyler says the sickest patients are seronegative, or produce little to no antibodies. 
"Individuals with a poor immune response tend to have worse disease"  



Gary Wormser, what the CDC calls post Lyme syndrome is really post sepsis or immunosuppression.  




Antibiotics cannot fix wrecked b-cells or viral infections. Where does this leave those who remain disabled for the rest of their lives with an acquired immune deficiency or post-sepsis like diseases? Antibiotics fail them, no treatment works for them. They are left to self treat in this do it alone disease while just trying to survive and while forced into poverty. Where is the treatment options, justice and validation for these victims? Why does LymeLand continue the antibiotic debate? What do we propose for these victims? The main question is, how can people who do reach remission leave others who faced the same scrutiny behind?


Anthony Fauci, head of National Institute of Allergy and Infectious Diseases, owns a patent for the treatment of all immunosuppressive diseases caused by fungal antigens/infections.
"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 opportunistic infections that occur in AIDS patients."  

It's not the truth we wanna hear, but this is the reality of millions of victims are left with. Ignoring the truth doesn't make it go away, you can't change what you refuse to confront. The only thing that can save all victims is criminal prosecution of the CDC/ALDF/IDSA psychopathic thugs so everyone can get a chance at the treatment and help they need. Not just the 50% who actually respond to treatment. We must all ban together and unite, not for ourselves but the children, future generations and destitute who have nothing left.
"Not knowing the truth doesn't make you ignorant, not wanting to know the truth is what makes you ignorant."


Medical Holocaust Files List; RICO, Lyme, ME/CFS, GWI, Fibro, Vaccines

Original by Whiste-blower Kathleen Dickson 1986 DuraySteere EBV Lymphoma.pdf   -- Steere in 1986 talking about how Lyme is like pos...