Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."
 


9 July 2017

Home


1988 Steere says Lyme is like a B cell leukemia

Assoc Blogs-n-Webs:
TruthCures.org
badlymeattitude.com/
immune2lies.com/
researchfraud.com/
may12.org
meadvocacy.org/
truthbetoldx81
lymecryme
crymedisease
theothersideofthestretcher
rjspiritualityandthe
truthaboutlymedisease
JC-LilnkedIn
KD-Linkedin.com
LD-LinkedIn
JC-academia.edu

KD-academia.edu

 


CDC "SPIDER"

Fungal Exosomes Inhibit Apoptosis

IDSA: "Vaccines serve the mfgs, not their victims"

RICO_filed_USDOJ

BlumenthalAntiTrust Lawsuit

Exosomes, Blebs

Spirochetal_Dementia


PDFs
CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
Dearborn, 1994
BarbourFishpdf.pdf
 

Pathogenic Fungi

Bush's warcrimes, Oct 2000

Trainer

170708

 



PLUM ISLAND

The more thoroughly I conduct scientific research, the more I believe that science excludes atheism. --Lord Kelvin
 

OUTLINE:

Introduction:  CDC shows us how to aersolize, dessicate, or weaponize Borrelia into the cyst or spheroplast form in 1964

I. Mycoplasma and Vector-Pathogen Competence Studies performed on Plum Island

Selling such fungi and other biological and chemical weapons to Saddam Hussein
http://www.actionlyme.org/US_SELLS_IRAQ_BIOWEAPONS.pdf

and Robin Cook);
Dead Iraqi scientist who worked with mycoplasma and allegedly on Plum Island (run over while changing a flat, much like Don Wiley)
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=Al-Aubaidi+jm[Author
Mycoplasma cause infertility and reduced milk production in livestock

Mycoplasma-Membrane Associated Lipoproteins inhibit the auto-kill kinases resulting in the activation of latent Epstein-Barr:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=16889623[uid]

Mycoplasma and Leukemias
http://www.ncbi.nlm.nih.gov/pubmed/14276278
Mycoplasma and other tumors:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=14329455

Isolation of mycoplasma from Leukemic bone marrow:
http://www.ncbi.nlm.nih.gov/pubmed/14287426
"Pleuropneumonia-like organisms associated with neoplastic disease":
http://www.ncbi.nlm.nih.gov/pubmed/14243415

Mycoplasma are molds that cause plant rot
 Stinking Smut and Iraq
    http://www.antiwar.com/prather/?articleid=10989

 

 II. Mycoplasma vs L-forms vs Spheroplasts  What's the difference?
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17586646


UConn's Justin Radolf and Dunn on stealth pathogens or stealth disablers
        Radolf (UConn):
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.


        Dunn (SUNY-SB and Brookhaven Nuclear Lab)
        Dark-field microscopy

Do L-forms cause disease?, Or, "Has science has gone backwards, which is why we're having this discussion?"

 

III. African Swine Fever and Durland Fish
   http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=9499019[uid]
    African Swine fever and Lyme Borrelia
    http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=209230&blobtype=pdf



IV. Borrelia phylogeny  (hermsii, anserina)


V. Bacteriophage vectored DNA & bioweaponeer bumbling


VI. Tully and Shope, bioweaponeers.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627593/



Joe Tully, the bioweaponeer and mycoplasma and tick, on MedLine:
http://www.ncbi.nlm.nih.gov/pubmed?term=tully%20jg[Author]%20AND%20%28%22mycoplasma%22[MeSH%20Terms]%20OR%20%22mycoplasma%22[All%20Fields]%29%20AND%20%28%22ticks%22[MeSH%20Terms]%20OR%20%22ticks%22[All%20Fields]%20OR%20%22tick%22[All%20Fields]%29&cmd=DetailsSearch

bioweaponeering, possibly with Rockefellers and SmithKline, Erythrocyte deformities in humans with human mycoplasmal infections, L-forms and mycoplasma look the same under a microscope but are different...)
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=377161&blobtype=pdf


VII. Rockefeller University
(The Biology of Parasitic Spirochetes)


VIII. Ed Bosler and UPenn on outbreak areas:

Evolution of a focus of Lyme disease
http://www.ncbi.nlm.nih.gov/pubmed/3577493
  (This supports the assertion that Plum Island was the original outbreak area.)


