Expanded Version of the Cryme Explainer-Trainer from the Summer of 2012

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

01 Oct 2017

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1988 Steere says Lyme is like a B cell leukemia

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

CDC "SPIDER"

Fungal Exosomes Inhibit Apoptosis

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

RICO_filed_USDOJ

BlumenthalAntiTrust Lawsuit

Exosomes, Blebs

Spirochetal_Dementia

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

Pathogenic Fungi

Bush's warcrimes, Oct 2000

Trainer

170708

PLAUSIBLE DENIABILITY - NIAID's Anthony Fauci tries to say he had no idea what his LYMErix-HIV vaccine was (see more about that below, including the images of the 2 antigens, OspA and HIV gp120) because that research (what goes on on Plum Island) is classified:

"Or, in some cases, the work might need to be classified. Fauci notes that the NIH does not do classified studies. 'We would have to refer it to an agency that does classified research, because we don't,' he says."
http://www.npr.org/2012/03/30/149664035/policy-on-high-risk-biological-research-tightened

Policy On High-Risk Biological Research Tightened : NPR
www.npr.org

The government released a new policy on how to handle legitimate biological research that could be misused in the wrong hands. The move comes as controversy still swirls around recent experiments with lab-altered bird flu. See More

It was said in a Congressional Hearing (120717;14:30) that "Lyme is totally, 100% incurable - and spirochetes return."
http://foreignaffairs.house.gov/hearings/view/?1455

Steven "Stealth Bomber" Barthold: "100% of the animals remain infected after treatment... Naysayers say this is dead DNA, but we can transfer it to normal animals and get viable spirochetes [Mouse Infectivity Test and of course the older data] ... In my written testimony... (publication underway) shows that 12 months post treatment you see a resurgence of spirochetes in mice."

SAYS BARTHOLD: "The viability of noncultivable [it takes months not weeks to reculture spirochetes from the spheroplast form and of course, see the older data on the viability of the "granule" form] spirochetes in antibiotic-treated mice (demonstrable by PCR) was confirmed by transplantation of tissue allografts from treated mice into SCID mice, with dissemination of spirochetal DNA to multiple recipient tissues, and by xenodiagnosis, including acquisition by ticks, transmission by ticks to SCID mice, and survival through molting into nymphs and then into adults. Furthermore, PCR-positive heart base tissue from antibiotic-treated mice revealed RNA transcription of several B. burgdorferi genes. These results extended previous studies with ceftriaxone, indicating that antibiotic treatment is unable to clear persisting spirochetes, which remain viable and infectious, but are nondividing or slowly dividing." http://www.ncbi.nlm.nih.gov/pubmed/19995919

Dattwyler talking about the incurability of Spirochetal Diseases in 1988:

From: http://www.actionlyme.org/DODD_KENNEDY.htm -- Dodd and Kennedy knew what goes on on Plum Island which is why Dodd and Kennedy never did anything for us.

See more on the incurability of Lyme - by the crooks - here:
http://www.actionlyme.org/BRAIN_PERMANENT.htm

The Testing Ruse & the BIG PICTURE:

There is no such thing as "Lyme Disease;"

it's all simply Relapsing Fever.

Since the 1994 Dearborn conference/redefinition, when the IDSA/ALDF.com Lyme crooks say "Lyme Disease" (especially when perjuring themselves in court cases) that means, to them, "just the HLA-linked bad-knee."

These are the documents you need to demonstrate fraud and mass-murder, so
please copy them, save them, update them as they're updated, and study them:

Previous known and documented uses of bioweapons by the USA in recent history:

1) African Swine Fever (something Durland Fish studied for bioweapons potential on Plum Island) dumped on Castro's Cuba story in 1971 (look it up on Wikipedia), which is apparently not denied and of course,

2) what the Chinese reported about US dropping all kinds of bioweapons junk and bugs on China - including RELAPSING FEVER BORRELIA - during the Korean War (See more scientific data supporting Lyme as the original, unnatural outbreak area here>>: http://www.actionlyme.org/PIIB.htm )

Go to MedLine and enter borrelia and host-adapted:
http://www.ncbi.nlm.nih.gov/pubmed?term=%28%22borrelia%22%5BMeSH%20Terms%5D%20OR%20%22borrelia%22%5BAll%20Fields%5D%29%20AND%20host-adapted%5BAll%20Fields%5D&cmd=DetailsSearch

Those are all the people who know Lyme is simply a Relapsing Fever organism, that vaccines won't work, and that the Dearborn case definition is research fraud.

Host-adapted means the spirochete won't be expressing the same antigens it did when it was fresh out of a tick due to antigenic variation, which is the nature of the relapse in Relapsing Fever. That means you can't use the Dearborn protocol late in the disease even if Dearborn WASN'T research fraud.

"Lyme Disease" is a commercialized accidental release from Plum Island:

Compare the following from the Congressional Record re US Bioweapons with
the "single spirochete" outcome:

From: http://www.actionlyme.org/US_SELLS_IRAQ_BIOWEAPONS.pdf

Infection with a single spirochete results in limitless varieties, overwhelming the immune system:

Could the variety show of antigens produced by even a single
spirochete be responsible for the variety show of symptoms for
which Relapsing Fever is famous?

See Mark Klempner not use any scientifically valid biomarkers in his non-
repeat treatment study, while himself discovering one of those biomarkers, and reporting that OspA was responsible for autoimmunity against myelin (although Roland Martin thought it was OspC).

From: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC441260/pdf/bactrev00144-0058.pdf

See more at http://www.actionlyme.org/RICOCHRON.htm

CONCLUDE:
Spirochetes themselves overwhelm the immune system, per the bioweapon Congressional Record design protocol, but also, fungal antigens like OspA turn off the immune response and render its victims the Hostez with the Mostez - overwhelming the immune system with other infections. It is no surprise, really, that OspA is basically the same thing as HIV gp120 (we think the latter is OspA in triplicate and comes from some other microbe with which they experimented on Plum Island like mycoplasma or Brucella).

RECENT HISTORY re PORTON DOWN VS CRAZY EDDIE'S ANTICS IN 1986:

According to an employee of Porton Down (presumably Susan O'Connell) when confronted by a member of the UK House of Lords over whether or not Porton Down and the CDC were still working with Borrelia as a bioweapon, the employee at first tried to deny that they were experimenting with Borrelia as a bioweapon (see what happened in Korea and China during the Korean War). The UK Lord said, 'nonsense, don't lie to me about that,' essentially, and again asked the Porton Down employee if they were still studying Lyme as a bioweapon. The Porton Down employee then admitted that the accidental release "was given over to industry." Soon thereafter, Susan O'Connell either quit or was fired by the UK NHS (end of March, 2012).

We knew this anyway, and all along said,

"We do not care if Lyme was an accidental release, but we do not need to be the victims of the RETards who handled it afterwards. REtards who clearly did not know the first thing about Borrelia, relapsing fever and especially its surface antigens, as revealed by Crazy Eddie McSweegan in his 1986 letter to Senator Goldwater where he speaks about 'cloned ehrlichial ligands' (code language for Lyme vaccines). These "Lyme" Special Eddies did not know enough basic science to even look to see if other vaccines of the same type had been tried before and what the outcome was (Tuberculosis TLR2-agonist failed vaccines). They're so stupid, they did not know that the nature of the relapse in relapsing fever is that antibodies (and vaccines) do no good."

Says Crazy Eddie McSweegan to Senator Barry Goldwater in 1986:

TRANSCRIPT OF THE ABOVE:

"I'm certain that the DoD would attempt to make a case for its continued in-house research programs. Yet, the defense department does not feel the need to make its own fighter planes, or Christmas fruitcakes, or nerve gas, or acetylcholinesterase [nerve agent antidote, revealing what a nerve agent is]. Why then to they feel that they need to have their own programs to study the mechanisms of campylobacter diarrhea, or lectin-ligand interactions, or the cloning of rickettsial surface proteins genes [means making Lyme vaccines]? These are projects for university graduates, not Navy and Army lieutenants. If the DoD thinks these are topics of military importance they should be willing to fund the research in the form of grants to universities, and contracts to businesses [like the ALDF.com which then parasitized the IDSociety.org]. The end result would be a leaner, cheaper defense department and stronger universities and biotechnical businesses. Everyone would benefit." - Eddie Da Sweeg

You will see in the following documents on this homepage... and on 120702.htm, both the bioweapons evidence and the efforts of the Special Ed "scientists" (Susan O'Connell's "industry") who conspired to sell a vaccine that they knew did not prevent Lyme and for the basic capital investment (royalties and a monopoly on the national blood to pharm patentable goodies from all our blood, not just vector borne diseases data, but genetic bioweapons susceptibility data) for their stated enterprise, the ALDF.com

The following is a snippet of an advertisement that was on Corixa.com's website where we see Corixa/Yale/Imugen being awarded an NIH Biodefense contract for lying about the outcome of LYMErix. Corixa was later purchased by SmithKline, so all that 11.5 million dollars worth of USA biodefense data is now owned by a foreign company:

http://www.actionlyme.org/CORIXA_NIH_BIODEFENCE.pdf (full advertisement taken from Corixa's website)

Keep reading for more on Corixa, Yale's L2 Diagnostics, and Imugen (the cabal within the cabal)

DEARBORN AND EARLIER:

