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Cryme Trainer (moved)


Non-HLA-linked Diseases
Hurricane Sandy and Mold-Related illnesses (like LYMErix and Lyme Disease, and CFIDS/FM).

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References for psychotropics-induced brain damage

Older data on the incurability of Relapsing Fever

1986, McSweegan trashes Navy for $$$ for ALDF.com

1988, Dattwyler & about immune-suppressing, seronegative Lyme

1990, CDC: "Diagnose Lyme as if it was Relapsing Fever."

Allen Steere  "NeuroLyme won't test positive," 1990.

1992, CDC officer Allen Steere falsifies testing in Europe

1992, CDC patents with SmithKline show 2 kinds of Lyme

Compare the 2 kinds of Lyme in the RICO complaint

1994, CDC's Dearborn Booklet .pdf

CDC's invitation to participate in Dearborn .pdf

Igenex, Harris, Dearborn .pdf

Evidence  Lyme criminals knew LYMErix produced the same "multisystem disease" as "Chronic Lyme"

LYMErix Damage Coverup (short)
 

120302 NIH Treatments
 

1998, CIA Oilmen & Israelis plan to overthrow Saddam for the oil.

Bush/Gore  Oil/War-(Oct,2000)  

Bush's own explainer (Oct 2000) re: Iraq Oil

 

This page not changed since early 2008, first created March-May, 2003.

Regarding other failed vaccines of the OspA type. 

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See also Chp 10 on Biomarkers for more data related to immune-suppression outcomes of Lyme and LYMErix vaccinations (Pam3Cys or OspA from fungi)
Previous Chp 15, PLUM ISLAND SLYME (OspA) AND IMMUNE-SUPPRESSION
 

CHAPTER 16, FUNGAL VACCINES 

First of all, What is OspA?  From Chp 3  and Chp 9, we know that these fungal antigens are a big problem.  At first they're very immunogenic, but then they seem to make the victim more susceptible through tolerization process and their downstream mechanisms, as well as the now well-known inhibition of the auto-kill kinases (activated latent viruses are not stopped from re-spreading):

 "These look like Epstein-Barr transformed or mutated lymphocytes... I wonder if Bb infection reactivates latent virus infections in tissues? "- Paul Duray.

I wonder if it's related to inhibition of the auto-kill kinases in latently, virally-infected cells that would otherwise undergo auto-kill when the viruses started replicating again, but don't due to the suppression of such functions caused by these fungal lipopeptides?

Mycoplasma are known to be associated with cancer. Perhaps it is due to the fact that they are associated with activated latent viral infections because we know for sure viruses are associated with the production of cancer or mutated cells.
 

HIV vaccine with OspA adjuvant stuck on it?

E.coli:

 

~OspA stuck on an HIV vaccine:
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=525594&blobtype=pdf 

 

 

 

Back when we knew LYMErix was not a vaccine because the Dearborn testing standard was bogus (misses 85% of all cases) and because of all the terrible outcomes of OspA vaccines, we looked into the matter of whether or not this idea of trying out a fungal or a triacyl Pam3Cys lipoprotein had been tried before and what were the results.

Here is what I found:

http://www.jimmunol.org/cgi/content/full/173/4/2683
LPS binding protein (LBP) is an acute-phase protein synthesized predominantly in the liver of the mammalian host. It was first described to bind LPS of Gram-negative bacteria and transfer it via a CD14-enhanced mechanism to a receptor complex including TLR-4 and MD-2, initiating a signal transduction cascade leading to the release of proinflammatory cytokines. In recent studies, we found that LBP also mediates cytokine induction caused by compounds derived from Gram-positive bacteria, including lipoteichoic acid and peptidoglycan fragments. Lipoproteins and lipopeptides have repeatedly been shown to act as potent cytokine inducers, interacting with TLR-2, in synergy with TLR-1 or -6. In this study, we show that these compounds also interact with LBP and CD14. We used triacylated lipopeptides, corresponding to lipoproteins of Borrelia burgdorferi, mycobacteria, and Escherichia coli, as well as diacylated lipopeptides, corresponding to, e.g., 2-kDa macrophage activating lipopeptide of Mycoplasma spp. Activation of Chinese hamster ovary cells transfected with TLR-2 by both lipopeptides was enhanced by cotransfection of CD14. Responsiveness of human mononuclear cells to these compounds was greatly enhanced in the presence of human LBP. Binding of lipopeptides to LBP as well as competitive inhibition of this interaction by LPS was demonstrated in a microplate assay. Furthermore, we were able to show that LBP transfers lipopeptides to CD14 on human monocytes using FACS analysis. These results support that LBP is a pattern recognition receptor transferring a variety of bacterial ligands including the two major types of lipopeptides to CD14 present in different receptor complexes.
 

