IDSA's Secrets:

Guardian: "New World Disorder"
IDSA's Persistence "Cryme Disease" book Klempner's Fraud USDOJ RICO Myco-Viral Synergy Bioweapons Attributes Kissinger NWO Beast
Relapsing Fever Dearborn Quotes Plum Island Corixa RICO Epstein▲Borreliosis Borrelia & B-cells Rx Brain Damage
Steere Falsifies Test Dearborn Booklet Russians & NYMC RICO Patents GarthNicolson-GWI Despite NIH CD20 Hell/NDEs
IDSA's Imitators Yale/SKB admit crime IDSA: "Cyst Viable" CDCs Patents w/SKB CT Med Board Grants Search "TLR2" Psychiatry
IDSA's ShellGame Schoen-LYMErix LYMErix ►Imitators DARPA Boots CDC 3 Kinds Lyme-MS DCF's-Penisbiter
IDSA's Biomarkers Weinstein's Frauds UConn's KidTuskegee Plum Stupid Fraud With Intent PubMed Updates: TLR2   DCF's Entrapment
IDSA's Stupid Rx
 
Dickson FDA Yale Yale's Congen Lyme
 
IDSA ▲ self-indicts
 

 
Penisbiter Update
 


09 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 


CDC Greed (won't answer the FOIA)

ELISA = arbitrary cutoff.

Disclaimer

Overview
 


TUSKEGEE - By Jerry Leonard


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.




 

 

 

DSM-IV  Dole-Bayh Act Disease: 

A psychosis related to the chronic defiance over having been exposed as a total fraud, from the Dearborn Hoax (Steere in Europe), to "Lyme Disease" (a bad knee that "goes away on its own in 4 years" without any treatment), to Magically Readable Unreadable Western Blots (Weinsteinium and Crooked Sour OspA Grapes), to the Negative Data Rule. 

This illness is similar to Borderline Personality Disorder (Drama Queens) in that the sufferers of the disease reliably throw in hysterical fits whenever confronted with their own conflicting statements.

Example: Yale's Durland Fish' Hit List:  2007 Fish Hysterical and hysterical comments to the Hartford Courant interviewer.

The Treatment is to get Durland Fish out of the Plum Island Lab, by removing 1) Plum Island from Yale's management, 2) completely de-funding Yale's Bumbling by giving out over a billion dollars worth of grants to everyone university lab group except Yale, 3) sending the CT Attorney General up their butts, 4) giving out the $500,000 Albany Award to the people who really understood immunology, and 5) recognizing Paul Duray who discovered the lymphocyte mutations in chronic Lyme victims and reported it to Yale et al in 1989 and 1992

Otherwise, just ignore them and move on with the new discovery, MALP-2, which will do what OspA did but not with the harmful effects such as causing Chronic Lyme (or the immune-suppression-related New Great Imitators or the New Yuppie AIDS or being "the Perfect Stealth Disabler" or the Trojan Horse Disease).
 

"It is well known that Borrelia burgdorferi indeed after asymptomatic infection can lurk or secrete itself in certain areas of the body, perhaps the central nervous system or perhaps the joint spaces, only to reappear months or maybe years later in the form of late stages of illness which are harder to diagnosis and treat.
-- Vijay Sikand, 1998 FDA OspA or LYMErix Vaccine Meeting.
 

======================================================

Allen Steere et al treating Lyme long-term because it is of benefit 


Crooked Sour OspA Grapes & Guidelines from Valhella (◄You can't make this stuff up.) 

The Big Enders and the Little Enders had a dispute about unreadable Western Blots... but who pissed on their OspA fire?
 



And what did these intellectual Lilliputians miss out on?

