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


08/29/2016 07:18:34
 

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1991 Steere appears to know this is about the secondary opportunistics not HLA-associated


dressler1994.pdf
golightly1988 - Copy (2).pdf
dattwyler1988 (1).pdf


Predicting Bush's warcrimes, Oct 2000

Criminal_Charges, Navigation of this site


Occam's Razor (EBV)

SASH: Vaccines & Common Mechanisms

Exosomes, Vesicles, Blebs

"Somatoform" (def.)

IDSA: "Vaccines are dangerous"

Fibro herpes ganglia

"Spirochetes Love Brain to Death"

Benach/IDSA, Lyme brain damage

Spirochetal Dementia

160725

2015 Lyme Mafia

SASH sites:
CrymeDisease.com
OhioActionLyme.org
Bad Lyme Attitude
MaineActionLyme.org
May12.org


151218 Merck's MMR monograph

151127 Predicting Bush's warcrime results, Fawaz Gerges


151027 Occam's,  Auwaerter,Johns Hopkins



 


 

Cryme Disease, the movie: https://vimeo.com/180529812

The fungal-ish OspA vaccine caused the same post-sepsis, immunosuppression disease as the one thrown out of the case definition at Dearborn.
Steere used a seronegative Lyme assay to assess chronic neuro Lyme, a disease he later falsified and now claims never existed.  Steere recently claimed in a radio interview that (June 14, 2016) he never knew Lyme caused a chronic neuro outcome.  The CDC would like to throw Allen Steere under the bus,... and Steere is trying to avoid being thrown under the bus.  Obviously not happening.
 

 


More Lyme Cryme movies, related, and expanded: https://www.youtube.com/channel/UC-QMTRlZUqZ992g8vVo9tZg


 

 

Lyme Cryme: How it all Went Down


 

 

 

The Autism pandemic is caused by children getting the actual brain-tropic viruses that are in the vaccine vials, either because those children are immunosuppressed or because the vaccines are contaminated with the likes of fungal antigens like LYMErix.  Thimerosal was put in vaccines, literally, to prevent the fungal Lyme vaccine, LYMErix, and antigens like it. 

Yes, the *ENTIRE* HHS.gov is that stupid.  Add to that, everyone with "MD" after their names.  YES, ALL OF THEM are THAT STUPID.

You have seen the MRIs of the heads of the ZIKA brain damaged children in the news.  The scientific literature says Borna virus is the model for the "neurodevelopmental brain damage" we call Autism.  The IDSA says vaccines are given too many, and too young, and none of them are properly vetted, and this was true since the 1970s.  The scientific literature on those MMR qualifications shows those children were never followed longer than a few days.  The MMR vaccine qualifications were even more criminal than the LYMErix stunt.  Go look for yourself on Pubmed.  You'll do it if you give a sh*t about other people.  But if you don't, you won't bother. 

It is the same with activism, in general.
 

If you are looking for the very simplest explainer on the Lyme crymes, see the RICO complaint already filed with the USDOJ.  I was talking to lawyers after all, so I had to really dumb it down.




 


 


ONLY IN
the United States of STUPID could you see the likes of the ALDF.com's founders, Edward McSweegan and Durland Fish
,
not knowing spirochetes were their own phylum (are not regular "bacteria"), are relapsing fever organisms, that the nature of the relapse was antigenic variation (vaccines would do no good), and that the McSweegan-Fish gang never even asked what OspA was (fungal, TLR2/1 agonist, causes permanent immunosuppression, never could have been a vaccine).  The CDC deployed the stupid and cowardly Allen Steere who went into Rheumatology to avoid VietNam (there are no old ladies who need aspirin among deployed US combat forces), probably because he was known to be too stupid to ask any questions about ticks or spirochetes.


What is the simplest way to explain that the ALDF dot com / Yale / CDC Lyme cabal threw out of the Dearborn, "2-tiered" "case definition" the very same disabling, chronic neurologic, "New Great Imitator" disease that was caused by the fungal toxin, Pam3Cys or OspA?  They knew OspA vaccination causes neurologic, immunosuppression disease before the Oct 1994 Dearborn, Michigan fake consensus conference ever took place (chronology here).
 