UNCOORDINATED PHYLOGEOGRAPHY OF BORRELIA BURGDORFERI AND ITS TICK
VECTOR, IXODES SCAPULARIS:
http://www.ncbi.nlm.nih.gov/pubmed?term=20394659[uid]&cmd=DetailsSearch
Despite the intimate association of B. burgdorferi and I. scapularis, the population structure, evolutionary history, and historical biogeography of the pathogen are all contrary to its arthropod vector.


IIX. PNAC "race-specific bioweapons" is moot
(nanobots and Morgellon's)


IX. OspA, HIV's gp120 and gp41
, HIV vaccines (1993 and Fauci's HIV patent and Fauci's immune suppression treatment patent) Pam3Cys and CCR5 and Africans


X. TLR2 and not 4 handles these lipoproteins:
Downregulation of HLA molecules is part of the tolerization process. (mentioned in Chapter 10, Biomarkers)
OspA-induced IL-10 which is an immune suppressing cytokine

Brucella's Pam3Cys lipoproteins also result in immune suppression.
http://www.ncbi.nlm.nih.gov/pubmed/17984211

So, AIDS (and their vaccines), Brucella (and their potential vaccines), Lyme (and LYMErix and ImmuLyme), and Tuberculosis (and their vaccines), all caused immune suppression.  But thanks to Yale's deliberate criminal incompetence, none of these LYMErix and Chronic Lyme outcomes were investigated and instead the Lyme and LYMErix victims were stalked and trashed.  This is a criminal matter. 

 

XI.  Garth Nicholson.  Large can of worms.  Fungal infections suppress the immune system:
http://www.immed.org/autoimmune/publications/CMIGWVC%20AutismPatients.pdf

Summary:
Downregulation of HLA (no antibodies are produced)
Inhibition of the autokill kinases
 


XXII:  New York Times Book review on USA dumping Borrelia on China and Korea:
http://www.nytimes.com/books/first/e/endicott-biological.html


 


I. Mycoplasma and Vector-Pathogen Competence Studies performed on Plum Island and in association with Yale.

Recall that 3 years ago I instructed Homelame Stupidity - who happens to work for us, remember, since we are the government - to look into the matter of the Lyme bullshit, and as regards Tully and Shope.  That would be because I have read just about everything those three (there are 2 Shope, RE's father and son and they're both in the same business).  I refer to Tully again in Chp 10 on Biomarkers which is a chapter now thankfully getting much attention by referral.

Because Homelame Stupidity is a joke (it was revealed to us all just one month later by Miss Katrina), we are still here, 3 years later, still battling these Yale/NYMC/ALDF lying profiteering creeps, who have the relentless audacity to claim they did not settle out of court with Mr. Blumenthal to avoid criminal charges.  Yet, anyone with eyes in their head can read the agreement and discover that that's exactly why they're terrified.  Still it is left to the real scientists out here to reveal what is the real deal on these criminals because we have no faith in the "US Government," whatsoever.  This crime belonged to the US Department of Justice ever since December 1998, when the FDA approved LYMErix because they were defrauded by Yale, and in particular, they were defrauded by Yale's Robert Schoen (see Chapter 4 on what I explained to the FDA vaccine committee and as regards the evidence that Robert Schoen has known since 1996 that he could not read his Western Blots in OspA vaccinated people).

Thus, I will expose what we all can find out about Plum Island and what kinds of goodies they messed with there.  Keep in mind that we want indictments.  We want these bastards charged with every crime they committed.  From the looks of things, they never appeared to investigate what the hell OspA really was, because they had first made a decision to make money off of this new epidemic.  I note that what happened here has similarities to Jurassic Park, where the scientists just grabbed the thing and tried to turn in into a money-maker without thinking of the consequences and Voila!  what do you know, Michael Crichton was one of the invitees to the ALDF.com's 2000 "GALA"
http://groups.google.com/group/sci.med.diseases.lyme/msg/508d7369ce25f5cc?hl=en&dmode=source

Either that's a coincidence or a sick joke, since Lyme appears to be one of the ones that "got away from" Plum Island.

