Paying an NIH Scientist for "Clairvoyance" and "Wishful Thinking"
Mort Zuckerman
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Subject: Paying an NIH Scientist for "Clairvoyance" and "Wishful
Thinking"
Date: Aug 6, 2008 8:45 AM
Dear Ed,
Are we paying you for clairvoyance and wishful thinking?
Let us know so we can call Grassley's office.
We know complaining to Zerhouni about you and Fauci won't
do any good because Zerhouni is the DHHS's Brownie.
Please let us know if you use the clairvoyance on your
work time so that we can inform India and Russia.
They'll probably not want any crazy stalking clairvoyants
in their country and may be insulted that the United States
would dare to send such nutcases into their countries under
the pretense of science.
Let us know.
Kathleen M. Dickson
http://www.actionlyme.org/index.htm
The Scientist and the Lunatic.
How the immune system damage caused by Lyme Disease (Relapsing
Fever plus a
fungal antigen, OspA) and LYMErix (OspA) vaccination, discovered by a
real scientist,
was blocked and buried for 16 years by a paranoid, stalking, vain-
arrogant-stupid,
grandiose lunatic, who trashed his co-workers throughout his entire
career as means
of advancement.
The bottom line is, did the HIV vaccines, if they have Pam3Cys
on them,
not work for the same reason OspA vaccination did not work?
Could years of research been put back on the right path in
both of these
diseases, starting in 1992, when this lymphocyte abnormality was first
recognized
by Paul Duray if it was followed up on instead of suppressed?
The suppression of the suppression data, is the crux of the
Lyme Cryme.
Paul Duray is a plain old genuine bioweaponeer.
Sweeg never was. He cut himself out of the loop due to
psychopathy.
Then he started just making it all up in his head.
The story of Crazy Eddie McSweegan and a real scientist, Paul
Duray.
Eddie is a psychopath and always wanted to be a famous scientist.
He worked
for the US Navy who had acquired the booty from the Japanese
Bioweapons Unit 731
in Manchuria after WWII. The Navy was clearly performing some
biological and chemical
weapons research, and Crazy Eddie learned about it:
http://www.actionlyme.org/GOLDWATER_LETTER.htm
It all went to his head.
He then thought himself a world-class bioweapons-insider spook.
We believe
he still thinks he is some kind of bioweapons insider, but as we will
later see,
he’s clueless and actually has been left out of the secret US
Biodefense bioweaponeers
loop for a long time. He then went into fantasy story writing, since
that’s all
the material he had to work with, so to speak.
Crazy Eddie admits to his early delusional, grandiose nature,
here:
http://www.actionlyme.org/BIOCRIMES_AND_MISDEMEANORS.htm
As a graduate student twenty years ago, I had a departmental
recruiting
poster
tacked up on the wall next to my desk. It read, in part, "If
you are
curious,
patient, and awfully damned intelligent, consider a Ph.D. in
microbiology."
In
1984 a degree in microbiology seemed like a good idea.
AIDS was just exploding on the scene. Lyme disease was racing
through the
Northeast. Evidence was emerging that a bizarre neurologic
disease might
be
caused by an equally bizarre infectious agent called a prion.
And recombinant
DNA techniques, discovered a decade earlier, were rapidly
helping to create
a
multi-billion dollar industry in the U.S.
After trashing the US Navy to Senator Goldwater and 20 other
senators and congressman,
Sweeg found himself at the NIH as the head of the “Lyme Program.”
Remind yourselves
that Willy Burgdorfer, a real scientist, says of Sweeg’s handling of
the Lyme Program:
“AFTER 30 YEARS, WE HAVE NOTHING!”
Those of us who have been following Crazy Eddie’s antics over the
last 20 years,
and I remind, as regards the lawsuits over his stalking, harassment,
and Deliberate
Release of internet disinformation campaign using a remailer to hide
his address,
we know from Karen Forschner of the Lyme Disease Foundation, one of
his first victims:
(DEPOSITION TRANSCRIPT):
http://groups.google.com/group/sci.med.diseases.lyme/msg/c5e50e5b067b2565?dmode=source
Message from discussion na...@cotse.com archive: Re: Submitted to
FDA with supporting
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Lines: 83
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From: writer0...@aol.com (Writer0608 = KAREN FORSCHNER OF THE
www.lyme.org
)
Newsgroups: sci.med.diseases.lyme
Date: 08 Feb 2001 17:58:31 GMT
References: <981546178.3...@webmail.cotse.com>
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Subject: Re: na...@cotse.com archive: Re: Submitted to FDA with
supporting
Message-ID: <20010208125831...@ng-md1.aol.com>
Anon:
Sorry you have so much confused and incorrect. Why would you keep
attributing
statements to me, that you know I did not say? You need to be
accurate.