In order for it to be prosecuted as a criminal case you have to show they knew ahead of time that there was this problem with their "vaccine" choice and that they CHANGED the testing definition after that, such as to leave out the chronic neurologic Lyme definition - the very disease caused by the fungal OspA vaccines
 

This is from June, 1993, by Alan Barbour and Durland Fish:



http://www.actionlyme.org/BarbourFishpdf.pdf

They said this ˄ BEFORE the CDC's Dearborn-"Let's-Leave-Out-the-Chronic-Neurologic-Form-of-the-Disease-Which-Is-Also-Caused-by-OspA-Injection-Alone" fake consensus conference took place (Oct, 1994). 
So, these criminals would have known there was a problem with OspA injections making people sick.  After all, OspA is a fungal endotoxin, TLR2/1-agonist.
 

The current, 1994, "Dearborn" case definition only detects the 15% of cases, only the late-, HLA-linked- arthritis cases, no early cases, and then these CDC (vaccine patent holding) criminals say this late manifestation needs no treatment.  The truth is that chronic neurologic disease is mainly caused by immunosuppression, reactivated Epstein-Barr and cross tolerance to other infections, or, technically, is post-sepsis syndrome or a kind of a B cell AIDS (see the Occam's Razor).

In this criminal case, you have to show to the DOJ that they CHANGED the diagnostic criteria from an older one that allowed more people to be diagnosed (the 1990 CDC version).  If the DOJ does not respond, clearly this was a bioweapon accident of some sort.  The circumstantial scientific, epidemiological evidence from Plum Island as the original outbreak area says so.    (Do the Russians know by now?  They knew in 2006.  The Chinese, a year later.  Site stats.)


The US press cant handle it, and no one has ever written about it in any book.

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

Whoever does not know what LYMErix-disease is, does not know what Lyme disease is.  This includes ILADS.org and all of the Lyme non-profits.  One has to know what the antigen is, in order to know what it does.  This is basic science. 

And it turns out that Lyme and Syphilis as "Great Imitators" are really Great Detonators of latent viruses and general immunosuppression - also known as post-sepsis syndrome.  It turns out that Pam3Cys (OspA), a triacyl lipopeptide, is a functional mimic of E. coli's Lipid A, a serious fungal (TLR2/1-agonist) ENDOTOXIN.  Think about that.  The CDC wanted to inject everyone with several blobs of bathroom scum.  And that's what happens with a tick bite, too. 



Baumgarth (UCDavis):

"For months after infection, those germinal centers fail to produce the specific cells — memory B cells and antibody-producing plasma cells — that are crucial for producing lasting immunity. In effect, the bacteria prevent the animal’s immune system from forming a “memory” of the invading bacteria and launching a protective immune response against future infections.

"The researchers found that following Borrelia burgdorferi infection, this process even prevented induction of strong immune responses to an influenza infection."

See https://scienceblog.com/79136/lyme-disease-subverts-immune-system-prevents-future-protection/#hiCzbjF13JBLGgQF.97

 

Cadavid on Septic Spirochetes:

"Finally, spirochetal lipoproteins have more prominent pro-inflammatory effects compared to other bacterial lipoproteins and synthetic lipopeptides ()."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4075078/



Who else says OspA alone is responsible for this sepsis-then-immunosuppression outcome?

1.)  Norman Latov on how OspA vaccination caused the same disease as chronic Lyme:

Neuropathy and cognitive impairment following vaccination with the OspA protein of Borrelia burgdorferi.

“Neurological syndromes that follow vaccination or infection are often attributed to autoimmune mechanisms. We report six patients who developed neuropathy or cognitive impairment, within several days to 2 months, following vaccination with the OspA antigen of Borrelia burgdorferi. Two of the patients developed cognitive impairment, one chronic inflammatory demyelinating polyneuropathy (CIDP), one multifocal motor neuropathy, one both cognitive impairment and CIDP, and one cognitive impairment and sensory axonal neuropathy. The patients with cognitive impairment had T2 hyperintense white matter lesions on magnetic resonance imaging. The similarity between the neurological sequelae observed in the OspA-vaccinated patients and those with chronic Lyme disease suggests a possible role for immune mechanisms in some of the manifestations of chronic Lyme disease that are resistant to antibiotic treatment.”  http://www.ncbi.nlm.nih.gov/pubmed/15363064



 

2.) Gary Wormser on OspA causing immunosuppression (which means it was the opposite of a "vaccine"):

Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA).