Steere's original, 1986, Lyme-diagnostic serology report which resulted in the 1990 CDC standard (and says Lyme is Relapsing Fever, and that the only valid antibody to use to detect all cases of Lyme was flagellin, or band 41):
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC423723/?tool=pubmed

A snippet from that 1986 report:

The above was mentioned at the 2001, Jan, FDA Meeting on LYMErix Adverse Events by Kathleen Dickson: "The standard changed at Dearborn, Lyme used to be considered Relapsing Fever according to Allen Steere, above, people with LYMErix Disease are like chronic Lyme victims, and that that could be because of the immunosuppression as per Mario Philipp (OspA results in the production of the immunosuppressive cytokine IL-10) and Ray Dattwyler's NK cell suppression studies):
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2.htm

1990 CDC Serology standard (same as Steere's 1986 report; means Lyme is Relapsing Fever):
1990 Case Definition for "Lyme Disease" was "Relapsing Fever"

Dearborn Invitations (connotes consensus, but it was not):
http://www.actionlyme.org/DEARBORNINVITATIONS.pdf

Dearborn, Who Approved:
http://www.actionlyme.org/Dearborn_Who_Approved.htm

Dearborn booklet (111 pages) showing no one agreed with Steere's proposal and who was on all the committees
http://www.actionlyme.org/DEARBORN_PDF.pdf

Gary Wormser's peer-reviewed assessment of Steere's Dearborn proposal where he says only 9/59 patients met the Steere/Dearborn criteria for IgG (85% of cases are missed):
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=266355&blobtype=pdf

Page 74 of the Dearborn booklet - Gary Wormser saying the Steere proposal sucked. Here is the full text of that assessment:
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=266355&blobtype=pdf

(missed 85% of the cases)

◄ Page 75 (Imugen's assessment = 14% accuracy of the Steere/Dressler antibody panel proposal) of the Dearborn booklet

◄ Page 76 (Wisconsin Lutheran's submission) of the Dearborn booklet:
IgG proposal detects 22% of the cases.

◄ Page 99 of the Dearborn booklet; Ron Schell:

"Dearborn is 15% accurate in IgG, or misses 85% of the cases," which was the same result as Imugen's and Gary Wormser's.

Nick Harris (Igenex, present at Dearborn and a participant) said Dearborn was 8% accurate. The rest were disqualified for one reason or another, including MarDx, UConn, and the CDC (who submitted a mouse antibody result, duh).

So, of the accuracy assessments of the Dressler/Steere proposal (based on research fraud) were:
15% (Wormser),
14% (Imugen),
22% (Lutheran Hosp),
8% (Igenex)
15% (Ron Schell, State of Wisconsin)

Average, 14.8%, or Dearborn misses 85% of the cases of "Lyme" and this was deliberate.

"Steere in Europe" [the other 1992 report missing from Dearborn booklet which shows the research fraud where OspA (band 31) and B (band 34) are left out of the Dearborn diagnostic standard panel http://www.actionlyme.org/STEERE_IN_EUROPE.htm (look at the ELISA cutoffs, this is clearly fraud)];

What it says in the report: http://www.ncbi.nlm.nih.gov/pubmed/8106763 (Antigens in Europe, as I call it):

“The group 1 strain of B. burgdorferi, G39/40, used in this study and in the previous study of US patients was isolated from an Ixodes damini tick in Guilford, Connecticut [21]. The group 2 strain, FRG [Federal Republic of Germany], was isolated from Ixodes ricinus near Cologne [22]. The group 3 strain, IP3, was isolated from Ixodes persulcatus near Leningrad [23]. All three strains used in this study were high passage isolates, which were classified by Richard Marconi (Rocky Mountain Laboratory, Hamilton, MT) using 16S ribosomal RNA sequence [revealing that he knows the OspA gene is the shell game] determination as described [11, 24]. The recombinant preparations of OspA and OspB used in this study were purified maltose- binding protein-Osp fusion proteins derived from group 1 strain B31 [25]. The fusion proteins contained the full-length OspA or OspB sequence without the lipid moiety or the signal sequence -" [OspA and B (encoded on the same plasmid) will not be seen in antibody-response without the lipids attached to the Osps. This was how OspA and B were left out of the Dearborn panel - pure research fraud.]

CDC staff (Barbara Johnson) patents (5 of them) from 1992 in Europe with SmithKline explaining that there are 2 kinds of Lyme, the HLA-linked and the non-HLA linked, meaning the same crooked characters who were there at the Dearborn conference, knew the outcome was scientific fraud and that it served their own patent interests for Lyme to be the fake disease it is now (high antibody concentration). There can be no vaccines or antibody tests other than flagellin for Relapsing Fever:
http://www.wikipatents.com/CA-Patent-2135800/compositions-useful-in-diagnosis-and-prophylaxis-of-lyme-disease

CDC's (Barbara Johnson) final (Dearborn) serology standard (No OspA and B, bands 31 and 34, which are encoded on the same plasmid)
http://wonder.cdc.gov/wonder/prevguid/m0038469/m0038469.asp

CDC's Barbara Johnson was present at Dearborn and approved a standard she knew was false and she did so to suit her own "patents in Europe with SmithKline" bottom line:
http://www.actionlyme.org/Dearborn_Who_Approved.htm
http://www.actionlyme.org/CDCS_PARTICIPATION_IN_LYME_CRIMES.htm

CDC Crooks (Barbara Johnson) say in their 5 European patents with SmithKline: "Certain of these antigens are characterized as being B. burgdorferi B31 strain specific and major histocompatibility complex (MHC) nonrestricted [these would be all the cases that are not "Bad-Knees-Only']. Certain other of these antigens are characterized as being MHC restricted [these would be all the cases of Dearborn-Positive-Bad-Knees-Only]...."

CONCLUSION: Lyme used to be considered Relapsing Fever and this was independently observed by Allen Steere, who said in 1986 that one only needed band 41 (flagellin) to be diagnosed with Lyme. The CDC then sent Steere on a junket to Europe to narrow the disease definition the same year other CDC staff (Steere became a CDC officer to avoid the draft and also, he's not too bright) claimed patents with SmithKline in the European patent database. Those CDC/SmithKline European patents identify two kinds of Lyme: 1) Steere's HLA-linked "bad-knees" and 2) the other, Great Imitator, seronegative outcomes.

The Great Imitator Neurologic Lyme outcomes are thrown out of the standard at the Dearborn Conference and only the Bad Knees (HLA-linked hypersensitivity or allergy response) outcome can be detected.

We find later that fungal antigens carried by borrelia - like OspA - are themselves responsible for the Great Imitator outcomes in that they appear to inhibit apoptosis in EBV-infected cells, and tolerize to fungal infections in the blood, which contribute to fatigue. Paralyzing fatigue is characteristic of late, chronic, neurologic Lyme.

WHO-DID-WHAT, ONCE OspA and B WERE DROPPED FROM THE STANDARD

1995- Mayo Clinic's David Persing and Yale's Robert Schoen's RICO (monopoly) strain (dropped OspA and B, but was determined to be burgdorferi via the DNA/RNA shell game) report:
http://jcm.asm.org/cgi/reprint/35/1/233?view=long&pmid=8968914

1995- Persing and Schoen's RICO strain and monopoly patent on post-LYMErix blood patent:
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=6045804.PN.&OS=PN/6045804&RS=PN/6045804
"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....

"The present invention provides a method useful to detect a B. burgdorferi infection in a subject. The method provided by the invention is particularly useful to discriminate B. burgdorferi infection from OspA vaccination, although it is sufficiently sensitive and specific to use in any general Lyme disease screening or diagnostic application. Thus, the method of the invention is particularly appropriate for large scale screening [THE MONOPOLY- this has implications for the current situation where this cabal now contracted with the Red Cross for a do-over of the same fraud-monopoly crime; they are interested only in patentable goodies in the blood while lying about everything else] or diagnostic applications where only part of the subject population has been vaccinated or where the vaccination status of the population is unknown. "

Evidence that Corixa, Imugen and Yale's L2 Diagnostics were officially SEC "partners"
https://groups.google.com/forum/?hl=en&fromgroups#!topic/sci.med.diseases.lyme/D6v-QHQdMbc

Evidence that Corixa did the advertising for the Corix-Imugen-L2 Diagnostics ("partners") cabal
https://groups.google.com/forum/?hl=en&fromgroups#!topic/sci.med.diseases.lyme/cy9beTF_Uqs

Evidence that the Yale Endowment Fund funded the former Yale Lyme and Lupus clinic, "L2 Diagnostics"
http://www.actionlyme.org/LYME_CORRUPTICUT.htm

Proof that Corixa's newest model of adjuvant was NOT tri-lipidated. Persing's company, Corixa, advertising selling a new form of OspA-adjuvant, monophosphoryl A, which is meant to be a mono-acyl version of OspA-the adjuvant, but not so toxic as OspA.
http://www.actionlyme.org/EMBASSIES_CORIXA_TLR_13_JULY_06.htm

CONCLUSION: We speculate that Steere is involved with Imugen financially and his payoff for putting his name on the Dressler/Steere falsified serology reports was an official partnership with Corixa and Steere's pal Robert Schoen at L2-Diagnostics, Yale's former Lyme and Lupus Clinic. Corixa, Imugen and L2 Diagnostics intended a monopoly on all blood in the United States after LYMErix was approved and on the market because in that national monopoly on blood would be new vector-borne diseases' DNA to patent. That blood-supply-monopoly also holds bioweapons value (HLA-differences among peoples) as you can see from the activities of the Russian scientists who publish in association with the ALDF.com cabal at New York Medical College, Valhalla, NY:
http://www.actionlyme.org/BOGUS_RUSSIAN_NYMC_ARTICLES.htm

May 2012: GARY WORMSER TALKING ABOUT HOW LYME AND LYMERIX CAUSE IMMUNOSUPPRESSION
AND SERONEGATIVE DISEASE (Note that if Wormser owns stock in Abbott- they won't produce a real
test for Lyme; an Abbott representative was at the Congressional Hearing 120717.):

Here we see Gary Wormser talking about immunosuppression from Lyme and LYMErix, yet how could that be if he also insists the Dearborn standard is real,... and subsequently Klempner's Non-Retreatment non-study, upon which the IDSA "guidelines" are based?