My concern is that you are fixated on me, and that fixation is
increasing.
Including increasing over the internet.
Ed did say "Buzz-off Karen." Not very mature. And, I did not go up
to him. I
noticed him after I was talking with Phil Baker. And, he was there
with Phil.
I wonder how his lawsuit against NIH is going. Is he claiming
conspiracy again?
And, the document was missing when it was FOI'd. Ed even sent an
email
to the
reporter, asking why she was interested in the document(s). But, I
guess you
know this.
You state "I heard both conversations went badly." What do you
think
you
"heard"? Now, be careful, because you need to cite first hand
information,
not
gossip. Who told you the information, Phil or Ed?
Lastly, I admit that I did cry during the deposition. Yup. It was
during a
reading of material Ed admitted writing, that mocked our dead son
and pets.
And, a number of such writings were done WHILE he was a public
official
working at NIH as LD Project Officer.
I was also surprised that Ed, (while a Public Official and LD
Program Officer)
was tracking my parents address and phone numbers; my home address
and phone
numbers; my travel agent's information; employee names, home
addresses,
home
phone numbers; my movements while working for the LDF; and had
been at the
LDF's office.
He even had tracked down and talked with a person working with Dr.
Joe
Burrascano. Keeping their informtion in his files. I was also
surprised to
see
his point system, giving himself a score when he was able to harm/
interfere
with an LDF/Karen initiative. This was happening while he was the
LD project
officer.
When was he working? And, who else did he track that he wasn't
caught tracking?
Anon, if you plan to cite depositions I suggest this format.
These are regarding various charges Ed made about the LDF. Ed's
deposition.
Q's
are by lawyers to Ed. A's are Eds answers.
p229 lines 11-13.
"Q. But you have no factual basis to rely on?
A. Not at the moment."
p 288 lines 1-8
"Q. And what was your basis for saying this may invite
investigation and
prosecution?
(ed -accusing the LDF of a wide range of things while NIH LD
Program Office)
A. Clairvoyance.
Q. Anything else?
A. Wishful thinking. I don't know.
Q. Clairvoyance and wishful thinking, okay. Anything else's?
A. No, I didn't have any knowledge of anything related to
investigations
at the
time."
p 147 lines 15-22 p 148 lines 1-6
"Q. Are the things you've said about them, the Forschners or the
Foundation,
that you believe to be true but that you didn't necessarily follow
up on
and
check yourself before you made those statements?
A. For example?
Q Anything
A. I don't think so.
Q In other words, if you made a statement about the Forschners or
the Lyme
Disease Foundation that you didn't have personal knowledge about,
did you
make
an inquiry about it before you would make that statement in
writing or orally
to make sure it was accurate?
A. Yes, but, in fact, I have no personal knowledge of anything."
The LDF received a lot of material from Ed during the time he was
suing the
LDF. Much of this crossed lines from NIH to CDC and to the FDA.
Ed appeared
to be very concerned with the activities of various people and we
were not the
only ones to receive threats, retaliation, or reporting to federal
authorities.
His own colleagues and a grantee was included as targets to be
turned in to
federal, state, and local officials accused of serious wrongdoing.
It wasn't just the LDF.
------
We know from the harassment of the Forschners that Crazy Eddie has
clairvoyance
and wishful thinking, and that he also harassed all his co-workers.
It wasn’t just
the LDF.
------
▼Willy's look of total disgust at what Sweeg and the gang did
with the
disease he discovered.