”… After exposure to either the unaltered vaccine preparation or OspA prepared in saline, normal lymphocyte responses to the mitogens concanavalin A, phytohemagglutinin-M or pokeweed mitogen, or the antigen BCG were consistently reduced. Whole cell extracts of B. burgdorferi also modulated immune responses but required a much greater quantity of protein than needed for theOspA preparation. The magnitude of modulation was directly dependent on the quantity of OspA. OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression. Future studies designed to delete the particular region or component of theOspA molecule responsible for this effect may lead to improved vaccine preparations.”
http://www.ncbi.nlm.nih.gov/pubmed/10865170

 

 

 


 

3.) Donald H. Marks - an OspA vaccine trial administrator - on how LYMErix caused the same disease as chronic Lyme:

Neurological complications of vaccination with outer surface protein A (OspA).

”A wide range of neurological complications have been reported via the medical literature and the VAERS system after vaccination with recombinant outer surface protein A (OspA) of Borrelia. To explore this issue, 24 patients reporting neurological adverse events (AE) after vaccination with Lymerix, out of a group of 94 patients reporting adverse events after Lymerix vaccination, were examined for causation. Five reports of cerebral ischemia, two transient Ischemic attacks, five demyelinating events, two optic neuritis, two reports of transverse myelitis, and one non-specific demyelinating condition are evaluated in this paper. Caution is raised on not actively looking for neurologic AE, and for not considering causation when the incidence rate is too low to raise a calculable difference to natural occurrence.”
http://www.ncbi.nlm.nih.gov/pubmed/21673416


It’s not “Autoimmune.”  It’s Subimmune.  This Subimmunity represents the entire class of the DSM's VooDoo Somatoformia – as well as cancer.  Cancer is in the Subimmune class, at the other end of the immunity spectrum from Autoimmunity.   This fact or condition completely flips the entire medical paradigm where you have to have a biomarker that is above-, or more-than- the normal range.  Lyme is not an inflammatory disease.  There are always negative correlations to biomarkers of autoimmunity or illness or infection except when using sophisticated DNA techniques using spinal fluid, in particular in these chronic, waste-basket diseases.  Henceforth, Autoimmunity will be an obsolete word that connotes the previous Medical Establishment where BigPharma is going to “block” something with their drugs.  They are dinosaurs.  You can’t block a mechanism that is already permanently blocked and you can’t unblock it.

It could be that a person has an HLA-linked outcome to one of the secondary infections like Epstein-Barr or HHV-6, reactivated by the AIDS-like Lyme and LYMErix.  Those people would for instance have the official, hypersensitivity outcomes of MS or Lupus or whatever.  But they are not also called Incompetent Incantation-ators and they are not mistreated by the entire universe (family, friends, Social Security, “doctors,” everyone, including ILADS and the non profits).

 


4.) Ben Luft at the 1998 FDA Vaccine Meeting on LYMErix:

 "The point that I wanted to make in regard to the study is that there is very heavy dependence on serologic confirmation. And when we start thinking about the adverse events, *** it was stated originally when we got the overview of the disease that the disease is really quite protean. And actually the adverse events are very similar to what the disease manifestations are.**** And if you start to, as I think Dr. Hall was eluding to -- if you start to kind of say well how often do you actually become seropositive, you can start to have a different take on when someone has an adverse event or whether it is disease specific or infection specific versus vaccine specific. And I think that that is an important issue that we have to deal with. ..."   http://www.fda.gov/ohrms/dockets/ac/98/transcpt/3422t1.rtf

 

 




5.) Dave Persing who together with Yale’s Robert Schoen developed this test in 1994 or 1995 says this about the similarities between Lyme and LYMErix disease:

"Additional uncertainty may arise if the vaccines are not completely protective; vaccinated patients with multisystem complaints characteristic of later presentations of Lyme disease may be difficult to distinguish from patients with vaccine failure....”