The crux of the crime is the Dearborn diagnostic standard.

FROM: http://onlinelibrary.wiley.com/doi/10.1002/art.34386/abstract;jsessionid=2BD998A181EC0AFF3A0F95E13D84B34F.d02t02

Note that Gary Wormser above discusses the mechanism of seronegative Lyme and the resultant immunosuppression
from exposure to OspA either thru blebbing or vaccination, resulting in LYMErix Disease being the
same disease as Chronic Lyme/Great Imitators:

Tolerance induced via TLR2 and TLR4 in human dendritic cells: role of IRAK-1

"Such tolerance of primary dendritic cells after TLR- ligation in settings of infection will likely contribute to a reduced immune response, which may be detrimental but could also be beneficial in that an over-reaction of the immune system is avoided."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628880/?tool=pubmed

And

Toll-Like Receptor 2 Deficiency Results in Impaired Antibody Responses and Septic Shock during Borrelia hermsii Infection
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2976319/?tool=pubmed

If LYMErix Disease is the same as Lyme Disease, it follows that A) the diagnostic standard of hypersensitivity and arthritis, alone, must be false, and B) the Lyme crooks falsified their vaccine outcomes as well as the Dearborn case definition, since the Dearborn case definition was claimed to have been used to assess the 2 OspA vaccines (where it was claimed that they were "76 and 92% safe and effective").

So why all these chronic lies? The crooks claimed Klempner's Non-long-term Non-retreatment Non-study was real merely in an effort to maintain the first lie, Dearborn.

They don't want to be prosecuted for the first lie, Dearborn, because that is a genocide charge.

THE ONLY SCIENTIFICALLY VALID ANTIBODY TEST FOR RELAPSING FEVER (flagellin, a non-variable antigen):

1991 Fikrig and Flavell's scientifically valid antibody test for B burgdorferi Relapsing Fever:
http://iai.asm.org/content/59/10/3531.full.pdf+html?view=long&pmid=1894359

1993 Fikrig and Flavell's scientifically valid antibody test patent (5,618,533)
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=5618533.PN.&OS=PN/5618533&RS=PN/5618533

1992 Fikrig and Magnarelli improve the above Fikrig Bb-Specific Flagellin test, by spiking in extras Bb-Specific Flagellin to capture cases of low flagellar antibody concentration (which is what happens in real validations):
http://www.ncbi.nlm.nih.gov/pubmed/1280650

See the Scientific Validity Powerpoint that discusses the above Bb-flagellin, increasing-sensitivity event:
http://www.actionlyme.org/SV_PPT_2.htm

FDA Criteria for Methods Validations, showing that one must improve/demonstrate the lowest quantity of analyte (Bb flagellar antibody in this case) http://www.fda.gov/downloads/Drugs/GuidanceComplianceRegulatoryInformation/Guidances/ucm122858.pdf

In a case of scientific fraud performed by Arthur Weinstein, he calls this a validation:

Western blot band intensity analysis. Application to the diagnosis of Lyme arthritis.
http://www.ncbi.nlm.nih.gov/pubmed/8053960

Here, Arthur Weinstein pretends he invented a chromatography detector:
http://www.actionlyme.org/CONNOLLY_FISH_WEINSTEIN.htm

More on the role Weinstein played in the fraud:
http://www.actionlyme.org/ARTHURWEINSTEIN.htm

Fikrig and Flavell's LYMErix OspA patent
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=5747294.PN.&OS=PN/5747294&RS=PN/5747294

See the PowerPoint Presentation here to see where Yale and the CT Dept of Agriculture spiked the Borrelia mix with extra flagellin to detect cases of Lyme where the antibody concentration is LOW - one of the goals and attributes of a scientifically valid method (FDA rules):
http://www.actionlyme.org/CRYMEDISEASE_CHP1.htm
Please see the PowerPoint Explainer on Scientific Validity:
http://www.actionlyme.org/SV_PPT_2.htm

The species determinant = Flagellin, See the Taxonomy database:
http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=138&lvl=3&lin=f&keep=1&srchmode=1&unlock

Barbour and NIAID say band 41 - generic - is valid to diagnose all Borreliae (H9724)
A Borrelia-specific monoclonal antibody binds to a flagellar epitope.

YALE AND ALAN BARBOUR SAY THERE CAN BE NO Osp-BASED VACCINES AGAINST RELAPSING FEVER

Fikrig and Flavell's report where they show LYMErix would not work because Lyme is Relapsing Fever ("selection pressure")
http://www.actionlyme.org/SELECTION_PRESSURE_NO_VACCINE_POSSIBLE.htm
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC173206/pdf/631658.pdf|

Alan Barbour in 1992 reported that OspA, too, undergoes antigenic variation and therefore could not have been a vaccine
http://www.actionlyme.org/BARBOUR_MUTANTS_1992.htm

Alan Barbour discussing antigenic variation in general and what that means re diagnostics and vaccines (can't):
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627965/?tool=pubmed

Andrew Pachner (formerly at Yale) Discussing...:
http://www.actionlyme.org/PACHNER_BRAINS_1990.htm :

"The plasmid content of N40Br was different from that of the infecting strain implying either a highly selective process during infection or DNA rearrangement in the organism in vivo. "

Discussing ▲ antigenic variation; meaning, you can't Western Blot someone with late Lyme with a tick fresh out of a tick, due to antigenic variation or what the crooks call host-adaptation. This means Dearborn is moot, and especially Klempner.

CONCLUSION: Fikrig and Flavell own the patents to Fla-burgdorferi and LYMErix OspA, and Barbour owns the patent for the ImmuLyme OspA vaccine, yet here they are saying the very idea is nonsense. Neither advised to stop the vaccine trials which were underway by 1993. Lyme is Relapsing Fever.

THE YALE, CORIXA, IMUGEN CABAL KNEW LYMErix (OspA) CAUSED A CHRONIC-LYME-LIKE ILLNESS

1) Yale's Robert Schoen says in 1998 not to test LYMErix victims and minimizes their symptoms knowing chronic Lyme is identical to what Schoen says is "nonspecific" because the exact reverse statement is in the Corixa-RICO patent "multisystem complaints characteristic of late Lyme", This is that textbook:
http://www.amazon.com/Lyme-Disease-Key-Diseases-Series/dp/0943126584/ref=sr_1_fkmr0_2?ie=UTF8&qid=1341914626&sr=8-2-fkmr0&keywords=lyme+disease+rhan+and+evans

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

2) Dave Persing discussing why you should not use the native or original Osps as vaccines (and Robert Schoen would know this too):
http://www.actionlyme.org/STEALTH_DISABLERS.htm

"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/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=/netahtml/PTO/srchnum.htm&r=1&f=G&l=50&s1=6,800,613.PN.&OS=PN/6,800,613&RS=PN/6,800,613
http://www.actionlyme.org/EMBASSIES_CORIXA_TLR_13_JULY_06.htm

3) Persing and Schoen's RICO strain and monopoly on post-LYMErix blood patent
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=6045804.PN.&OS=PN/6045804&RS=PN/6045804

"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....

4) the Corixa ad where they sell a new adjuvant product that is not a TLR2-agonist > bottom of this page)
http://www.actionlyme.org/CORIXA_NIH_BIODEFENCE.pdf

5) SmithKline bought Corixa to keep all that OspA-failure-and-harm data proprietary.

6) The Phase IV of the LYMErix trial. Schoen says the adverse events were as described by Allen Steere, which means he does not consider the Chronic Neurologic Lyme outcomes of LYMErix. Please read the whole report carefully: OspA_4.htm

7) Fish and Barbour in 1993 report start their psychiatric spin, while admitting the Phase I and Phase II trials of the OspA vaccines were underway. From this you can tell they knew OspA caused one what are now known as wastebasket diagnoses:
http://www.actionlyme.org/BarbourFishpdf.pdf

Munchausen's accusations against people they clearly knew were sick (1998) in this book:
http://www.amazon.com/Lyme-Disease-Key-Diseases-Series/dp/0943126584/ref=sr_1_fkmr0_2?ie=UTF8&qid=1341914626&sr=8-2-fkmr0&keywords=lyme+disease+rhan+and+evans

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

On the previous page of this Munchausen's book:

Study hard, my people. These douchebags are going to jail and this is why...