It appears, I say, since no one knows exactly what went on on Plum Island. But I guess there are records of Paperclipped NAZIs and we know the OSS-CIA-Rockefellers were involved in that crazy Double-Oh "Medicine" baloney and have always been interested in, um, race refinement.  There is not one thing that is associated with either the Rockefellers or the Bushies that does not have the aroma of "sinister."  (Chapter 24

Page 60 re "race specific bioweapons" ►PNAC document removed from the web.  Download here.


In the end, it does not matter what the hell they ever did on Plum Island.  I never actually cared, since the issue is not how it happened but when are we going to get better?  The real deal is that the country is beyond bankrupt and collapsing into the Great Depression II. There will be little for treatments and research.  We lost the window of opportunity when Bush stole the election from Al Gore in 2000.  That was our last chance to re-tool for new energy.

There will be no money to fight the global-warming related emerging infectious diseases.  There are new discoveries of fungi and various tick borne diseases all the time.  In 2004 there was an outbreak of 5 vector borne diseases in one heard of cattle in Switzerland:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15297529

Plain old regular household molds are a problem.  Rare is the house in New England that does not have a mold problem.  Two years ago they officially moved "Fall Foliage Peak Week" in New England back two weeks into late October.  Are we to not think spring might have gained an extra half month? 

Plum Island accidents are not the issue.  The cover up of the Lyme/LYMErix crime and the deliberate falsification of diagnostic tests, vaccines and especially the alleged "treatment" protocols are the issue.  The only real value in revealing all we know about what happened when and where is in the hopes that the perpetrators of these crimes against humanity committed by Kaiser and the ALDF.com brigade are indicted, deprived of their liberty and especially, deprived of their assets since we think Kaiser might be worth big property- something tradable on the foreign market for something other than worthless US dollars.


 

The first record that we can find on the OspA kind of antigen:
1983: Synthesis of the mitogenic S-[2,3-bis(palmitoyloxy)propyl]-N-palmitoylpentapeptide from Escherichia coli lipoprotein.
http://www.ncbi.nlm.nih.gov/pubmed/6347861?ordinalpos=131&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

 

As you recall from Chp 3, this is what OspA looks like/is

The following looks like an attempt at an HIV vaccine with an OspA adjuvant:

 

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


 

OspA basically comes from or is common to E. coli, HIV.  Some reports say B. burgdorferi and E. coli are the sources of the triacylated P3C lipopeptides and that mycoplasma produced diacylated lipopeptides  There may be something else similar but not identical in other pathogens but it appears that few are the sources of this particular general antigen shape ( Pam3Cys).

 

One of the Plum Island strains of mycoplasma (fungi); stealth disablers:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=6190898[uid]

PubMed:

: J Hyg (Lond). 1983 Jun;90(3):441-9. Links

 

Immunogenic variation among the so-called LC strains of Mycoplasma mycoides subspecies mycoides.   

"Much evidence of immunogenic heterogeneity among the LC strains of Mycoplasma mycoides ssp. mycoides emerged from cross-immunization and -hyper-immunization experiments in mice in which three LC strains (Vom/Plum Island, 74/2488, and Mankefar 2833) were used for challenge purposes. All heterologous LC-strain vaccines cross-immunized against the three challenge strains, but protection was usually only 'partial', i.e. significantly less than that given by homologous vaccine. Cross-hyperimmunization with all heterologous LC but not SC strains produced protection against challenge with Vom/Plum Island that was virtually 'complete', i.e. similar to that produced by homologous vaccine. Challenge with 74/2488 gave generally similar results; but against Mankefar 2833 six heterologous LC vaccines gave complete protection and six did not. Vaccines prepared from the Smith (1423) strain of M. mycoides ssp. capri gave some protection against Vom/Plum Island but none against 74/2488 or Mankefar 2833. The cross-immunizing ability of three further M. mycoides ssp. capri strains appeared to resemble that of Smith (1423). In a cross-hyperimmunization experiment, vaccines prepared from SC strains of M. mycoides ssp. mycoides varied greatly in their ability to protect against challenge with strains 74/2488 and Mankefar 2833.   PMID: 6190898 [PubMed - indexed for MEDLINE]

 

So, there are Plum Island strains of mycoplasma.