"AFTER 30 YEARS WE HAVE NOTHING!!!" - Willy Burgdorfer
Willy Burgdorfer's "NOTHING!!" quote... was..The LymeLiers Speak
(Libel = intent to cause harm)
Willy Burgdorfer’s 30 Years of Nothing and Paul Duray’s mutated
chronic Lyme
lymphocytes:
The false claims;
1) The lies about chronic Lyme being instead some hypothetical
psychiatric (since
all of psychiatry is hypothetical) hysteria or some sort of [fill in
the blank]
subconscious need,
2) that LYMErix or OspA caused the same immune suppression
outcomes as chronic
Lyme,
3) that Yale and Gary Wormser knew about but lied about these
outcomes,
http://www.actionlyme.org/SCHOEN_INSTRUCTING_DOCS_TO_BLOW_OFF_LYMERIX_INJUREES.htm
4) that the RICO data stolen off CT AG Richard Blumenthal's desk
was given
to two Yale associates who said under oath that this stolen RICO data
meant I was
"dangerously intelligent," "a chemist," and "like Ted Kaszynski,"
http://www.actionlyme.org/BLUMENTHALS_MAIL_STOLEN_BY_JESSICA_GAUVIN.htm
http://www.actionlyme.org/PHILLIPS_JE_PERVERT.htm
http://www.actionlyme.org/MARCUS_DANGEROUS_INCOMPETENCE.htm
5) that the years and years of lies about what chronic Lyme is /
was in the
interests of Kaiser-Permanente at New York Medical College and
***their relationship
with CDC officers in the ALDF.com cabal*** (Steere and Barbour),
http://www.actionlyme.org/JUNE_13_2005_LETTER_TO_SPITZER.htm
http://www.actionlyme.org/CONNOLLY_FISH_WEINSTEIN.htm
http://www.actionlyme.org/ALDF_BOARD.htm
http://groups.google.com/group/sci.med.diseases.lyme/browse_thread/thread/94e9d21309f76177/508d7369ce25f5cc?hl=en&lnk=gst&q=evan+greenberg+mortimer+zuckerman+ALDF+sponsors#508d7369ce25f5cc
http://www.actionlyme.org/OTHER_ALDF_SPONSORS..htm
http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm
6) the fact that the deliberate suppression of the New Great
Imitator outcomes,
cases not detected by the Steere/Dearborn Method or a Lyme ELISA until
they progress
into the deadlier stages- ALS, MS, Lupus, Dementia, Cancer:
http://www.actionlyme.org/CHP_9_IDSA_REVIEWS.htm
http://www.actionlyme.org/CRYMEDISEASE_CHP3_B.htm
http://www.actionlyme.org/ALSLYME47.htm
http://www.actionlyme.org/IDSA_GREATIMITATOR.htm
http://www.actionlyme.org/MARTIN_NIH_OLIGOCLONAL.htm
http://www.actionlyme.org/MARTIN_MS_1988.htm
http://www.actionlyme.org/LYME_AND_LUPUS_STEERE.htm
http://www.actionlyme.org/GANGLIOSIDES_STEERE_BENACH.htm
http://www.actionlyme.org/BRAIN_PERMANENT.htm
very much appear to be the result of this lipopeptide-induced
tolerance and
immune-suppression related activation of latent viruses of all kinds
(Epstein-Barr,
Cytomegalovirus, HHV-6, etc), and were noticed and mentioned by NCI,
NIH, and US
Army Pathologist (Ft. Detrick) Paul Duray at the Cold Spring Harbor
Conference in
1992, were recorded in a book by Steve Schutzer, and very strongly
appears to have
adversely affected HIV vaccine and other medical research development
for at least
10 years. (This is probably a world record for longest sentence.)
http://www.actionlyme.org/BIOMARKERS2.htm
http://www.actionlyme.org/FUNGAL_VACCINES.htm
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." - Paul Duray, NCI, NIH, Ft. Detrick, at
the 1992
Cold Spring Harbor Crooks' Conference, published in Steve Schutzer's
Lyme
Disease: Molecular and Immunologic Approaches.
http://www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770/ref=sr_1_2?ie=UTF8&s=books&qid=1214848669&sr=1-2
"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?"
Now let’s assume the limits in immune system pathologies are
unknown. There
is no AIDS vaccine, there is no Lyme vaccine, attempts at fungal
vaccines failed
previously (tuberculosis), no one quite understands all the mechanisms
of allergies
shots, and much data on immunity is buried in lies because it has
bioweapons potential.