Steere says "seronegative Lyme is a conflict in terms when talking about arthritis" meaning that after the Dearborn conference,
"Lyme Disease" officially became the arthritis, only (in the Munchausen's/Schoen lies book here>>
http://www.amazon.com/Lyme-Disease-Key-Diseases-Series/dp/0943126584/ref=sr_1_fkmr0_2?ie=UTF8&qid=1341914626&sr=8-2-fkmr0&keywords=lyme+disease+rhan+and+evans

Seronegative Lyme disease is a subtle, attenuated illness, says Steere, in 1998. He means "low antibody concentration" - see the Western Blots in the RICO complaint to see the difference: http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm

Steere was at this 1994 FDA meeting:

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

Steere says Lyme is like Syphilis at that same meeting:

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

1989 IDSA Reviews, Special Supplement on Spirochetal Diseases (you have to look at all of them)
http://www.actionlyme.org/CHP_9_IDSA_REVIEWS.htm

Paul Duray twice reports that chronic Lyme victims have mutated B cells (1989, IDSA's Journal and 1992, Schutzer's book)
http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm
http://www.actionlyme.org/Duray.htm

Dattwyler and Luft report that one has to look for new IgM bands (the old standard) in order to diagnose Lyme
(1992, Schutzer's book)

http://www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770

Trinity Biotech bought MarDx (Jeremy Gray is in Dublin; Gray is criminal partners with Susan O'Connell at Porton Down/ UK's NHS) to keep all the OspA vaccines trial data (unreadable blots) out of the United States.

Dave Persing and Lenny Sigal report that the Western Blots of OspA vaccinated people assessed with MarDx were unreadable (blot smudging is due to the fact that the OspA molecules were not micellized enough by the carrier; people were injected with blobs of various sized lipids, resulting in all the strokes associated with the Phase III vaccine trial
http://www.journals.uchicago.edu/doi/pdf/10.1086/313920

Robert Schoen reports in the Phase III & IV LYMErix trial that tons of people died (vascular events) or were made sick or got cancer (OspA helps activate Epstein-Barr), and this would be because OspA sticks to itself, as also reported by the Koreans when they reported that the HIV gp120 antigen is the same thing as LYMErix (triacyl lipopeptide).
http://www.actionlyme.org/OspA_IV.htm
Korean Pam3Cys = HIVgp120 PDF

These are the essentials to demonstrate fraud over the testing and that the intention of it was to falsify the vaccines outcomes and changed the definition of the disease to "arthritis" or hypersensitivity, alone, and as shown in the RICO complaint to the USDOJ http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm

Look at the blots in the RICO complaint. This crime is so obvious....

TRAINING:

The IDSA "Guidelines," based on the 2001 bogus Klempner non-re-treatment article, are "Offense as the Best Defense" against a charge that the Dearborn "case definition," was FRAUD and a homicide charge.

◄THE IDSA CRAZY-WHEEL - A Brief History, from 1986 to 2012, where Clifford Harding reports on: 1) the mechanism of Steere's Dearborn "Only-Bad-Knees-Disease," 2) How OspA and Lyme turn off the antibody response, and 3) Harding mentions something like Fungal-Viral Synergy is going on in other diseases. And Allen Steere doesn't discover anything. Ever.

THE FOLLOWING 3 ARTICLES RELATED TO THE IDSA CRAZY WHEEL- THIS IS CLIFFORD HARDING DESCRIBING THE MECHANISMS OF ALL OUTCOMES OF LYME AND LYMERIX EXPOSURE (FUNGI):

Clifford Harding, 2010 on the 37 year old mystery of "Steere's Bad Knees":
Mycobacterium tuberculosis synergizes with ATP to induce release of microvesicles and exosomes containing major histocompatibility complex class II molecules capable of antigen presentation. http://www.ncbi.nlm.nih.gov/pubmed/20837713

Clifford Harding in 2000 reveals why Lyme is seronegative and OspA does not produce antibodies:
"Despite the ability of MTB 19-kDa lipoprotein to activate microbicidal and innate immune functions early in infection, TLR 2-dependent inhibition of MHC-II expression and Ag processing by MTB 19-kDa lipoprotein during later phases of macrophage infection may prevent presentation of MTB Ags and decrease recognition by T cells. This mechanism may allow intracellular MTB to evade immune surveillance and maintain chronic infection. http://www.jimmunol.org/cgi/content/full/167/2/910

Clifford Harding on Fungal-Viral Synergy or Lyme and LYMErix activating Epstein-Barr/Similars, 2012:
TLR2 [fungi, like OspA or Lyme antigens] Signaling Depletes IRAK1 and Inhibits Induction of Type 1 by TLR7/9 (viruses)--
http://www.ncbi.nlm.nih.gov/pubmed/22227568

See more at: CV Harding and LYMErix-Disease

TERMINOLOGY:
http://www.youtube.com/playlist?list=PL7A9646BC5110CF64&feature=plcp
Kahn Academy B Cells http://www.youtube.com/watch?v=Z36dUduOk1Y&feature=relmfu
Kahn Academy Overview of Adaptive and Innate Immunity
http://www.youtube.com/watch?v=rp7T4IItbtM&feature=relmfu

Review of Dearborn
http://www.actionlyme.org/DEARBORNINVITATION.pdf
http://www.actionlyme.org/DEARBORN_PDF.pdf
EXACTLY how Steere falsified the test (no-OspA-B) http://www.actionlyme.org/STEERE_IN_EUROPE.htm

The Corixa-Yale RICO, and the CDC's Patents
http://www.actionlyme.org/CENTRAL_LYME_RICO_PATENTS.htm

PROOF that Corixa-Yale knew OspA caused systemic illness:
1) Schoen in the "Munchausen's" book discussing chronic Lyme, but blaming the victim,
2,3) the two Corixa patents,
4) the Corixa ad where they sell a new adjuvant product that is not a TLR2-agonist > bottom of this page)

1) http://www.actionlyme.org/SCHOEN_INSTRUCTING_DOCS_TO_BLOW_OFF_LYMERIX_INJUREES.htm

2) "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/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=/netahtml/PTO/srchnum.htm&r=1&f=G&l=50&s1=6,800,613.PN.&OS=PN/6,800,613&RS=PN/6,800,613

3) "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=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6045804.PN.&OS=PN/6045804&RS=PN/6045804

4) http://www.actionlyme.org/CORIXA_NIH_BIODEFENCE.pdf The TLR2-agonist OspA, they found, was too toxic so they were going with a TLR4-agonist in their new Adjuvant business.

Lyme is Relapsing Fever (Taxonomy Database, Basic Genetics)
http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=138

Yale's Valid Antibody testing http://www.actionlyme.org/CRYMEDISEASE_CHP1.htm

Barbour and NIAID say band 41 - generic - is valid to diagnose all Borreliae (H9724)
A Borrelia-specific monoclonal antibody binds to a flagellar epitope.

CONCLUSION: Lyme is Relapsing Fever; they falsified the test so that only the HLA-linked hypersensitivity response is allowed to be a "case;" they knew all along how to diagnose especially EARLY Lyme or any Relapsing Fever organism via flagellin antibody; Schoen, Persing, Steere and Molloy (Imugen) knew all along that LYMErix vaccination produced a chronic-Lyme-like illness but they trashed LYMErix victims the same way they trashed Chronic Lyme (formerly called Relapsing Fever, the name implying chronicity) victims.

The History of Relapsing Fever
http://www.actionlyme.org/RICOCHRON.htm

http://ijs.sgmjournals.org/content/46/4/898.long

Plum Island and Durland Fish:
http://www.actionlyme.org/PIIB.htm
(Durland Fish playing with African Swine Fever Virus in new bugs)

Here is how this anserina adapted to the Ixodid ticks as explained by Willy Burgdorfer and Alan Barbour, both bioweaponeers
who worked at the NIH's Rocky Mountain Bioweapons Lab:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC217620/pdf/jbacter00247-0414.pdf
[Bacteriophage-delivered DNA; possibly from Brucella or mycoplasma in the case of acquiring OspA; See the Plum Island
Chapter of Cryme Disease for more details: http://www.actionlyme.org/PIIB.htm on TLR2-agonists in ticks (Joe Tully, etc)]
OspA allowed this spirochete to penetrate the hard body of the hard-body tick.
See http://www.actionlyme.org/BURGDORFER_CYST.htm for more data related.)

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC228430/pdf/332427.pdf

Blumenthal AntiTrust Subpoenaed all IDSA's Self-Incriminating documents, but for a year and half,
the crooks refused; those documents were:

IDSA reports that Lyme is incurable with about 20 articles of their own:
http://www.actionlyme.org/BRAIN_PERMANENT.htm

Patents and Alan Barbour http://www.actionlyme.org/CENTRAL_LYME_RICO_PATENTS.htm and flagella-less borrelia patent and statements about antigenic variation in OspA and in other VBDs (meaning vaccines and test kits are useless)

Scientifically Valid Biomarkers Discovered by the Crooks and Mark Klempner http://www.actionlyme.org/BIOMARKERS.htm http://www.actionlyme.org/MKLEMPNER.htm ; Klempner does not use the valid biomarkers- including one of his own, MMP-130, to assess the standard of care (and not retreatment) 4.7 million dollar study which is the basis of the "guidelines."
This is research fraud of the psychiatric "check-list" type.