Murdered Iraqi scientist who studied infertility in cattle due to mycoplasmas on Plum Island
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=Al-Aubaidi+jm[Author

 

Use of biological weapons by Don Saddam Rumsfeld:

http://www.fas.org/irp/congress/2002_cr/s092002.html   Congressional Record- Bioweapons sold by USA to Iraq to use against Iran: Page S8987-S8998


"...Over the protest of some Pentagon skeptics, 
     the Reagan administration began allowing the Iraqis to buy a 
     wide variety of "dual use" equipment and materials from 
     American suppliers. According to confidential Commerce 
     Department export-control documents obtained by NEWSWEEK, the 
     shopping list included a computerized database for Saddam's 
     Interior Ministry (presumably to help keep track of political 
     opponents); helicopters to transport Iraqi officials; 
     television cameras for "video surveillance applications"; 
     chemical-analysis equipment for the Iraq Atomic Energy 
     Commission (IAEC), and, most unsettling, numerous shipments 
     of "bacteria/fungi/protozoa" to the IAEC. According to 
     former officials, the bacterial cultures could be used to 
     make biological weapons, including anthrax...."

 

What was the fungi?

One we know about was "stinking smut"
http://ipm.uiuc.edu/diseases/series100/rpd112/index.html

It would seem that the UNSCOM weapons inspectors had found any biowarfare agents that we had sold Saddam Hussein, then, methinks someone with a .gov domain would be guilty of a warcrime?  The only people squawking about it is Iran and they don't count since they have oil and they're not the USA, which makes them... bad, bad, terrorists and insane and threatening criminals etc etc Islamofascist Hitlers intent on a global extermination Christianity and Judaism and so on and so forth and faster please and all of that fairy-ass neocon bullshit... 

"Iran exists and they're not Israelis; Iran is an existential threat to Israel!!"

"The ALDF exists and they're not truthful; the ALDF is an existential threat to mankind and must be wiped off the map!" 

Experiment: Everyone should be able to try on this crazy bullshit and see if they don't get carried off to the nearest psychiatric emergency room.  Only the Israelicons get away with it because crazy is not crazy when referring to Israelis.  Everyone knows that's just how they are.

 

No one cares.  This is not pursued.  White phosphorus, anthrax, all sorts of illegal biological and chemical weapons, were and are used in Iran/Iraq but supplied by the US and the UK.  It's no big deal.  It's only a big deal when an Israeli-US scientist who worked at Ft. Detrick mailed some around the US after 9/11 and tried to blame it on Arabs.  Zack and the Dancing Israelis, and whoever else from Israel is allowed to do whatever they want in America and the go back home.  'Like the State Department's Mark Grossman and Sibel Edmonds.  'Like Michael Ledeen and the fake Niger letter.  There's tons of crime around here.  Whoever is an Israeli is pretty much immune to prosecution anywhere in the Western world.

 

There was a murdered Iraqi scientist who worked in the United States with mycoplasmas with regard to causing bovine infertility.

So far, no big secrets.  Mycoplasma are a rather new discovery.  JG Tully was fascinated with them and spiroplasma

http://www.cdc.gov/ncidod/eid/vol3no1/baseman.htm ◄1997 Tully on Mycoplasma associated with arthritis and immune suppression.

 

http://jcm.asm.org/cgi/reprint/2/3/165?view=long&pmid=1176623:

 

MEDLINE search for mycoplasma and L form:

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=(%22mycoplasma%22[MeSH+Terms]+OR+%22mycoplasma%22[All+Fields])+AND+L-form[All+Fields]

 

Characterization of the physiological requirements for the bactericidal effects of a monoclonal antibody to OspB of Borrelia burgdorferi by confocal microscopy.

 

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=175240&blobtype=pdf 

Department of Pathology, State University of New York, Stony Brook 11794, USA.