 

http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=/netahtml/PTO/srchnum.htm&r=1&f=G&l=50&s1=6045804.PN.&OS=PN/6045804&RS=PN/6045804


 

Who else says OspA alone is responsible for the immunosuppression with brain inflammation that is characteristic of "Chronic Lyme?"

6.) THE NIH (Martin and Marques):

Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression (2006).

The spirochete Borrelia burgdorferi is the agent of Lyme disease, which causes central nervous system manifestations in up to 20% of patients. We investigated the response of human brain microglial cells, glial progenitors, neurons, astrocytes, as well as peripheral blood monocytes to stimulation with B. burgdorferi. We used oligoarrays to detect changes in the expression of genes important for shaping adaptive and innate immune responses. We found that stimulation with B. burgdorferi lysate increased the expression of Toll-like receptors (TLRs) 1 and 2 in all cell types except neurons. However, despite similarities in global gene profiles of monocytes and microglia, only microglial cells responded to the stimulation with a robust increase in HLA-DR, HLA-DQ, and also coexpressed CD11-c, a dendritic cell marker. In contrast, a large number of HLA-related molecules were repressed at both the RNA and the protein levels in stimulated monocytes, whereas secretion of IL-10 and TNF-alpha was strongly induced. These results show that signaling through TLR1/2 in response to B. burgdorferi can elicit opposite immunoregulatory effects in blood and in brain immune cells, which could play a role in the different susceptibility of these compartments to infection.
http://www.ncbi.nlm.nih.gov/pubmed/16783164 

 

The NIH patent explaining how Lyme causes LYMErix-disease (“stealth bomber”):

"The invention relates to novel antigens associated with Borrelia burgdorferi which are exported (or shed) in vivo and whose detection is a means of diagnosing Lyme disease. The antigens are extracellular membranevesicles and other bioproducts including the major extracellular protein antigen. Another object of the invention is to provide antibodies, monoclonal and/or polyclonal, labeled and/or unlabeled, that are raised against the antigens. A further object of the invention is to provide a method of diagnosing Lyme disease by detecting the antigens in a biological sample taken from a host using the antibodies in conventional immunoassay formats. Another object of the invention is to provide kits, for the diagnosis of Lyme disease, comprising the antibodies and ancillary reagents. The advantage of the antibodies used in the invention is that they react with the antigens from geographically diverse strains of Borrelia burgdorferi, but do not react with antigens from related Borrelia spirochetes."
http://patft.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=5,217,872.PN.&OS=PN/5,217,872&RS=PN/5,217,872
 


The shed blebs (or exosomes or vesicles) have LYMErix on them (delayed fuse or “time bomb”):

Characterization of multiprotein complexes of the Borrelia burgdorferi outer membrane vesicles.

"Although we uncovered the existence of at least 10 distinct OM complexes harboring several unique subunits, the complexome is dominated by the frequent occurrence of a limited diversity of membrane proteins, most notably P13, outer surface protein (Osp) A, -B, -C, and -D and Lp6.6." 
http://www.ncbi.nlm.nih.gov/pubmed/21875077
 

 

 

7.)  Dattwyler and Luft in 1989, in IDSA's own "journal," saying "treatment fails in half the cases." And the OspA vaccine caused the same systemic disease, say the crooks, themselves.  See the Occam's Razor report for who says so. 

Steere was at this 1994 FDA meeting: 

DATTWYLER:  "-- the ones that (sic) failed to mount a vigrous immune response tended to do worse.  So, there is an inverse correlation between the degree of serologic response and the outcome. 
"So, individuals with a poor immune response tend to have worse disease."