CDC reports that Borreliae are intracellular http://www.ncbi.nlm.nih.gov/pubmed/17045505

Klempner reports that Borreliae are intracellular http://www.actionlyme.org/MarkKlempner_Fibroblasts.htm

IDSA Reviews http://www.actionlyme.org/CHP_9_IDSA_REVIEWS.htm
(There are numerous reports, here, and they all have to be looked at, because it is the crooks claiming Lyme is the New Great Imitator, and does not just produce "bad-knee")

IDSA's Other Patent Claims http://www.actionlyme.org/CENTRAL_LYME_RICO_PATENTS.htm

IDSA's Treatment Failure Data http://www.actionlyme.org/IDSA_TMTFAILS.htm ("fails in half the cases")
http://www.actionlyme.org/BRAIN_PERMANENT.htm (about 20 reports, total)

Evidence that the crooks are playing a DNA/RNA shell game: http://www.actionlyme.org/PRIMERSHELLGAME.htm

Gary Wormser's peer reviewed article about how Dearborn detected 15% of the cases
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=266355&blobtype=pdf

Gary Wormser's peer-reviewed article about how OspA was immunosuppressive
http://www.ncbi.nlm.nih.gov/pubmed/10865170

UConn's Justin Radolf and Clifford Harding discover that OspA is Pam3Cys and causes
A) immunosuppression and
B) Steere's HLA-linked hypersensitivity response (see also Dave Dorward)
http://www.actionlyme.org/101016/htm
http://www.actionlyme.org/PIIB.htm

Ray Dattwyler and Allen Steere discuss seronegative Lyme (NK Cell Suppression)
http://www.actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm
http://www.actionlyme.org/STEERES_SERONEG_LYME_ASSAY.htm

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

Paul Duray publishing for IDSA (EBV and cancerous B cells) 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.actionlyme.org/IDSA_CLINIPATH_DURAY.htm

"Immature B cells can also be seen in the spinal fluid.
These cells can appear quite atypical- not unlike those
of transformed or neoplastic lymphocytes." --

--1989, IDSA's Journal

CONCLUSION: The Klempner "retreatment" article is research fraud and can be thrown out. They all proved Relapsing Fever is a permanent infection of the brain, and intracellular. The "guidelines," based on Klempner, were merely an attempt to reinforce the notion that the Dearborn diagnostic standard was real and valid.

[Evidence for Mouse Gammaherpesvirus being transmitted by ticks:
http://www.ncbi.nlm.nih.gov/pubmed?term=21732020 ]

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

Plum Island and Bioweapons data:

http://www.actionlyme.org/PIIB.htm and
http://www.actionlyme.org/120702.htm (Congressional Record re what would be the characteristics of a bioweapon - delayed response, stealth, no antibodies & "overwhelm" the immune system; that happens to be exactly what OspA does.)

CDC writes "bogus articles" http://www.actionlyme.org/120305_CDC_BOGUSARTICLES.htm

Durland Fish writes "bogus articles" http://www.actionlyme.org/TICK_BITE_CONSPIRACY.htm

Russians at NYMC write bogus articles about intracellular spirochetes and the spheroplast form, while being interested in the HLA-haplotypes of peoples from all sorts of nations (this is bioweaponeering and disease-spin to hide what really is a bioweapon/stealth disabler)
http://www.actionlyme.org/BOGUS_RUSSIAN_NYMC_ARTICLES.htm

McSweegan reveals he stalked and harassed me, Karen Forschner (Lyme.org), and Janice Beers :
http://www.actionlyme.org/SWEEG_WATCH.html
http://www.actionlyme.org/McSweegan_Relentless.htm

More evidence of Victim-Blaming and Anonymous Internet Harassment (a federal cryme) of Lyme victims:
http://www.actionlyme.org/GOLDWATER_LETTER.htm

McSweegan discusses his trip to an Israeli Bioweapons Plant
http://groups.google.com/group/scilyme2/browse_thread/thread/97145b659573ba9d/91f61251f09c793f?hl=en&lnk=gst&q=double-oh#91f61251f09c793f

John Dunn at Brookhaven and the discussion of Lyme, stealth disablers and MS all in the same paragraph. http://www.actionlyme.org/JohnDunn_Brookhaven.htm

Evidence for OspA/Lyme and EBV inhibiting apoptosis (potential synergy)

http://www.actionlyme.org/101016.htm -- Lyme is the New AIDS.

What we know about what goes on on Plum Island:
http://www.actionlyme.org/PIIB.htm (mycoplasma and mycobacteria turning off the immune response, fungi as stealth disablers, Stinking Smut)

Gary Wormser's peer-reviewed article about how OspA was immunosuppressive
http://www.ncbi.nlm.nih.gov/pubmed/10865170

Dattwyler and Steere discuss seronegative Lyme (NK Cell Activity Suppression)
http://www.actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm
http://www.actionlyme.org/STEERES_SERONEG_LYME_ASSAY.htm

Evidence for Mouse Gammaherpesvirus being transmitted by ticks:
http://www.ncbi.nlm.nih.gov/pubmed?term=21732020

Lyme/LYMErix Cryme Reveals New Paradigm in Health/Disease:
"Bacterial/Viral Coinfections"; TLR2 (fungi)Signaling Depletes IRAK1 and Inhibits Induction of Type 1 by TLR7/9 (viruses)-- -CV Harding, 2012

Chapter 5 of "Cryme Disease",

The RNA and DNA Primers Shell Game- where the crooks use one set of primers to indentify spirochetes to patent, but another to find "NOT-LYME" in humans :)))

Background:

A) The Klempner - No-DNA/RNA-primers-listed-in-the-Method - report; Mass Medical Society (publishes the New England Journal of Medicine, wherein Klempner reported his nonsense "retreatment" "study") never noticed that Klempner did not report what primers he used to exclude people who were DNA positive in spinal fluid (yes, there were some, we know of one person who was excluded).

B) CDC officer Alan Barbour (owner of the ImmuLyme OspA vaccine) reports in 1992 that like all other antigens in Relapsing Fever spirochetes, OspA undergoes antigenic variation or "selection pressure" (means vaccines and antibody testing based on variable surface anitgens are useless): BARBOUR_MUTANTS_1992.htm :

Note that this is GENETIC variation of the OspA gene, meaning an OspA primer is useless for detecting Lyme in humans or anything else. It means Lyme is just Relapsing Fever. It also means Barbour knew his OspA vaccine was a joke.

C) Yale's Erol Fikrig (owner of Yale's OspA/LYMErix vaccine) reported that due to antigenic variation and selection pressure, OspA, one of the variable surface antigens in Lyme Relapsing Fever would be useless as a vaccine.

Note: The antigens vary in ticks and in mammals. Therefore, you have to use non-variable antigens if you are to perform an antibody test, and guess what, Yale developed such an accurate and specific test in 1991: CRYMEDISEASE_CHP1.htm

Please see the PowerPoint Explainer on Scientific Validity:
http://www.actionlyme.org/SV_PPT_2.htm

The PPT shows that Yale and others are completely aware and certain that the only scientifically valid antibody test for Lyme is flagellin, and the current NIH Lyme Program Officer not only agreed with me, but said we should be using all the recombinant flagellin from all the borreliae to detect "Lyme" (real name of the disease is Relapsing Fever).

"Lyme Disease" is a ruse. When the crooks use that phrase, they are talking about their own, Dearborn, re-definition of "autoimmune arthritis in a knee."

ILADS.org does not give you this information for 2 reasons: 1) the concept of scientific validation would backfire on a bunch of psychiatrists, and 2) they simply aren't trained scientists (which is the same as the first reason).

1) [GARY WORMSER] Genetic diversity of Borrelia burgdorferi in lyme disease patients as determined by culture versus direct PCR with clinical specimens:

Liveris D, Varde S, Iyer R, Koenig S, Bittker S, Cooper D, McKenna D, Nowakowski J, Nadelman RB, Wormser GP, Schwartz I.

Departments of Biochemistry and Molecular Biology, New York Medical College, Valhalla, New York 10595, USA.

Two hundred seventeen isolates of Borrelia burgdorferi originally cultured from skin biopsy samples or blood of early Lyme disease patients were genetically characterized by PCR-restriction fragment length polymorphism (RFLP) typing of the 16S-23S ribosomal DNA intergenic spacer. Three major RFLP types were observed. Of the cultured isolates, 63 of 217 (29.0%) were type 1, 85 of 217 (39.2%) were type 2, and 58 of 217 (26.7%) were type 3; mixtures of two RFLP types were obtained in 6.0% (13 of 217) of the cultures. Comparison of typing of B. burgdorferi performed directly on 51 patient skin specimens with typing of cultures originally isolated from the same tissue revealed that a much larger proportion of direct tissue samples had mixtures of RFLP types (43.1% by direct typing versus 5.9% by culture [P < 0.001). In addition, identical RFLP types were observed in only 35.5% (11 of 31) of the paired samples. RFLP type 3 organisms were recovered from blood at a significantly lower rate than were either type 1 or type 2 strains. These studies demonstrate that the genetic diversity of B. burgdorferi patient isolates as determined by cultivation differs from that assessed by PCR performed directly on patient tissue.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=9986813

2) Yale's Robert Schoen discussing how the species determinant is not the OspA gene, but RNA:

http://jcm.asm.org/cgi/reprint/35/1/233?view=long&pmid=8968914

3) When CDC officer Alan Barbour patented Masters' Disease, he went straight for the flagellin DNA, since he knows that is the species determinant, and not the OspA gene:

1996 B. theileri patent (Master's Disease is Cow Relapsing Fever) Alan Barbour patent application for Masters' Disease 5,932,220

4) Here Gary Wormser uses the correct RNA to determine that 2/9 people with Lyme rashes still had spirochetes in their skin after treatment for tick attachment:

http://jcm.asm.org/cgi/reprint/30/12/3082?view=long&pmid=1452688

5) Here Durland Fish uses the correct RNA to determine that spirochetes were present (he did not use the OspA gene, which is used by the crooks on humans to determine "NO LYME"):

"PCR.