(See the PNAC document, page 60, on race specific bioweapons
http://www.actionlyme.org/PNAC.pdf )
Dr. Roland Martin at NINDS did not find Lyme to be an autoimmune T
cell disease
through the ridiculous library method (so, he went back home to
Germany):
http://www.actionlyme.org/MARTIN_NINDS_MS_CHRONIC_LYME.htm
And Allen Steere did not find Lyme to be an autoimmune T cell
disease through
the ridiculous library method (so he hid in his high security lab with
the T cells
and the violin blah, blah, poor thing with the depression and the
paranoid delusions
about being stalked):
http://www.ncbi.nlm.nih.gov/pubmed/18191206?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
http://www.actionlyme.org/STEERE_FAIRY_UNSTALKED.htm
“…Steere's lab and private office were in their own section of
the hospital,
tightly guarded by bolts and alarms. When I rang the bell at his lab,
a woman looked
at me through a glass pane and then buzzed me in. Since Steere's
testimony in
Congress, his hair had receded, leaving him nearly bald, and with his
white coat
and pale skin there was something slightly ghostly about him…”
Yale, et al, deliberately lied to the FDA about the outcomes of
LYMErix, the
2 OspA vaccine trial administrators (ImmuLyme and LYMErix) reported 4
times that
they actually could not read their Western Blots in LYMErix vaccinated
people, yet
they reported 92% and 76% safe and affective vaccines anyway, they
lied about what
Lyme was in order to have a fake vaccine trial (Steere in Europe with
the bogus
high-passage strains in Europe to falsify the antibody panel), and
then they stalked
and trashed the victims and the whistleblowers.
LYMErix disease® is basically the same disease as Lyme disease®-
the immune
suppression related disorders that we do not expect to be unlike Sick-
Building Syndrome
or the immune suppression outcomes of chronic mold exposure:
http://en.wikipedia.org/wiki/Sick_building_syndrome
It’s almost useless to hypothesize what are the possible outcomes
from the already-identified
and numerous immune dysregulation mechanisms caused by exposure to
molds or fungal
antigens. Insurance companies recognize the Sick Building and Asthma
outcomes of
new mold exposures. If BigInsurance won’t insure molds exposures,
this suggests
that BigInsurance knows Lyme is a chronic illness.
Note there are two HLA-esque (race-specific PNAC bioweapons) ends
of the inhaled
fungi spectrum- asthma and Chronic Fatigue Syndrome, and possibly
extra, induced,
chemical sensitivities, due to the constant morphing of spirochetal
antigens. If
someone has a new autoimmune hypersensitivity disease as a result of
chronic Lyme,
one would expect that to be probably the result of antigenic
variation. We don't
know. With this many variables and this many impediments to
discovery, we have
barely scratches the surface. Perhaps it is possible that sooner or
later the bug
could create something that your antibodies (or-HLA-complex) find to
be hyperstimulatory.
This can happen even with immune suppression, since the antigens are
of different
types and can affect different TLRs.
Says Alan Barbour in one of his patents:
http://www.actionlyme.org/CENTRAL_LYME_RICO_PATENTS.htm
You don't know how exhausted I am or how hard it is to concentrate
on making
all these variables and data and crime fit into a logical essay on how
Edward McSweegan,
Inc (Ed is the missing fourth partner at www.aldf.com ) bungled all
aspects of
US Medicine with a monstrous migraine and a my-head-feels-like-someone-
opened-it-up-and-poured-cement-in
chronic, daily condition. No, that's not what Barbour says. He says:
http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6,719,983.PN.&OS=PN/6,719,983&RS=PN/6,719,983
2.1 Methods of Treatment
"An important aspect of the invention is the recognition that
Borrelia
VMP-like sequences recombine at the vls site, with the result that
antigenic variation
is virtually limitless. Multiclonal populations therefore can exist in
an infected
patient so that immunological defenses are severely tested if not
totally overwhelmed."
That means the Yale/Steere/Dearborn method is useless for
people who do
not have Steere's haplotypes.
As an aside, says the murdered Don Wiley:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=11877480
This is the story of how Sweeg and Yale obstructed research in all
chronic diseases
with their lies about LYMErix and Lyme disease, and especially HIV
research. The
NIH has now admitted that they have to throw in the towel and start
over on HIV,
and that entire disastrous condition and event looks very much like
the effect of
the immune suppression results of Pam3Cys (OspA) used as an adjuvant
on the HIV
vaccine.
Where to find Pam3Cys and Pam2Cys:
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.
Pam3Cys (it may be Pam2Cys) activates HIV replication:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15312143
Immunology. 2004 September; 113(1): 121–129.