1994 FDA Meeting Transcripts where Ray Dattwyler tells the FDA Vaccine Committee that the
patients with low or no antibodies are the sickest:  http://www.actionlyme.org/Dattwyler_Luft_DNA_in_CSF.htm




 


Ray Dattwyler (SUNY-SB) says in 1988 that exposure to Lyme or even just its supernatants (OspA-like molecules) turn off the NK cell activity (or is immunosuppressive):




"Effect of B burgdorferi Culture on Normal PBL




"..when lymphocytes are cultured in the presence of growing Bb there is a marked inhibition ( p < .0005 ) of NK activity on days 3, 5, and 7 when compared to lymphocytes cultured in BSKII media in the absence of spirochetes.  This effect is not due to a selective depletion or or toxicity to endogenous NK since viability studies and monoclonal antibodies demonstrate no significant changes after culture with the organism.

 



"The inhibition is directly attributable to the organism or its supernatants (data not shown)."
 

From: Modulation of natural killer cell activity by Borrelia burgdorferi.

Golightly M, Thomas J, Volkman D, Dattwyler R.
Department of Pathology, State University of New York, Stony Brook 11794.
PMID: 3056196 [PubMed - indexed for MEDLINE]
Ann N Y Acad Sci. 1988;539:103-11.

http://www.actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm

 

Dattwyler on Seronegative Lyme and how that is like fungal diseases:

DOWNLOAD THE FULL TEXT of Dattwyler talking about seronegative, neuroLyme, HERE:
dattwyler1988 (1).pdf



Lyme is like Jeopardy!  Ask the right question:  "Something that causes a 'multi-system disease' and is IDSA's own 'New Great Imitator.'" 

The answer is, "What is OspA?"


 

UCSF says Lyme and LYMErix-Disease are a diseases of immunosuppression, and they say that half the Lyme/tick bite victims remain ill and are not cured with antibiotics
Feb 12, 2016:

“Early Lyme disease prior to antibiotic therapy was characterized by marked upregulation of Toll-like receptor signaling but lack of activation of the inflammatory T-cell apoptotic and B-cell developmental pathways seen in other acute infectious syndromes,” wrote the study’s authors. “Six months after completion of therapy, Lyme disease patients were found to have 31 to 60% of their pathways in common with three different immune-mediated chronic diseases. No differential gene expression signature was observed between Lyme disease patients with resolved illness to those with persistent symptoms at six months post-treatment.”

http://www.genengnews.com/gen-news-highlights/lyme-disease-may-be-diagnosable-via-transcriptome-signature/81252365/



See more below from UC Davis,
and in the Occam's Razor report. The Great Imitator is EBV, the Great Initiator is the fungal antigen OspA, shed by spirochetes - their own phylum, and not regular "bacteria" - on blebs, says the NIH.  America is a really stupid country, when you consider that nearly every disease is an outcome of the first immune disordered step - inhibition of apoptosis of infected B cells.


Look at the experience of Lewis Bull, East Lyme, CT, back in the OspA "vaccines" trials days (late 1990s) to see exactly what these evil bastards of the CDC (Barbour, Johnson, Steere) had planned from the beginning to do with LYMErix - "multisystem (read: "sepsis")," Chronic Fatigue Syndrome-like - outcomes.   'Says it all.
 

 

University of California, Davis, says the CDC, Allen Steere, Gary Wormser, Edward McSweegan, et al must be lying their faces off:  Lyme and LYMErix cause permanent immunosuppression or is like a B cell AIDS.

http://www.ccm.ucdavis.edu/our-science/lyme-disease 

       

Lyme is not an "inflammatory," "autoimmune disease," it is the Great Initiator of latent viruses, as a fungal antigen shedder, SPIROCHETE (its own phylum).  Fungal antigens like triacyl lipopeptides (OspA) have always been known to cause immunosuppression. The complete opposite of an "autoimmune" or "inflammatory" disease.  The only biomarkers will be signs of nerve and brain degradation in the cerebral spinal fluid; no antibodies in the blood.
 

 

 


 

 So what exactly is OspA? 