"To identify the Borrelia genospecies and to detect Borrelia double infections within the produced tick batches, ticks were analysed by PCR using Borrelia genus-specific amplification of 16S rDNA and subsequent dot-blot hybridization.

http://mic.sgmjournals.org/cgi/content/full/147/6/1425?view=long&pmid=11390674

6) And of course, the ever-infamous...:

..."Steere in Europe" [the other report missing from Dearborn booklet which shows the research fraud where OspA (band 31) and B (band 34) are left out of the Dearborn diagnostic standard panel http://www.actionlyme.org/STEERE_IN_EUROPE.htm (look at the ELISA cutoffs, this is clearly fraud)];

What it says in the report: http://www.ncbi.nlm.nih.gov/pubmed/8106763 (Antigens in Europe, as I call it):

“The group 1 strain of B. burgdorferi, G39/40, used in this study and in the previous study of US patients was isolated from an Ixodes damini tick in Guilford, Connecticut [21]. The group 2 strain, FRG [Federal Republic of Germany], was isolated from Ixodes ricinus near Cologne [22]. The group 3 strain, IP3, was isolated from Ixodes persulcatus near Leningrad [23]. All three strains used in this study were high passage isolates, which were classified by Richard Marconi (Rocky Mountain Laboratory, Hamilton, MT) using 16S ribosomal RNA sequence [revealing that he knows the OspA gene is the shell game] determination as described [11, 24]. The recombinant preparations of OspA and OspB used in this study were purified maltose- binding protein-Osp fusion proteins derived from group 1 strain B31 [25]. The fusion proteins contained the full-length OspA or OspB sequence without the lipid moiety or the signal sequence -" [OspA and B (encoded on the same plasmid) will not be seen in antibody-response without the lipids attached to the Osps. This was how OspA and B were left out of the Dearborn panel - pure research fraud.]

These crooks did not think they would get caught. And they had very good reason to think so because the vast majority of American MDS have no science training and the rest are cowards.

OspA

The NIH, CDC, Yale, Paul Auwaerter, NIAID, Anthony Fauci, Francis Collins, Kathleen Sebelius, and IDSociety.org all refuse to answer, "What is OspA," ...

... because what OspA is, is the disease, stuff doing what it is, at the molecular level. (Chemists speak in structures for this reason.)

They all refuse to tell us what OspA is/does for 1 of 2 reasons: 1) They're stupid or 2) they won't admit it because they know that if they admitted what OspA was, the "Lyme Disease" (means "bad knees, only") house of cards would come down.

This is the crux of it all, my fine people.

The bad guys and the NIH refuse to answer the question of what OspA is/does, because if they did, they would have to admit the whole thing, from Dearborn to even the name, "Lyme Disease," was a lie.

BACKGROUND - Blebbing (or autovaccination by spirochetal shedding):

CDC Officer and Lyme Crook Alan Barbour explains in 1996 and shows graphically:

"He finds that during the early stages of infection, B. burgdorferi avoids immune detection by decreasing its expression of surface proteins or cloaking its expressed surface proteins under a layer of slime [ALSO, BIOFILMS FROM OTHER ORGANISMS ARE COVERED WITH OSP-A-LIKE ANTIGENS; it's really slyme- the older terminology was "mucoproteins"]. "It's using some sort of stealth-bomber-type mechanism," he says. Or, using another diversionary tactic called blebbing, the spirochete can pinch off bits of its membrane in order to release its surface proteins. Explains Barbour: "It's like a bacterial Star Wars defense program [I prefer the term flak since I think that is more accurate for what he describes]," in which released surface proteins might intercept incoming host antibodies, keeping the spirochete safe from immunological attack."

OspA-like Blebs (see arrows in the below micrograph by Alan Barbour) are shed lipoproteins, so everyone with "Lyme disease," also has LYMErix Disease, because that is actually the disease - the chronic exposure to Borrelial OspA-like blebs resulting in immunosuppression, tolerance to mycoplasma in the blood (causes fatigue), results in no antibodies being produced, and the activation of Epstein-Barr/Similars.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=7103461

FROM LYMERIX-DISEASE WE KNOW THAT:

Tolerance induced by the lipopeptide Pam3Cys is due to ablation of IL-1R-associated kinase-1.

"Preculture of the cells with Pam(3)Cys [LYMErix or OspA Blebs, as shown below- KMD] at 1 microg/ml leads to a reduced response after subsequent stimulation with Pam(3)Cys at 10 microg/ml, indicating that the cells have become tolerant to Pam(3)Cys. The CD14 and TLR2 expression is not decreased on the surface of the tolerant cells, but rather up-regulated. Analysis of the NF-kappaB binding in Pam(3)Cys-tolerant cells shows a failure to mobilize NF-kappaB-p50p65 heterodimers, while NF-kappaB-p50p50 homodimers remain unchanged. Pam(3)Cys-tolerant cells showed neither IkappaBalpha-Ser(32) phosphorylation nor IkappaBalpha degradation but MyD88 protein was unaltered." http://www.ncbi.nlm.nih.gov/pubmed/15294992

More here

All aspects of the crime, including:

1) Klempner's bogus retreatment study of patients (66% of whom had never had ceftriaxone before; it wasn't a "retreatment" "study"),
2) the IDSA "guidelines,"
3) the fake OspA "vaccines", and
4) perjury cases where the crooks claimed under oath that a person did not have Lyme because they did not have the HLA-linked, hypersensitivity response (the "Steere in Europe"/Dearborn falsified case definition)

are based on/dependent upon the bogus Dearborn "case definition."

If the Dearborn case definition is shown to be false and bogus, all the rest of Yale's/IDSA's Baloney can be thrown out as well. There will be no limitations on testing and treating. All the crap and nonsense out of Yale and IDSA will have no reference point. Their crap will not hold up in court.

Everyone can win their own private lawsuit. Yale's Endowment Fund - the fund that established Schoen's L2 Diagnostics - is today worth nearly 20 Billion Dollars.

1996; KOREANS identify the structure of the OspA and HIV gp120:

: Characterization of Extremely Hydrophobic Immunostimulatory Lipoidal Peptides by Matrix Assisted Laser Desorption Ionization Mass Spectrometry

Synthetic lipoidal peptides based on viral protein sequences have been prepared. These peptides contain an N-palmitoyl group at the N-terminal residue, which is a modified cysteine, containing a S-[2,3-bis(acyloxy)-(2-R,S)-propyl] moiety. When this residue (Pam3Cys) is at the N-terminus of a synthetic peptide, it acts as potent immunoadjuvant to enhance both IgM and IgG antibody responses to the attached peptide. Conventional analytical procedures (e.g., Edman degradation and amino acid analysis) are either not applicable due to the N-terminal modification, or do not provide confirmation of the intact structure. Chromatographic analysis is also hindered by the tendency of these lipoidal Pam3Cys peptides to form large aggregates, and in some cases to be permanently adsorbed on reversed phase columns. We have applied several mass spectrometric techniques, including fast atom bombardment (FAB), electrospray ionization (ESI) and matrix assisted laser desorption ionization (MALDI) to characterize the intact structures of a number of different Pam3Cys synthetic peptides. The MALDI-MS has been found to be the most sensitive for the analysis of the structure of Pam3Cys peptides. PDF

Go to http://www.actionlyme.org/101016.htm for more:

and see...

1988, Distinction between HIV-1 and HIV-2 infection using novel synthetic lipopeptide conjugates as antigens in enzyme immunoassays.

“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.”
http://www.ncbi.nlm.nih.gov/pubmed/2464607

and...

People with HIV have antibodies to LYMErix, and as we will see later, apparently it was put into a vaccine for HIV and failed in the same way LYMErix failed - it did not produce antibodies and it made existing infections worse (Fauci).

Fauci the Fumbler on the outcomes of the ▲▲ HIV/LYMErix Vaccine:

‎"The initial empirical approach of immunizing with VaxGen's AIDSVax, a recombinant form of the outer glycoprotein-120 (gp120) portion of the HIV envelope, which was based on a strategy that was successful with hepatitis B, failed to protect volunteers from infection, apparently because the vaccine did not induce broadly neutralizing antibodies.3"

An HIV Vaccine — Challenges and Prospects — NEJM
www.nejm.org

▲ FAUCI SAYS: "LYMErix did not produce antibodies. Therefore, it was not a vaccine. Therefore, it must have been falsely qualified. Therefore, the Dearborn standard was false, which is a crime - a homicide charge."