Copyright © 2004 Blackwell Publishing Ltd
Lipid-associated membrane proteins of Mycoplasma fermentans and M.
penetrans
activate human immunodeficiency virus long-terminal repeats through
Toll-like receptors
Mycoplasmas are known to enhance human immunodeficiency virus
(HIV) replication,
and mycoplasma-derived lipid extracts have been reported to activate
nuclear factor-κB
(NF-κB) through Toll-like receptors (TLRs). In this study, we examined
the involvement
of TLRs in the activation of HIV long-terminal repeats (LTR) by
mycoplasma and their
active components responsible for the TLR activation. Lipid-associated
membrane
proteins (LAMPs) from two species of mycoplasma (Mycoplasma fermentans
and M. penetrans)
that are associated with acquired immune-deficiency syndrome (AIDS),
were found
to activate HIV LTRs in a human monocytic cell line, THP-1. NF-κB
deletion from
the LTR resulted in inhibition of the activation. The LTR activation
by M. fermentans
LAMPs was inhibited by a dominant negative (DN) construct of TLR1 and
TLR6, whereas
HIV LTR activation by M. penetrans LAMPs was inhibited by DN TLR1, but
not by DN
TLR6. These results indicate that the activation of HIV LTRs by M.
fermentans and
M. penetrans LAMPs is dependent on NF-κB, and that the activation of
HIV LTR by
M. fermentans LAMPs is mediated through TLR1, TLR2 and TLR6. In
contrast, the LTR
activation by M. penetrans LAMPs is carried out through TLR1 and TLR2,
but not TLR6.
Subsequently, the active component of M. penetrans and M. fermentans
LAMPs was purified
by reverse-phase high-performance liquid chromatography (HPLC).
Interestingly, the
purified lipoprotein of M. penetrans LAMPs (LPMp) was able to activate
NF-κB through
TLR1 and TLR2. On the other hand, the activation of NF-κB by purified
lipoprotein
of M. fermentans LAMPs (LPMf) was mediated through TLR2 and TLR6, but
not TLR1.
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
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.
http://www.actionlyme.org/FUNGAL_VACCINES.htm
And:
"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
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.***
OspA anchors the auto-kill kinase. Latent virally infected cells
become, unlatent
virally infected cells. They don't autokill before the viruses break
free of
the cells and spread around in the system again when the works are
gunked up by
OspA, or shed borrelial lipoproteins, or:
"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?"
More from FUNGAL VACCINES:
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."
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 don't know if these are Pam3Cys or Pam2Cys or what these
antigens are
(at the present time), but one could say that this stupid Lyme clique
either did
not look into other known fungal vaccine antigens or they did not
care, or both.
Nevertheless, not only did LYMErix not work and appear to activate
latent infections
of all kinds, as Paul Duray says and as I suggested to the FDA in
2001, but tuberculosis
vaccines seem to have failed in the same way. Now the HIV vaccine has
also failed
in the same way.
All fungal vaccines appear to have failed because they suppress
the immune system.
Now ask yourself: If all fungal antigens as vaccines failed
because they suppressed
the immune system, how could Lyme be an inflammatory disease, only?
With this much
data showing the known mechanisms of illness caused by these strange
lipids,
There are several patents related to Pam3Cys (tripalmitoyl) as an
adjuvant and
HIV:
http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&p=1&u=/netahtml/PTO/search-bool.html&r=0&f=S&l=50&TERM1=tripalmitoyl&FIELD1=&co1=AND&TERM2=HIV&FIELD2=&d=PTXT
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.
Several reports which make it appear as if the Pam3Cys type of
antigen was used
as an HIV vaccine adjuvant or is actually part of the HIV gp120 and
gp41 (I cannot
find out officially):
1) http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1421990&blobtype=pdf
2) http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=1349173
3) http://www.ncbi.nlm.nih.gov/pubmed/18524817?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
We found decreased Toll-like receptor 1 (TLR1) and TLR4
surface expression
in HIV-infected U1 monocytic cells compared to the uninfected parental
U937 cell
line and decreased TLR message in alveolar macrophages (AMs) from HIV-
positive subjects.
In addition, stimulation with TLR1/2 ligand (Pam(3)Cys) or TLR4 ligand
(lipopolysaccharide)
resulted in decreased intracellular phosphorylated extracellular
signal-regulated
kinase and subsequent decreased transcription and expression of TNF-
alpha in U1
cells compared to U937 cells.
