01 Oct 2017
File List, RICO
1988 Steere says Lyme is like a B cell leukemia
Fungal Exosomes Inhibit Apoptosis
"Vaccines serve the mfgs, not their victims"
CDC Admits Fraud, 2016
Bush's warcrimes, Oct 2000
thoroughly I conduct scientific research, the more I believe that
science excludes atheism.
us how to aersolize, dessicate, or weaponize Borrelia into the cyst or
spheroplast form in 1964
and Vector-Pathogen Competence Studies performed on Plum Island
Toll-like receptor 2-dependent inhibition of
macrophage class II MHC expression and antigen processing by 19-kDa
lipoprotein of Mycobacterium tuberculosis.
Selling such fungi and
other biological and chemical weapons to Saddam Hussein
and Robin Cook);
Dead Iraqi scientist who worked with mycoplasma and allegedly on Plum
(run over while
changing a flat, much like Don Wiley)
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:
Mycoplasma and Leukemias
Mycoplasma and other tumors:
Isolation of mycoplasma from Leukemic bone marrow:
"Pleuropneumonia-like organisms associated with neoplastic disease":
Mycoplasma are molds
that cause plant rot
Stinking Smut and Iraq
Department of Pathology, Case Western Reserve University and University
Hospitals of Cleveland, Cleveland, OH 44106, USA.
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)
Do L-forms cause disease?, Or, "Has science has gone backwards, which is why
we're having this discussion?"
African Swine Fever and Durland Fish
Swine fever and Lyme Borrelia
IV. Borrelia phylogeny
Bacteriophage vectored DNA & bioweaponeer bumbling
Tully and Shope, bioweaponeers.
Joe Tully, the bioweaponeer and mycoplasma and tick, on MedLine:
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...)
VII. Rockefeller University
(The Biology of Parasitic Spirochetes)
Ed Bosler and UPenn on outbreak areas:
Evolution of a focus of Lyme disease
(This supports the assertion
that Plum Island was the original outbreak area.)
PHYLOGEOGRAPHY OF BORRELIA BURGDORFERI AND ITS TICK
VECTOR, IXODES SCAPULARIS:
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
IIX. PNAC "race-specific bioweapons" is moot
(nanobots and Morgellon's)
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,
OspA-induced IL-10 which is an immune suppressing cytokine
lipoproteins also result in immune suppression.
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:
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:
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
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)
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
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:
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
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:
Synthesis of the mitogenic
S-[2,3-bis(palmitoyloxy)propyl]-N-palmitoylpentapeptide from Escherichia
As you recall from Chp 3,
is what OspA looks like/is
The following looks like an attempt at an HIV
vaccine with an OspA adjuvant:
From an HIV vaccine:
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:
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
So, there are Plum Island strains of mycoplasma.
Murdered Iraqi scientist who studied infertility in cattle due to
mycoplasmas on Plum Island
Use of biological weapons by Don Saddam Rumsfeld:
Congressional Record- Bioweapons sold by USA to Iraq to use against Iran:
"...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"
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...
exists and they're not Israelis; Iran is an existential threat to
"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
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.
MEDLINE search for mycoplasma and L form:
Characterization of the physiological requirements
for the bactericidal effects of a monoclonal antibody to OspB of Borrelia
burgdorferi by confocal microscopy.
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:
Proposed Life Cycle for the Reiter
Treponeme (validity of
"cysts," or spheroplasts or
◄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
tuberculosis LprG (Rv1411c): A Novel TLR-2 Ligand That Inhibits Human
Macrophage Class II MHC Antigen Processing1
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
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."
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:
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:
"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
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?
Weaponeer Pathologist in 1992, at the Cold Spring Harbor Bioweaponeer-
Conference says the lymphocytes of Chronic Lyme victims look like
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?
"We don't know how LYMErix is making people sick, but it could be due
the immune dysregulation known to be caused by OspA..."
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
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,
Mycoplasma have been shown to be involved in the alteration of several
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) inhibited tumour necrosis factor (TNF-alpha)-induced
apoptosis. Mycoplasmal membrane lipoproteins are considered to be the
initiators of inflammatory reactions in mycoplasmal
infections. The aim of this
study was to clarify whether the inhibitory effect on TNFalpha-induced
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
proteins LPMf and MALP-2, but not AqMf, downregulated the formation of
caspase-8.*** NF-kappaB was transactivated in cells treated
with M. fermentans
lipoproteins, and was essential for host cell survival, but not for the
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