 

090618.htm

 

When people begin to realize that the association between OspA-like-induced or fungal immunosuppression and vaccines extends to the parallel epidemics of asthma and autism in children (the former is hypersensitivity and the latter is the opposite), then they'll be interested in "Lyme Disease": http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=17265454[uid]
 

 

Lipopolysaccharide Binding Protein Binds to Triacylated and Diacylated Lipopeptides and Mediates Innate Immune Responses1
http://www.jimmunol.org/cgi/content/full/173/4/2683
 

"Lipoproteins and lipopeptides have been identified in a large number of microorganisms, the most prominent ones being mycobacteria, mycoplasms, and spirochetes. They have been found to exhibit both a strong innate inflammatory response in the host and an enduring adaptive immune response in mammalian hosts (16).  The strong proinflammatory capacities of lipoproteins were first described for outer surface proteins A and B of Borrelia burgdorferi, which are also highly immunogenic (17) and have lately been the basis for a Lyme disease vaccine development (18). These compounds exhibit an triacylated lipid anchor structure comprising an N-palmitoyl-S-[2,3-bis(palmitoyloxy)-(2RS)-propyl]-(R)-cysteinyl (Pam3Cys) moiety at the N terminus (19), a feature that was previously described for the Braun lipoprotein from Escherichia coli (20). Because the N-terminal Pam3Cys modification is essential for immunoactivation caused by lipoproteins of B. burgdorferi as well as of another spirochete, Treponema pallidum (21), subsequent studies investigating immune responses to spirochetes used synthetic lipopeptides (22). The Pam3Cys moiety was also reported to be present in cytokine-inducing lipoproteins of Mycobacterium and Mycoplasma spp. (23, 24); thus, it can be regarded as a highly conserved molecular motif among different classes of bacteria. In Mycoplasma fermentans, the presence of a macrophage stimulating lipopeptide, termed 2-kDa macrophage-activating lipopeptide (MALP-2), was observed, being stimulatory active at picomolar concentrations (25). This compound, in contrast to the predominant lipopeptide structures present in lipoproteins of E. coli, B. burgdorferi, and mycobacteria, lacks the N-palmitoyl group, thus containing a diacylated (Pam2Cys) lipid anchor structure at the N terminus. Following studies revealed the presence of closely related compounds in other Mycoplasma spp. (26).."   

 

 J Immunol. 2001 Jul 15;167(2):910-8. Links (While LYMErix Pam3Cys was still on the market)
http://www.jimmunol.org/cgi/content/full/167/2/910
 

Toll-like receptor 2-dependent inhibition of macrophage class II MHC expression and antigen processing by 19-kDa lipoprotein of Mycobacterium tuberculosis.
Department of Pathology, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, OH 44106, USA.
Noss EH, Pai RK, Sellati TJ, Radolf JD, Belisle J, Golenbock DT, Boom WH, Harding CV.

Mycobacterium tuberculosis (MTB) induces vigorous immune responses, yet persists inside macrophages, evading host immunity. MTB bacilli or lysate was found to inhibit macrophage expression of class II MHC (MHC-II) molecules and MHC-II Ag processing. This report characterizes and identifies a specific component of MTB that mediates these inhibitory effects. The inhibitor was extracted from MTB lysate with Triton X-114, isolated by gel electroelution, and identified with Abs to be MTB 19-kDa lipoprotein. Electroelution- or immunoaffinity-purified MTB 19-kDa lipoprotein inhibited MHC-II expression and processing of both soluble Ags and Ag 85B from intact MTB bacilli. Inhibition of MHC-II Ag processing by either MTB bacilli or purified MTB 19-kDa lipoprotein was dependent on Toll-like receptor (TLR) 2 and independent of TLR 4. Synthetic analogs of lipopeptides from Treponema pallidum also inhibited Ag processing. Despite the ability of MTB 19-kDa lipoprotein to activate microbicidal and innate immune functions early in infection, TLR 2-dependent inhibition of MHC-II expression and Ag processing by MTB 19-kDa lipoprotein during later phases of macrophage infection may prevent presentation of MTB Ags and decrease recognition by T cells. This mechanism may allow intracellular MTB to evade immune surveillance and maintain chronic infection.

 

FEMS Immunol Med Microbiol. 2000 Jul;28(3):193-6.Click here to read

Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA).
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=10865170[uid]
 

Department of Medicine, New York Medical College, Valhalla, NY 10595, USA.

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.