4) http://journal.kcsnet.or.kr/main/j_search/j_download.htm?code=B961118
(Korean Journal where they blew up this HIV-Pam3Cys thing to look for
“We are currently using several mass spectral techniques to
characterize
the amino acid sequences of the Pam3Cys peptides found in the envelop
glycoproteins
of the HIV-1 and the Simian Immunodeficiency Virus (SIV).(17)
Convential FAB-MS
analysis using standard matrices, such as glycerol and nitrobenzyl
alcohol, is not
particularly effective for these molecules, largely due to their
tendency to aggregate”
[“their tendency to aggregate” …like what happened with LYMErix
and the Western
blot smudging, we think. We think they could never guarantee
completely free OspA
antigens in a vial of vaccine, and previous reports about HPLC assay
of OspA, I
suspect had a –prefiltering and pre-HPLC step because we always knew
OspA was a
sticky lipid and even sticks to itself, since Alan Barbour reported
that phenomenon.
The most important information to be gleaned from that Korean
report above is
that it appears that Pam3Cys is stuck on HIV antigens either
naturally, or as an
adjuvant (or both, inadvertantly). Previously we learned that
something in tick
saliva blocks HIV transmission. I hypothesize that whatever blocks
HIV in tick
saliva also blocks OspA (given OspA’s tendency to cause spirochetes to
even stick
together), and that that would be advantageous to the tick, not having
spirochetes
and perhaps antibodies or mammal immune cells sticking to its mouth
parts.
Movie about HIV attachment. gp20 and gp41, it appears, are
Pam3Cys-120 and
Pam3Cys-41.
http://www.youtube.com/watch?v=RO8MP3wMvqg
Biochem Biophys Res Commun. 2008 Feb 29;367(1):41-6. Epub 2007
Dec 26. Links
The Ixodes scapularis salivary protein, salp15, prevents the
association of
HIV-1 gp120 and CD4.
Juncadella IJ, Garg R, Bates TC, Olivera ER, Anguita J.
Department of Veterinary and Animal Sciences, University of
Massachusetts Amherst,
103 Paige Laboratory, 161 Holdsworth Way, Amherst, MA 01003, USA.
Ixodes scapularis salivary protein, Salp15, inhibits CD4(+) T cell
activation
by binding to the most-extracellular domains of the CD4 molecule,
potentially overlapping
with the gp120-binding region. We now show that Salp15 inhibits the
interaction
of gp120 and CD4. Furthermore, Salp15 prevents syncytia formation
between HL2/3
(a stable HeLa cell line expressing the envelope protein) and CD4-
expressing cells.
Salp15 prevented gp120-CD4 interaction at least partially through its
direct interaction
with the envelope glycoprotein. A phage display library screen
provided the interacting
residues in the C1 domain of gp120. These results provide a potential
basis to define
exposed gp120 epitopes for the generation of neutralizing vaccines.
https://www.aidsreagent.org/program_info.cfm#5
It is pretty difficult to tell what is blocked by salp15, but if
it prevents
spirochetes from sticking to the mouth parts of the tick, and if it is
true that
the lipid portion of the HIV gp120 and gp41 is indeed Pam3Cys, then it
would make
sense that the tick saliva component blocks Pam3Cys. We don't know.
Either
it is a bioweapons secret or because of the insanity in Lymeland on
the part of
the perps sued by the Connecticut Attorney General, no one is allowed
to discover
which end is up.
Would an antibody alone, such as anti-OspA antibody, be enough to
block the
HIV "glyco"-proteins if the "glyco" were the same as the OspA
lipids?
ON MEDLINE, searching for Pam3Cys and HIV or tripalmitoyl and HIV:
: J Virol Methods. 1988 Dec;22(2-3):173-82.Links
Distinction between HIV-1 and HIV-2 infection using novel
synthetic lipopeptide
conjugates as antigens in enzyme immunoassays.
Böltz T, Hummel RP, Tröger W, Rübsamen-Waigmann H, Biesert L,
Müller-Lantzsch
N, Koch P, Bessler W, Jung G.
Institut für Immunobiologie, Universität Freiburg, F.R.G.
A novel immunoassay technique using synthetic lipopeptide (Pam3Cys-
Ser) linked
to immunodominant peptide domains of HIV-1 and HIV-2 envelope proteins
as an antigen
adsorbent has been developed. Attachment of peptides to microtiter
plates can be
considerably improved with this method by employing the hydrophobic
properties of
lipopeptide. From the sera of 121 HIV-1 infected patients 117 reacted
with Pam3Cys-Ser-[HIV-1(598-609)cyclic
disulfide]. Five of 5 HIV-2 positive sera were positive with Pam3Cys-
Ser-[HIV-2(593-603)cyclic
disulfide]. Control sera failed to react with these conjugates.