A confocal microscopy study was undertaken to characterize the bactericidal effects of the Fab fragments of CB2, an immunoglobulin G1kappa murine monoclonal antibody, to an epitope in the carboxy region of the outer surface protein B (OspB) of Borrelia burgdorferi. Simultaneous direct labeling of both fixed and live spirochetes with fluorochrome-labeled Fab-CB2 and 11G1, and an immunoglobulin Mkappa monoclonal antibody to OspA, showed that OspA and OspB seem to colocalize in dead spirochetes but do not appear to be physically associated when the organisms are alive. A polar bleb composed of a Fab-CB2-OspB complex, followed by incorporation of 11G1-OspA, precedes the formation of a spheroplast. The spheroplasts contain both OspA and OspB and are a terminal stage in the bactericidal process induced by Fab-CB2. Outer membrane destabilization by Fab-CB2, but not cell wall or cytoplasmic membrane alterations, was demonstrated experimentally by the sequential treatment of spirochetes with Fab-CB2 and monoclonal antibodies to flagellin and DnaK. The action of Fab-CB2 is epitope specific, as another monoclonal antibody to an epitope in the amino terminus of OspB was not bactericidal. The bactericidal effect of Fab-CB2 is not dependent on the induction of spirochetal proteases but is dependent on the presence of Ca2+ and Mg2+. Supplementation of Ca2(+)- and Mg2(+)-free medium with these cations restored the bactericidal effects of Fab-CB2. The mechanism by which a Fab fragment of an antibody destroys a bacterium directly may represent a novel form of antibody-organism interaction.


 

URI's Dave Nelson "Reversion of cyst form to intact spirochetes within one minute of addition of rabbit blood:"

http://mic.sgmjournals.org/cgi/reprint/146/1/119  (This was published in the United States in recent time so the CDC can't reject it which is what they always do with data they don't like from Europe.)

 

Question:  If spirochetes, when driven into the cyst form, replicate, do we end up with even more spirochetes than we would have had we not taken antibiotics?
 

Fikrig mentions that OspA vaccination makes the spirochete population increases in ticks in the presence of OspA antibodies:

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=7729870

 

--1983, Proposed Life Cycle for the Reiter Treponeme  (validity of "cysts," or spheroplasts or regeneration forms)


 

--1982, Willy Burgdorfer:

 

http://www.pnas.org/content/90/15/6966.full.pdf  ◄Lynn Margulis; different spirochetal life forms.

1) "Composite, large spirochetes from microbial mats: spirochete structure review."

Morphological changes may be responsible for relapsing, persisting illness.

 

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

 

How Lyme Borreliosis and LYMErix cause immune-suppression illnesses- Downregulation of the antigen-presenting HLAs mean no antibodies will be produced:

The Journal of Immunology, 2004, 173: 2660-2668.
Copyright 2004 by The American Association of Immunologists
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."   http://www.jimmunol.org/cgi/content/full/173/4/2660    
 

 


See also, the Russian Scientists, Intracellular, and the spheroplast forms (& "starvation forms," "stringent forms," "L-forms," cysts, mycoplasma-like formations, and/or whatever else they do)

 

"Toll-like receptors (TLRs) 2 and 4 are signal transducers for lipopolysaccharide, the major proinflammatory constituent in the outer membrane of Gram-negative bacteria. We observed that membrane lipoproteins/lipopeptides from Borrelia burgdorferi, Treponema pallidum, and Mycoplasma fermentans activated cells heterologously expressing TLR2 but not those expressing TLR1 or TLR4. These TLR2-expressing cells were also stimulated by living motile B. burgdorferi, suggesting that TLR2 recognition of lipoproteins is relevant to natural Borrelia infection. Importantly, a TLR2 antibody inhibited bacterial lipoprotein/lipopeptide-induced tumor necrosis factor release from human peripheral blood mononuclear cells, and TLR2-null Chinese hamster macrophages were insensitive to lipoprotein/lipopeptide challenge. The data suggest a role for the native protein in cellular activation by these ligands. In addition, TLR2-dependent responses were seen using whole Mycobacterium avium and Staphylococcus aureus, demonstrating that this receptor can function as a signal transducer for a wide spectrum of bacterial products. We conclude that diverse pathogens activate cells through TLR2 and propose that this molecule is a central pattern recognition receptor in host immune responses to microbial invasion."   http://www.jimmunol.org/cgi/content/full/173/4/2683