"Cause Known" - Japanese also identify the structure of OspA; It appears to be Pam3Cys:

A delicate interplay of structure, dynamics, and thermodynamics for function: a high pressure NMR study of outer surface protein A.
http://www.sciencedirect.com/science/article/pii/S0006349511054075

The Free LYMErix Receptor, TLR2, when found in breast milk, protects babies from HIV by "(2) directly inhibiting cell-free HIV-1 infection." CONFIRMING THAT LYMERIX CONTAINS HIV gp120, as shown on actionlyme.org

http://www.ncbi.nlm.nih.gov/pubmed/22792230

Milk Matters: Soluble Toll-Like Receptor 2 (sTLR2) ... [PLoS One. 2012] - PubMed - NCBI

www.ncbi.nlm.nih.gov

PubMed comprises more than 21 million citations for biomedical literature from MEDLINE, life science journals,

MEET THE INFERTILITY ANTIGEN PAM3CYS, FOUND IN LYME AND HIV AND KNOWN AS OSP-A, THE LYMERIX VACCINE:
"We previously showed that lipoproteins from M. fermentans enhance human immunodeficiency virus replication through TLR2 and TLR6 but lipop...roteins from M. penetrans facilitate human immunodeficiency virus replication through TLR1, TLR2, and TLR6 (42). We also reported that the lipoproteins isolated from M. pneumoniae, as well as the synthetic lipopeptides containing three acyl chains, induce NF-κB through TLR1- and TLR2-dependent but TLR6-independent pathways (44). Taken together, these findings support the idea that triacylated lipoproteins are present in mycoplasma species.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493199/?tool=pubmedSee More

A Triacylated Lipoprotein from Mycoplasma genitalium Activates NF-κB through Toll-Like Receptor 1 (T

www.ncbi.nlm.nih.gov'

Go back to the 1950s to see Rockefeller Bioweapons Inc experimenting with mycoplasma antigens like OspA - Enhancing Mouse Leukemia Virus (Clue: HIV and "Lyme" bearing the same immunosuppressing triacyl lipopeptide fungal antigen, OspA):

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136329/?tool=pubmed

In Swiss mice, animals with high natural resistance to hepatitis virus, the pathogenicity of this agent was markedly enhanced by combined infection with eperythrozoa. Eperythrozoa were maintained throughout 18 successive passages in normal Princeton and Swiss weanlings with intact spleens. The combined infection of Princeton mice with eperythrozoa and the virus component of Gledhill, Dick, and Andrewes, which is nearly inactive when injected alone, resulted in acute hepatitis with fatal outcome.

The Next Plum Island Experiment: ...

http://www.ncbi.nlm.nih.gov/pubmed/13192255
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136378/pdf/311.pdf

"Let me be clear: we will not tolerate health care fraud. And, in every instance where we uncover it, we will use all available tools to hold those responsible to account."
http://www.justice.gov/iso/opa/dag/speeches/2012/dag-speech-1207021.html

In this case, the world outside the USA will hold the USA to account.

Lyme/LYMErix Cryme Reveals New Paradigm in Health/Disease:
"Bacterial/Viral Coinfections";
TLR2 [fungi, like OspA vaccination or blebbing] Signaling Depletes IRAK1 and Inhibits Induction of Type 1 by TLR7/9 [manages viruses, like latent EBV]-- -CV Harding, 2012

Vaccines' Brain Damage - these are the scientific reports which demonstrate that the CDC knows what "autism" is.

Epstein-OspA-Borreliosis - these are these scientific reports (most of which are by the Lyme bad-guys, themselves) that demonstrate that Lyme/OspA cause immunosuppression, tolerance to mycoplasma in the blood, and apparently the reactivation of Epstein-Barr/Similars.

A few years ago Roland Martin who headed the NIH's MS-Lyme research group wanted to try Leukophoresis to get rid of the badly cloned B cells in the MS version of "Lyme Disease." Later came Rituximab. Clue.

Soon after Roland Martin discovered that LYMErix or OspA vaccination produced the antibody-negative, MS-version of Chronic, Incurable Lyme that he was hired to study for the NIH, he went back home to Germany.

Clue.

Go here for more data on fungal-viral synergy and why OspA exposure seems to reactivate EBV/Similars. We don't know the exact mechanism, but there is an undeniable synergy discussed by many people, and especially Clifford Harding, the man who identified the mechanisms of Steere's bad knee, whereas for 35-plus years, Steere could not (he's not too smart).

WHO, AMONG THE LYME CROOKS, IS AWARE OF THE VIABILITY OF
THE SPHEROPLAST FORM?

See more at http://www.actionlyme.org/RICOCHRON.htm

ALL THE ONES WHO REFERENCED THIS:

URI's Dave Nelson "Reversion of cyst form to intact spirochetes within one minute of addition of rabbit blood:"
http://mic.sgmjournals.org/cgi/reprint/146/1/119 (This was published in the United States in recent time so the CDC can't reject it which is what they always do with data they don't like from Europe or Brazil.)

Here are all the crooks who cited the report above:

http://www.ncbi.nlm.nih.gov/pubmed?linkname=pubmed_pubmed_citedin&from_uid=10658658

Bockenstedt (Yale), Steere, Wormser, Radolf, ...

US Army tells soldiers to be careful not to inhale desiccated spirochetes, LOL (page 13 of the .pdf):

http://www.afpmb.org/pubs/dveps/haiti.pdf

MEDLINE LINK: Allen Steere using the Dattwyler Seronegative Lyme T-cell assay to determine that nearly half his lab workers had inhaled spirochetes

1946; HAMPP:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC518649/pdf/jbacter00652-0074.pdf

--1982, Willy Burgdorfer:

Discovers the spirochete and discusses cyst or spheroplast or starvation forms

"Ever since it was demonstrated that the body louse (Pediculus humanus humanus) and the African O moubata were the vectors of the relapsing fever spirochetes known today as Borrelia recurrentis and B duttonii, respectively, intense studies have been carried out on the development of these microorganisms in their vectors, and on the mode of transmission to humans. Thus, in 1912, the French worker Charles Nicolle and coworkers studied the behavior of B recurrentis in lice and noted that the spirochetes had disappeared from the midgut 24 hours after they had been ingested; they were no longer detectable until days 6 to 8 when they suddenly reappeared in the hemolymph.

A similar "negative phase" had previously been reported for B duttonii in O moubata by Dutton and Todd (1905-1907), Leishman and other investigators (1907-1920), Fantham (1911-1915), Hindle (1911), and later also by Hatt (1929) and Nicolle and associates (1930). According to these investigators, ingested spirochetes invade the gut epithelium where they lose motility and after 3 to 4 days develop into cysts (blebs, vesicles) that contain granules or chromatin bodies (Fig. 4). Duton and Todd postulated that these spherules are formed by protuberance of the spirochetes periplasmic membranes; they may occur at any point along the spirochete. At some time during their development, these spherules or cysts were said to burst and release their granules. By the 10th day after infectious feeding, Dutton and Todd no longer found morphologically typical spirochetes, but instead large numbers of granules from which eventually new spirochetes developed provided the ticks were maintained at temperatures above 25° C.

Figure 12

Thus, RML scientists Dave Dorward and Claude Gron using silver staining, transmission and scanning electron microscopy investigated the nature of naturally elaborated membrane blebs on the surface of cultured B burgdorferi or free in the medium, and found both linear and circular DNA (Fig. 13). The fact that his material was packaged within the membrane-derived vesicles suggested that it might play a role in the protection of genetic markers. In vivo and in vitro exposure of B burgdorferi to antibiotics (penicillin G, ceftriaxon) were shown by Preac-Mursic and associates to produce cytomorphic atypical but motile spirochetes with numerous membrane-derived vesicles (spheroblast -- L-forms) (Fig. 14).^[1]

In their recent publication, Brorson and Brorson reported on the "In vitro Conversion of Borrellia burgdorferi to Cystic Forms in Spinal Fluid, and on the Transformation to Mobile Spirochetes by Incubation in BSK-H Medium."^[2] Accordingly, B burgdorferi converted rapidly to cystic forms when transferred to spinal fluid. No normal spirochetes were left after 24 hours of incubation at 37° C; all were converted to cysts. When these cystic forms were transferred to a rich (BSK-H) medium, the cysts were converted back to normal, mobile spirochetes after incubation for 9 to 17 days.

These most recent findings do confirm the development of membrane-derived cysts, blebs, spherules, vesicles and the potential transformation to motile, helical spirochetes, not as part of a complex developmental cycle -- as postulated by Dutton and associates -- but rather as a "survival mechanism" of spirochetes to overcome or escape unfavorable conditions. Such conditions prevail during early phases of infection when spirochetes ingested into the midgut of ticks or lice become exposed to the vectors' digestive enzymes and tissue barriers (peritrophic membrane, gut epithelium). As a result, most detectable spirochetes produce numerous cysts often filled with granular material.

Other in vitro and in vivo factors shown to induce development of cysts include unsatisfactory culturing conditions, presence of antibodies and the effects of antibiotics.

Using silver impregnations and immunochemical staining, cystic material has been demonstrated in every animal and human tissue infected by B burgdorferi. As yet, it is not known whether these forms of Borrelia represent products of degenerated spirochetes or of surviving organisms capable of transforming to typical spirochetes once the faborable environmental conditions are restored. It is tempting to speculate, however, that the survival mechanism of spirochetes is responsible for the diverse pathology of these organisms as well as for their ability to survive as cystic forms thereby producing prolonged, chronic and periodically recurrent disease.