“I did not get the vaccine so this does not concern me.”   Oh, yes, you got the vaccine.  Everyone with Lyme got LYMErix.  Here is what LYMErix is, and how this "vaccine-was-the-disease" works:
 

This is image is of Pam3Cys or OspA.  What is variable is the protein end "("peptide"), but what is immunogenic (seen as an invader to the immune system) are the fatty acids or acyl groups and the very electronegative cysteine core:

 


Pam3Cys is a triacylated lipoprotein, the degree of acylation is equated with its toxicity.   So what is acylation?  It’s the zig-zaggy lines that mean Carbon-Carbon-Carbon, yes, hydrocarbons, like margarine or octane.  Exactly, the name just refers to the number of carbons in each carboxyl or acyl group.  Palmitic (the Pam in Pam3Cys) has X number of carbons, gasoline, 8, linoleic acids, like 14. Look up what are alkanes then add a COOH group and you have one of these fatty acids. 

Something highly acylated like this (3 or more fatty acids hanging off) are managed by Toll-like Receptor (TLR) 2 and TLR1, together.  Therefore a “TLR2/1-agonist” is another term that generally refers to lipoproteins like those from Borrelia, mycoplasma, mycobacteria, and others like Brucella.  (But they can manage other compounds.)

This thing, Pam3Cys and fungal lipid molecules like it, is shed with the blebs.  In other words, like this:
 

 
The likes of OspA is on these blebs.  They go to the brain, inflame it, get eaten up by immune cells - which renders them incompetent-, they go to the kidneys (LUAT), etc. You will find this to be so in an NIH-owned patent (5,217,872) and elsewhere.


So, the fungal antigens are on the shed blebs and they go everywhere and they render the immune cells incompetent, resulting in an AIDS-like disease.  Everyone who has Lyme disease also has LYMErix disease. 
 


 

8.) Cadavid and the NIH say these shed vesicles or blebs go to the brain and inflame it:

 

 

 

 

 

 

 

 

 

http://www.ncbi.nlm.nih.gov/pubmed/?term=Cadavid+and+borrelia+and+brain  

 

In other words, the NIH is saying that thanks to exposure to shed blebs with TLR2/1 agonists like OspA on them, the HLA molecules will be downregulated and that you will make no antibodies.  This mechanism is mimicked elsewhere, in other fungal diseases models.  It is also CALLED endotoxin tolerance.

 

Endotoxin Tolerance Inhibits Lyn and c-Src Phosphorylation and Association with Toll-Like Receptor 4 but Increases Expression and Activity of Protein Phosphatases.

“Endotoxin tolerance protects the host by limiting excessive 'cytokine storm' during sepsis, but compromises the ability to counteract infections in septic shock survivors. It reprograms Toll-like receptor (TLR) 4 responses by attenuating the expression of proinflammatory cytokines without suppressing anti-inflammatory and antimicrobial mediators, but the mechanisms of reprogramming remain unclear. In this study, we demonstrate that the induction of endotoxin tolerance in human monocytes, THP-1 and MonoMac-6 cells inhibited lipopolysaccharide (LPS)-mediated phosphorylation of Lyn, c-Src and their recruitment to TLR4, but increased total protein phosphatase (PP) activity and the expression of protein tyrosine phosphatase (PTP) 1B, PP2A, PTP nonreceptor type (PTPN) 22 and mitogen-activated protein kinase phosphatase (MKP)-1. Chemical PP inhibitors, okadaic acid, dephostatin and cantharidic acid markedly decreased or completely abolished LPS tolerance, indicating the importance of phosphatases in endotoxin tolerization. Overexpression of PTPN22 decreased LPS-mediated nuclear factor (NF)-x03BA;B activation, p38 phosphorylation and CXCL8 gene expression, while PTPN22 ablation upregulated LPS-induced p65 NF-x03BA;B and p38 phosphorylation and the expression of TNF-α and pro-IL-1β mRNA, indicating PTPN22 as an inhibitor of TLR4 signaling. Thus, LPS tolerance interferes with TLR4 signaling by inhibiting Lyn and c-Src phosphorylation and their recruitment to TLR4, while increasing the phosphatase activity and expression of PP2A, PTPN22, PTP1B and MKP1.
http://www.ncbi.nlm.nih.gov/pubmed/26457672
 

 

See more at:  http://www.actionlyme.org/151026_OCCAMS_RAZOR.htm