That 1988 report sort of speaks for itself. OspA's type of
lipids attached
to some proteins associated with the AIDS virus produced a product
against which
HIV positive patients had antibodies.
Since we know the chronic exposure to borrelial lipoproteins
causes the immune
suppression diseases known as LYMErix disease® and chronic Lyme
disease®, then a
Pam3Cys vaccine might not be a good idea for HIV prevention. We
don’t know.
The typical vaccination strategy (producing antibodies in humans)
may have to
be abandoned here, in HIV-land, if human antibodies alone are not
enough to prevent
gp120 attachment to CD4+ cells. If HIV vaccines fail because of
antigenic variation,
and the strategy at the current time for Lyme vaccination is to
produce multivalent
OspA (Baxter, see:
http://www.actionlyme.org/WORMSER_INSISTS_LYME_A_KNEE_DISEASE.htm
then one wonders if they intend to produce a multivalent HIV
vaccine. The "selection
pressure" of borreliosis, we think is simply the deliberate mechanism
of immune
evasion which make Relapsing Fever organisms Relapsing Fever
organisms. The plasmid
encoded DNA constantly undergo antigenic variation, but generally, the
plasmid surface
antigen code for the TYPES of antigens generally remain the same
(example: there
is a gene for OspC which attaches to integrins or red blood cells, it
is believed,
but OspA attaches to something like chitinous tissue. We don't expect
OspC
to mutate, like for example, so drastically that it becomes OspA.).
For some reason, the selection pressure forcing changes in
borrelia spirochetal
surface antigens is more dramatically observed, than, for example,
among influenzas.
I myself, can't capture all the variables, here. I suppose it would
take years
and years of training, and reading the work of Donald C. Wiley to see
where we are
on what we know about infectious organisms mutations adding virulence,
and also
know all there is to know about human immunity. The latter is clearly
an impossibility.
That's why it is so hard to fathom any of these Lyme criminals could
ever have
thought they could put this disease into a neat little box. And then
dare to say
the box actually contains, the ever infamous, NOTHING!
Let’s assume mice are more accustomed to eating dirt, rotting food
particles,
and animal poopies than humans, since OspA comes from E. coli. There
is not a record
of OspA vaccination causing immune suppression in mice, although Gary
Wormser published
that it caused immune suppression in dogs. So, just because it
produced a prolonged
immune response in mice, one cannot and should not have assumed the
same principle
applied to humans or even primates (primates do not cook their meat,
if they eat
meat). Also, rotting food with molds on it, are not part of the usual
human diet.
Perhaps it would be better if we did consume a little rot as young
children since
adult autoimmune diseases appear to be a function of later-life
exposures. Childhood
allergies could be due to the confluence of non-dirt-exposure, a
sedentary lifestyle,
and immune dysregulation from multiple vaccinations. Whatever the
root reasons
for these epidemics, the discovery of them has not been helped by
social engineering,
BigInsurance and BigPharma. Epidemics of childhood diseases such as
allergies could
be a function of hyperprotection as much as they are global warming
and emerging
infectious diseases. The point here being, this lying, profit-driven
and Kaiser-driven
medicine destroys not only medicine, but the adult intellectual
potential in children,
decreasing the likelihood that these disasters can be managed
adequately by our
children.
I choke over the word “protection” because I almost sound like
Simon Wessely
when he accuses the Gulf War Illness Vets of being fairies, especially
since it
is truer that GWI is due to vaccinal “protection,” DEET, and nerve
agent antidote
prophylaxis "protection":
http://www.actionlyme.org/ROCKET_SCIENCE.htm
The bottom line is, did the HIV vaccines, if they have Pam3Cys
on them,
not work for the same reason OspA vaccination did not work?
Could years of research been put back on the right path in
both of these
diseases, starting in 1992, when this lymphocyte abnormality was first
recognized
by Paul Duray if it was followed up on instead of suppressed?
The suppression of the suppression data, is the crux of the
Lyme Cryme.
Paul Duray is a plain old genuine bioweaponeer.
Sweeg never was. He cut himself out of the loop due to
psychopathy.
Then he started just making it all up in his head.