 

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=12874328 related on MedLine

 

Here is Dave Persing (Lyme testing RICO patent owner) Corixa's "We modified OspA for use to sell in our adjuvant business because the real OspA is too awful" advertisement which has since been taken off the web, and Corixa has since been purchased by SmithKline:  EMBASSIES_CORIXA_TLR_13_JULY_06.htm

And here is Dave Persing of Corixa talking about how the native OspA proteins are too awful to be used alone as a vaccine in another patent:
http://patft.uspto.gov/6,800,613

"While not wishing to be bound by theory, it is believed that the efficacy of the prophylactic and therapeutic applications described above are based at least in part on the involvement of the mono- and disaccharide compounds in the modulation of Toll-like receptor activity. In particular, Toll-like receptors Tlr2, Tlr4, and others, are believed to be specifically activated, competitively inhibited or otherwise affected by the non-toxic LPS derivatives and mimetics disclosed herein. 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."

 

In this instance they are talking about a polysaccharide in place of the protein, but it's the union and the opposing solubilities that are toxic or immunostimulatory or "too immunostimulatory in the native form."

Note that one of the claims for this modified OspA vaccine as an adjuvant or immune-booster is that this could be used for:
7. A method in accordance with claim 2, wherein said infectious disease is a chronic infection.

 

I don't know of any "chronic infectious diseases," do you?

 

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

 

Top US Weaponeer Pathologist in 1992, at the Cold Spring Harbor Bioweaponeer- Crooks'
Conference says the lymphocytes of Chronic Lyme victims look like Epstein-Barr transformed
cells:
http://www.actionlyme.org/Duray.htm
http://www.actionlyme.org/COLDSPRINGHARBOR.htm


And so, what explains the viral-like (Lyme-like) activation of illness caused by
LYMErix, which I mentioned to the FDA Vaccine Committee in Jan 2001?
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf


"We don't know how LYMErix is making people sick, but it could be due to
the immune dysregulation known to be caused by OspA..."




http://www.ncbi.nlm.nih.gov/pubmed/16889623?ordinalpos=8&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Cell Microbiol. 2007 Jan;9(1):142-53. Epub 2006 Aug 2.Click here to read Links


    The inhibitory effect of Mycoplasma fermentans on tumour necrosis factor (TNF)-alpha-induced
apoptosis resides in the membrane lipoproteins.


    Gerlic M, Horowitz J, Farkash S, Horowitz S.

    Department of Microbiology and Immunology, Faculty of Health Sciences, Soroka
University Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel,
84105.

    Mycoplasma have been shown to be involved in the alteration of several eukaryotic
cell functions, such as cytokine production, gene expression and more. We have previously
reported that infection of human myelomonocytic U937 cell line with live Mycoplasma
fermentans (M. fermentans) inhibited tumour necrosis factor (TNF-alpha)-induced
apoptosis. Mycoplasmal membrane lipoproteins are considered to be the most potent
initiators of inflammatory reactions in mycoplasmal infections. The aim of this
study was to clarify whether the inhibitory effect on TNFalpha-induced apoptosis
is exerted by M. fermentans lipoproteins (LPMf). A significant reduction in TNFalpha-induced
apoptosis was demonstrated by stimulation of U937 cells with M. fermentans total
proteins, LPMf or MALP-2 (M. fermentans synthetic lipopeptide), but not with M.
fermentans hydrophilic protein preparation (AqMf).  ***To investigate the mechanism
of M. fermentans antiapoptotic effect, the reduction of mitochondrial transmembrane
potential (delta psi m) was measured. M. fermentans total proteins LPMf and MALP-2,
but not AqMf, inhibited the reduction of delta psi m. In addition, M. fermentans
total proteins LPMf and MALP-2, but not AqMf, downregulated the formation of active
caspase-8.***  NF-kappaB was transactivated in cells treated with M. fermentans
lipoproteins, and was essential for host cell survival, but not for the inhibition
of TNFalpha-induced apoptosis by LPMf. *** Our results suggest that the inhibitory
effect exerted by M. fermentans on TNFalpha-induced apoptosis in U937 cells is due
to the membrane lipoproteins of these bacteria.***