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CDC Greed (won't answer the FOIA)

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Overview

TUSKEGEE - By Jerry Leonard

1998, CIA Oilmen & Israelis plan to overthrow Saddam for the oil.

Bush/Gore  Oil/War-(Oct,2000)  

Bush's own explainer (Oct 2000) re: Iraq Oil

The Scientist and the Lunatic-  The story of Crazy Eddie McSweegan and a real scientist, Paul Duray.

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.

 

  

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, 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 nadie@cotse.com archive: Re: Submitted to FDA with supporting
View parsed - Show only message text
Path: supernews.google.com!sn-xit-02!sn-xit-04!supernews.com!europa.netcrusader.net!152.163.239.129!portc01.blue.aol.com!audrey05.news.aol.com!not-for-mail

Lines: 83

X-Admin: n...@aol.com

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: <981546178.3a8134c2ca3e5@webmail.cotse.com>

Organization: AOL http://www.aol.com

Subject: Re: na...@cotse.com archive: Re: Submitted to FDA with supporting

Message-ID: <20010208125831.05749.00000046@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

http://www.ncbi.nlm.nih.gov/pubmed/10865170?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

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 (airborne fungal antigens like OspA) 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 scratched 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
 

 

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.***

 

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."

 B) http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11179309&dopt=Abstract

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.

http://www.ncbi.nlm.nih.gov/pubmed/6347861?ordinalpos=131&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

  

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

 

http://www.ncbi.nlm.nih.gov/pubmed/18162176?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

 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.

 

 

Perhaps now that the FBI are experts in bacterial strains, they can find out why Allen Steere took strain "high passage" Borrelia burgdorferi G39/40 to Europe to use with a strain from the Federal Republic of Germany (strain FRG) to invent the bogus CDC Dearborn diagnostic criteria for "Lyme Disease."  [See Chp 3 of CRYME DISEASE.]  We'd also like the FBI to look into the coincidence where Imugen Labs in Norwood, Massachusetts, used those exact two strains, G39/40 and FRG, to discover "NO LYME" in America for years.  How else would Imugen get that FRG strain, if not from Steere's solitary trip to Germany in 1992, intending to leave OspA and B out of the diagnostic standard to facilitate the post-LYMErix approval national monopoly on vaccines and testing for vector borne diseases?  Imugen and L2 Diagnostics were to be the only labs licensed to use the "No-OspA-B-in-the-standard" Dave Persing/Corixa-L2-Imugen RICO method, and therefore the only labs in the country qualified to test for Lyme after everyone received Yale's bogus LYMErix vaccine.

Imugen Report Form showing the use of strains G39/40 and FRG, after the Dearborn Conference where it was stated which strains should be used.  Quest Labs uses strain B31 which has no OspC or band 23 in it.  See Chapter 1 of CRYME DISEASE, where we see several people from Yale and UConn try to develop a Lyme assay with OspC from strain 2591 and see also all the RICO movies, especially the PATENTS movie.  This cabal is playing a strains game.  Quest bought the Lyme Western Blot testing from SmithKline, who used strain B31 to Western Blot (unreadable anyway) people in the LYMErix trial. Quest to this day is still using strain B31, which has no OspC in it.  OspC is associated with brain invasion.   SmithKline and Kaiser-Permanente are in cahoots with the www.aldf.com cabal.  Although the three people who allegedly established the aldf.com (Gary Wormser, John J. Connolly, and Durland Fish) are not NIH staff or CDC officers, NIH and CDC staff are deeply involved in this criminal entity with SKB (GSK) and Kaiser, to not detect neurologic Lyme or the immune suppression outcomes (the New Great Imitator outcomes).  We think NIH's Crazy Eddie McSweegan (this week's topic) was the fourth founding partner of the aldf.com, based on what he did (trashing the US Navy) to insert himself into the top of the NIH's "Lyme Program," in order to be in charge of all the funding, to give all the money to his criminally insane friends.

Murder and the Strains Game Time to boot NIH's Elias Zerhouni

Murder and the Strains Game, Part II, Quest and Yale and Lou Magnarelli and the airhead Governor Jodi Rell

http://www.youtube.com/watch?v=o7pVjl4Rrtc&feature=related ◄ "You may ask yourself, How did I get here?"   Looneyland Corrupticut, Land of the Brainless Automatons (Jodi Rell).  "Same as it ever was same as it ever was same as it EVER WAS!!!"

------------

McSweegan's Latest Harassment of Lyme Activist/Victims    Crazy Eddie gets caught stalking and harassing Lyme victims once again.  (He must be very nervous.)

Announcement-  Read Sweeg's letter above and refrain from responding to his crazy Op-Eds.  You can see that he's baiting Lyme victims because he is under investigation from a federal authority and he wants to pretend to be the victim.

Paying an NIH Scientist for "Clairvoyance" and "Wishful Thinking"
Russia and India ought to know about McSweegan and the NIH.

Fort Detrick: From Biowarfare To Biodefense (Brucella, Incline Village, the CDC and the FBI; Is it Howdy Doody Time??)

http://www.counterpunch.org/sheehan08062008.html   Cindy!  You Go!