14 Feb 2012
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Pharma/CDC on Brain damage from vaccines, Fauci, Phages, Bioweapons manufacture
HHS.gov is Incompetent; BMJ calls fraud "crime.")
Official: CFIDS and MS-Lyme are the
same disease; Epstein-Barr
ELISA = arbitrary cutoff.
Disclaimer
1998, CIA Oilmen & Israelis plan to overthrow Saddam for the oil.
Bush/Gore Oil/War-(Oct,2000)
Bush's own explainer (Oct
2000):
Iraq Oil
Iraq was an oil-theft war.
MayDay refers to a protest scheduled for May 21 in Washington. More details coming...
http://issuu.com/orpheus68/docs/mayday_press_release_cp_05-09-11?mode=a_p
http://www.youtube.com/watch?v=dNB8o5nFaOQ ◄ Interview about the history of the discovery of the FRAUD (Dearborn and Karen Forschner's Lyme.org)
http://www.youtube.com/watch?v=fAhlpLJk1Ck&feature=youtu.be
MayDay Rally Video
Falsified Testing = Falsified Outcomes of OspA Vaccines = Falsified "Guidelines."
Do your homework and first review this PowerPoint presentation:
http://www.actionlyme.org/SV_PPT_2_files/v3_document.htm
The new, Dearborn, definition of "Lyme disease" excludes all the neurologic cases. This was by arrangement with Kaiser-Permanente who landed a New England Forward Base at New York Medical College and founded the RICO entity, the ALDF.com (1990), which later co-opted the IDSociety.org (which no one should worry about, since these ID "experts" fumbled HIV, Tb, Lyme, MRSA, Lupus, MS, ALS, Cancer and YouNameIt).
So, what is Dearborn?
It was a conference put on by the CDC in 1994 allegedly to "standardize" the testing for Lyme. Instead it was a farce where none of the participants agreed with Allen Steere's scientific fraud proposal based on bogus "high passage" strains and recombinant OspA and B without the lipids attached. Without the lipids attached, the lipoproteins would not be immunogenic (produce antibodies).
Here is what the contributors to the Dearborn Conference "Proceedings" said about Steere's proposal for new diagnostic criteria for Lyme: DEARBORN_WHO_SAID_WHAT.htm (Everyone said Steere's proposal sucked and missed 92% to 78% of the cases, including Gary Wormser).
Look at the graphics in the USDOJ RICO complaint to see what this means in terms of HLA-linked hypersensitivity-Lyme ("Just a Knee") vs. everyone else: USDOJ_COMPLAINT_RICO.htm
What is OspA or TLR2-agonists? (Remember that Structure = Function; first I will demonstrate Structure)
Graphics:
FROM:
Pam3Cys_Version15.htm
PAM3CYS_IMMUNE_SUPPRESSION.htm :
LYMErix as HIV gp120:
http://newjournal.kcsnet.or.kr/main/j_search/j_abstract_view.htm?code=B961118&qpage=j_search&spage=b_bkcs&dpage=ar
MORE of the same structure of Pam3Cys:
http://www3.interscience.wiley.com/cgi-bin/fulltext/120763430/PDFSTART
Watch the animation:
http://www.youtube.com/watch?v=RO8MP3wMvqg
HIV vaccine with Pam3Cys or something a lot like LYMErix stuck on it:
◄ This is supposedly how OspA lies in borrelia. The lipid portion appears to be buried in the spirochete membrane. I do not not know how the glyco-lipids of HIV lie (the protein portion appears to be scrambled into the lipid portion), or even if for certain they're Pam3Cys, although I have no information that they're not. I only have information that OspA and Pam3Cys have the same linear chemistry structure (but this is no predictor of presentation; the DNA can be sequenced, in other words).
From:
https://www.aidsreagent.org/program_info.cfm
The FUNCTION of TLR2 Agonists:
They, as a class, suppress the immune system and activate latent viruses. They also TOLERIZE people to fungal infections in the blood.
Introductory and Lead Evidence:
Paul Duray and "the lymphocytes of Chronic Lyme
victims look like Epstein-Barr transformed cells":
A) 1989, IDSA's Special Supplement on Lyme
and Spirochetal Diseases:
IDSA_CLINIPATH_DURAY.htm ("Epstein-Barr-like transformed B
cells")
"Immature B cells can also be seen in the spinal fluid. These cells can
appear quite atypical - not unlike those of transformed or neoplastic
lymphocytes."
and B) 1992, in Steve Schutzer's Book, "Lyme Disease, Molecular and
Immunologic Approaches":
http://www.actionlyme.org/Duray.htm
"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."
-
1) See http://www.actionlyme.org/PIIB.htm
where Justin Radolf and Clifford Harding demonstrated that TLR2 agonists (found
in spirochetes and mycobacteria and mycoplasma), render the HLA molecules
incompetent (no antibodies are produced after a time, or "Lyme becomes
seronegative and chronic, because it is chronic, and chronically shedding Osps -
AKA the auto-vaccination known as 'blebbing'").