A) http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10792376&dopt=Abstract
The 19-kD antigen and protective immunity in a murine model of tuberculosis. 
Yeremeev VV, Lyadova IV, Nikonenko BV, Apt AS, Abou-Zeid C, Inwald J, Young DB.

"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."

 

 B) http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11179309&dopt=Abstract

Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits Mycobacterium smegmatis-induced cytokine production by human macrophages in vitro.

Post FA, Manca C, Neyrolles O, Ryffel B, Young DB, Kaplan G.
 

Vaccination of mice with Mycobacterium vaccae or M. smegmatis induces some protection against M. tuberculosis challenge. The 19-kDa lipoprotein of M. tuberculosis, expressed in M. vaccae or M. smegmatis (M. smeg19kDa), abrogates this protective immunity. To investigate the mechanism of this suppression of immunity, human monocyte-derived macrophages (MDM) were infected with M. smeg19kDa. Infection resulted in reduced production of tumor necrosis factor alpha (TNF-alpha) (P < 0.01), interleukin-12 (IL-12) (P < 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared to infection with M. smegmatis vector (M. smegV). Infection with M. smeg19kDa and with M. smegV had no differential effect on expression of costimulatory molecules on MDM, nor did it affect the proliferation of presensitized T cells cocultured with infected MDM. When MDM were infected with M. smegmatis expressing mutated forms of the 19-kDa lipoprotein, including non-O-glycosylated (M. smeg19NOG), nonsecreted (M. smeg19NS), and nonacylated (M. smeg19NA) variants, the reduced production of TNF-alpha or IL-12 was not observed. When the purified 19-kDa lipoprotein was added directly to cultures of infected monocytes, there was little effect on either induction of cytokine production or its inhibition. Thus, the immunosuppressive effect is dependent on glycosylated and acylated 19-kDa lipoprotein present in the phagosome containing the mycobacterium. These results suggest that the diminished protection against challenge with M. tuberculosis seen in mice vaccinated with M. smegmatis expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha and IL-12 production, possibly leading to reduced induction of T-cell activation."

 

C) http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12761093

 

Infect Immun. 2003 Jun;71(6):3146-54. Related Articles, Links

 

 
The Mycobacterium tuberculosis recombinant 27-kilodalton lipoprotein induces a strong Th1-type immune response deleterious to protection.

Hovav AH, Mullerad J, Davidovitch L, Fishman Y, Bigi F, Cataldi A, Bercovier H.

Department of Clinical Microbiology, Faculty of Medicine, The Hebrew University, Jerusalem, Israel.

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.
 

 

 

We looked into the matter of whether or not the Lyme criminals had actually published anything that really proved they had a vaccine.  We found numerous reports that showed this vaccine failed in animal studies.

"Accordingly, the methods of the invention provide a powerful and selective approach for modulating the innate immune response pathways in animals without giving rise to the toxicities often associated with the native bacterial components that normally stimulate those pathways."   http://patft.uspto.gov/6,800,613

"Although a single ligation of TLRs induces responses such as TNF production, repeated ligation will lead to a loss of response, i.e., the cells become tolerant."   http://www.jimmunol.org/cgi/content/full/173/4/2736

"Borrelia burgdorferi-Induced Tolerance as a Model of Persistence via Immunosuppression" -  "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."
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12819085
 

http://www.jimmunol.org/cgi/content/full/173/4/2660
Mycobacterium tuberculosis LprG (Rv1411c): A Novel TLR-2 Ligand That Inhibits Human Macrophage Class II MHC Antigen Processing¹

 "Signaling through TLR-2 by lipoproteins may represent a double-edged sword for host responses to chronic intracellular pathogens such as M. tuberculosis. Short-term signaling through TLR-2 activates macrophages and initiates acute inflammation that may help control initial infection. In contrast, prolonged TLR-2 signaling in macrophages results in down-regulation of certain critical immune functions, such as MHC-II Ag processing. M. tuberculosis infects, survives, and persists in macrophages. The ability of M. tuberculosis to survive acute inflammation positions the bacilli to take advantage, through secretion of lipoproteins such as LprG and LpqH, of this down-regulation of macrophage immune function." 