2) See where Dattwyler and Steere reported that
fungal antigens suppress the immune system and cause the
seronegative./MS-Lyme outcomes:
http://www.actionlyme.org/STEERES_SERONEG_LYME_ASSAY.htm
Immunosuppression observed in persons with fungal infections (OspA is a fungal antigen):
"The disorder in these seronegative patients reflected a dissociation between T-cell and B-cell immune responses, in which the cell-mediated arm of the immune response was intact yet the humoral portion of the response to B. burgdorferi appeared to be blunted. This diminished antibody response is in contrast to the T-cell anergy commonly observed in several chronic infections (e.g., infection with Mycobacterium leprae or M. marinum, filariasis, and some chronic fungal infections (20-30)."
29.)
http://www.ncbi.nlm.nih.gov/pubmed?term=3499107[uid]&cmd=DetailsSearch
30.)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC436656/?tool=pubmed
31.)
http://www.ncbi.nlm.nih.gov/pubmed/158056
32.)
http://www.nature.com/nature/journal/v279/n5708/abs/279021a0.html
33.)
http://www.ncbi.nlm.nih.gov/pubmed/6444695
http://www.actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm
Says Dattwyler:
"The
inhibition is directly attributable to the organism of its products [OspA
shedding], since supernatants from the organism cultures also inhibit endogenous
NK without prior exposure (data not shown)."
OspA was the ▲thing that subdued normal Natural Killer Cell Activity, it turns
out.
Spirochetes go ▲ intracellular and into the brain/CNS (immunologically-privileged sites).
3) Steere in 1991 publishing that the MS version of Lyme is seronegative
(or rather, "not the RA-HLA-linked hypersensitivity response")
http://groups.google.com/group/sci.med.diseases.lyme/browse_thread/thread/530029f01871c005/4bc196d47f719923?hl=en&q=steere+rheumatology+news#4bc196d47f719923
4) 1994 (June, before Dearborn) FDA Meeting Minutes where Ray Dattwyler told the
FDA that the seronegative (Non-Dearborn, Non-Knee-Only) Lyme patients are the
SICKEST:
5) TLR2-agonists activate Epstein-Barr:
Interaction of Borrelia burgdorferi sensu lato
with Epstein-Barr virus in lymphoblastoid cells.
Toll-like receptor agonists
synergistically increase proliferation and activation of B cells by epstein-barr
virus.
Epstein-Barr virus induces MCP-1 secretion by human monocytes via TLR2.
And this is key: ▲ HOW do Epstein-Barr and Mycoplasmal lipoproteins inhibit apoptosis in infected B cells?
Infection of human B lymphoma cells by Mycoplasma fermentans induces interaction of its elongation factor with the intracytoplasmic domain of Epstein-Barr virus receptor (gp140, EBV/C3dR, CR2, CD21).
http://www.ncbi.nlm.nih.gov/pubmed/16054780 See more on this topic at 101016.htm
Apparently the lipoproteins stick to internal cell components and literally gum up the works.
The inhibitory effect of Mycoplasma fermentans on tumour necrosis factor (TNF)-alpha-induced apoptosis resides in the membrane lipoproteins.(See all related for the mechanisms of inhibition of apoptosis in cells infected with these fungi)
[Raji, P3HR-1 and Namalwa cells as a model for the study of Epstein-Barr virus (EBV) reactivation].
Involvement of TLR2 in recognition of acute gammaherpesvirus-68 infection.
Etc, See http://www.actionlyme.org/101016.htm
6) CDC Officer and former head of the NIH's
Rocky Mountain Bioweapons Lab, Alan Barbour, has now applied for a grant to
study the STRUCTURE of OspC, the brain invasion antigen:
http://projectreporter.nih
That tells you that these clowns are in no way
scientists or "experts" and have no business dictating to anyone what "Lyme
Disease" is, if after all these years they finally GET IT about
Structure Equaling Function.
7) Clifford Harding: "TLR2-agonists
Suppress the Immune System" (and therefore OspA could never have been a
vaccine and therefore must have been falsely qualified):
http://projectreporter.nih.gov/project_info_description.cfm?aid=7994850&icde=8012983
If OspA, a TLR2 agonist, could never have been a vaccine, it must have been falsely qualified.
So, what does that mean as regards the "guidelines?"
The Definition of Lyme Disease Changed at Dearborn (1994) to Falsify the OspA Vaccines Outcomes.
The "Guidelines" are a continuation of that same lie - that "Lyme Disease" is only the HLA-linked hypersensitivity response to OspA.
So, the conflict of interest at present, in putting out "Guidelines," is their own personal interest in not going to jail on a manslaughter charge over the blood test 1994 definition of "Lyme Disease" - which they all know to be false.
Go Here for More on this topic: GUIDELINES COI OSPA VACCINES (1994)
8) "NKT cells are specialized lymphocytes
that consist of several subtypes and can respond to glycolipids from infectious
organisms, such as borrelia burgdorferi the causative agent of
Lyme disease and self-lipids, during the course of autoimmune disease such as
multiple sclerosis."
http://projectreporter.nih.gov/project_info_description.cfm?aid=8019102&icde=8026015