The Journal of Immunology, 2004, 173: 2660-2668.
Copyright © 2004 by The American Association of Immunologists
 

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FROM THE 2003 ACTIONLYME.com WEBSITE:

 

1) OspA vaccination was not demonstrated to protect monkeys from infection:

The outer surface protein A (OspA) vaccine against Lyme disease: efficacy in the rhesus monkey.
Philipp MT, Lobet Y, Bohm RP Jr, Roberts ED, Dennis VA, Gu Y, Lowrie RC Jr, Desmons P, Duray PH, England JD, Hauser P, Piesman J, Xu K.
Vaccine. 1997 Dec;15(17-18):1872-87.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9413097&dopt=Abstract

 

2) rOspA vaccination did not protect rabbits:

Comparison of protection in rabbits against host-adapted and cultivated Borrelia burgdorferi following infection-derived immunity or immunization with outer membrane vesicles or outer surface protein A.

Shang ES, Champion CI, Wu XY, Skare JT, Blanco DR, Miller JN, Lovett MA.

Department of Microbiology and Immunology, Department of Medicine, School of Medicine, University of California, Los Angeles, California 90095, USA.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10858236&dopt=Abstract

"Analysis of the antibody responses to outer membrane proteins, including DbpA, OspA, and OspC, suggests that the remarkable protection exhibited by the infection-immune rabbits is due to antibodies directed at antigens unique to or markedly up-regulated in host-adapted B. burgdorferi." 

 

3) OspA was not shown to protect mice, and why, by Russell Johnson:

Resistance to tick-borne spirochete challenge induced by Borrelia burgdorferi strains that differ in expression of outer surface proteins.

Kurtti TJ, Munderloh UG, Hughes CA, Engstrom SM, Johnson RC.
Infect Immun. 1996 Oct;64(10):4148-53

There was no reduction of strain 297 spirochetes in ticks that fed on four hamsters immunized with M297, but the hamsters were protected.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8926082&dopt=Abstract

The journal publications of Russell Johnson-->  MEDLINE:  "Johnson RC [au] and spirochete"

 

 

4) rOspA vaccination results in escape mutants or variants spirochetes which INCREASE at a greater rate than normal.

Selection of variant Borrelia burgdorferi isolates from mice immunized with outer surface protein A or B.
Fikrig E, Tao H, Barthold SW, Flavell RA.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7729870&dopt=Abstract

 

Experiments in vitro in which complement is added demonstrate the antibodies to rOspA alone do not kill the spirochetes:

Borrelia burgdorferi escape mutants that survive in the presence of antiserum to the OspA vaccine are killed when complement is also present.
Sole M, Bantar C, Indest K, Gu Y, Ramamoorthy R, Coughlin R, Philipp MT.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9596714&dopt=Abstract

 

5) Yale did not demonstrate that there were not spirochetes in the ticks after vaccination and then feeding ticks on animal blood, then assaying for spirochetes:

 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1608951&dopt=Abstract

Elimination of Borrelia burgdorferi from vector ticks feeding on OspA-immunized mice. 
Fikrig E, Telford SR 3rd, Barthold SW, Kantor FS, Spielman A, Flavell RA.
Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5418-21.

 

As we Lyme warriors cannot engage any earthly assistance;
As the entire US medical community chooses not to assist sick and abused people and put a stop to this;
As there is not one MD or group in the entire USA who will take these criminals to court;
As there is not one lawyer or Department of Justice official who will do the job they were hired to do and protect us from corporate crime;
As there are no men left among us:

http://www.ourladyswarriors.org/prayer/michael.htm

Saint Michael the Archangel,
defend us in battle.
Be our protection against the wickedness and snares of the devil.
May God rebuke him, we humbly pray;
and do Thou, O Prince of the Heavenly Host -
by the Divine Power of God -
cast into hell, satan and all the evil spirits,
who roam throughout the world seeking the ruin of souls.