WILLY BURGDORFER REVEALING THE VIABLE SPHEROPLAST INFORMATION

"After 30 years we have NOTHING"

http://www.underourskin.com/news/lyme-discoverer-willy-burgdorfer-breaks-silence-heated-controversy

But, of course, he did. The viability of the spheroplast form is what makes it a stealth bioweapon as per the Congressional Record. Changing its surface antigens, the ability to revert to a starvation form and be dessicated and inhaled, overwhelming the immune system....

MORE on the History of Epstein-Barr-Lyme (PubMed: TLR2 and Virus)

"Immature B cells can also be seen in the spinal fluid. These cells can appear quite atypical- not unlike those
of transformed or neoplastic lymphocytes." --

--1989, IDSA's Journal, Paul Duray

"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 subsets
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, US Army.

Interleuken-10 (caused by Lyme & LYMErix) inhibits the management of EBV (1991) This article was cited over 100 times. H. pylori works with EBV (stomach cancer) Stevil Straus: Characterization & treatment of chronic active EBV disease: 28yrs, USA (CFIDS is Chronic EBV)	Interleukin-10 [produced by exposure to OspA] inhibits apoptotic cell death in infectious mononucleosis T cells.(1994) PubMed: "Endotoxin Tolerance and TLR2" [means LYMErix (OspA) was not a vaccine, Dearborn is a lie, and Borrelial antigens are immunosuppressive as TLR2 agonists.]	The latent membrane protein 1 (LMP1) oncogene of Epstein-Barr* virus can simultaneously induce and inhibit apoptosis in B cells.* EBV transformed cells help present fungal antigens 15950179 - EBV alters mitochondrial membrane (as do mycoplasma)	CFIDS = Seronegative (4 reports) Down-regulation of MHC class II expression through... [J Immunol. 2009] - PubMed - NCBI Innate immune modulation in EBV infection The lytic cycle of Epstein-Barr virus is associated ... [J Virol. 2002 Epstein-Barr virus evasion of CD8(+) and C... [Semin Cancer Biol. 2008] - PubMed - NCBI	EBV DNA in the spinal fluid but not peripheral blood 22038015 OspA delays apoptosis through inhibition f caspase-3 activity: CD14&TLR-2. (Ireland, BLP (OspA) inhibits neutrophil mitochondrial membrane depolarization" EBV LMP1 reduces p53 protein levels independent of the PI3K-Akt pathway. Dec 21, 2011	TLR2 and Virus (PubMed)(Simplex) NINDS' Roland Martin on exposure to OspA or Lyme: Bb Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression. Bb lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes.
Stress steroid hormones literally activates EBV Which means psych.org is trashed, once again Psych.org is trashed (NYT) Update, Mayo Clinic on RA and Cytomegalovirus (120202) *A profile of immune response to herpesvirus... [Arthritis Res Ther. 2012] - PubMed - NCBI*	"Conclusions: EBV DNA was often found together with other microbial findings in CSF of immunocompromised [LYMErix- or Lyme-Disease] patients." Clinical Characteristics Of Patients With Epstein Barr Virus In Cerebrospinal Fluid TLR2 Signaling Depletes IRAK1 and Inhibits Induction of Type 1 by TLR7/9 (viruses)--, 2012, Clifford Harding, "Bacterial/Viral Coinfections"	Herpes simplex virus immediate-early ICP0 protein inhibits Toll-like receptor 2-dependent inflammatory responses and NF-kappaB signaling. 20686034 EBV inhibits p53 auto-kill kinase BCL-2 Homolog BHRF1 Oncogene BCL2-like in EBV Herpes Simplex Immunosuppression (NF-kappa)	Tolerance induced Pam3Cys (Yale's LYMErix "vaccine") is due to ablation of IL-1R-associated kinase-1. 15294992	"Pam3Cys keeps the precursors in a more immature stage" (IL-17) Borrelia & IL-17 IL10>>CD4- = EBV EBV & IL-10
111222: HSV-1 Infection Activates the Epstein-Barr Virus Replicative Cycle via a CREB-Dependent Mechanism	TLR2 agonists [OspA, Lyme] synergistically increase the proliferation of EBV	H. Pylori/EBV affect NF-kappa-B Harold Varmus, Denise Huber Huber says there is 2 kinds of Lyme: the EBV evoking kind and Steere's "knees"	Formation of cysts within cells results in the release of flagellin (See H. pylori & EBV Flagellin (and other antigens) activates Mouse Gammaherpes
Despite the NIH anti-CD20 datapage	Interleukin-10 [produced by exposure to OspA] inhibits apoptotic cell death in infectious mononucleosis T cells.(1994)
Seronegative EBV (downregulation of MHC-II)
EBV & LMP1
EBV & mycoplasma
NF-Kappa B and Herpes (PubMed, General search)
Epstein-Barr and anti-CD20 (Rituximab) (PubMed, 500+)(and CFIDS)

120713.htm

PANDEMIC FLU: H9N5

Remember, whatever the "government" says - and especially, whatever the CDC says - is 180 degrees from the truth.

Here is what we know about what is the requirement for a pandemic flu human strain to take off (would be more like a swine H9):

1)
Chinese: Characterization of H9 subtype influenza viruses from the ducks of southern China: a candidate for the next influenza pandemic in humans?
http://www.ncbi.nlm.nih.gov/pubmed/12768017

2)
Don Wiley, 2001, before he was murdered "changing a flat tire":

Human and Swine HA Receptor-Binding Sites Are Wider than Those of the Avian HA.
"The distance between the 130 loop and the loop formed by residues 223–228, the 220 loop, which form two sides of the receptor-binding sites, is greater by ≈0.5Å (rms backbone atom average) in the human H3 (Leu-226/Ser-228) and swine H9 (Leu-226/Gly-228) HAs than in the Avian H5 HA (Gln-226/Gly-228) (Fig. (Fig.4). 4). ...

"α2,6-Linked sialosides bind in a cis conformation, exposing the glycosidic oxygen to solution and nonpolar atoms of the receptor to Leu-226, a human-specific residue. ...

..."Evidently, the “closed” geometry of the avian H5 HA, which prefers α2,3 linkages, results from the Gln-226/Gly-228 pair. This geometry appears optimal for positioning Gln-226 to hydrogen-bond to the α2,3 trans motif composed of the 4-OH of Gal-2 and the glycosidic oxygen (Fig. (Fig.22c). The human H3 HA with the Leu-226/Ser-228 pair is at the opposite extreme, more “open” at both 228 and 226, which may be optimal for Leu-226 to make nonpolar contacts to α2,6 cis linkages. Swine H9 HA (Leu-226/Gly-228) and the L226Q variant of human H3 HA (Gln-226/Ser-228) appear to be intermediate, with partial avian and partial human character and the nonstandard Leu/Gly and Gln/Ser pairs
(Fig. (Fig.22f)." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC58807/?tool=pubmed

3)
CDC, Jan 2012: In vitro evolution of H5N1 avian influenza virus toward human-type receptor specificity.

"Acquisition of α2-6 sialoside receptor specificity by α2-3 specific highly-pathogenic avian influenza viruses (H5N1) is thought to be a prerequisite for efficient transmission in humans. By in vitro selection for binding α2-6 sialosides, we identified four variant viruses with amino acid substitutions in the hemagglutinin (S227N, D187G, E190G, and Q196R) that revealed modestly increased α2-6 and minimally decreased α2-3 binding by glycan array analysis. However, a mutant virus combining Q196R with mutations from previous pandemic viruses (Q226L and G228S) revealed predominantly α2-6 binding. Unlike the wild type H5N1, this mutant virus was transmitted by direct contact in the ferret model although not by airborne respiratory droplets. However, a reassortant virus with the mutant hemagglutinin, a human N2 neuraminidase and internal genes from an H5N1 virus was partially transmitted via respiratory droplets. The complex changes required for airborne transmissibility in ferrets suggest that extensive evolution is needed for H5N1 transmissibility in humans." http://www.ncbi.nlm.nih.gov/pubmed?term=22056389

Pandemic flu and the "Unknown Intermediate" host being a pig: "Reassortant viruses appear to have caused the pandemics of 1957 and 1968; the 1957 H2 virus differed by three genes, those for HA, NA and the RNA polymerase subunit PB1, from the H1 virus that infected humans between 1918 and 1957; the 1968 H3 virus differed by two genes, those for HA and PB1, from the H2 virus that infected humans between 1957 and 1968 (Kawaoka et al., 1989). In both cases, the genes for the H2 and H3 HAs are proposed to have been contributed by avian viruses, ***during infection of an unknown host that was infected simultaneously by the prevalent human virus."***
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC125880/?tool=pubmed

See More of the Following at: KISSINGER_NAZI_PAPERCLIP.htm

"Also in "Emerging Viruses: AIDS & Ebola," you will learn exactly what was done with the $10 million Congress gave the DOD for the development of AIDS-like viruses, because I published the relevant contracts. You will learn that Dr. Robert Gallo, the famous NCI molecular biologist, pardoned by President Clinton last year for scientific fraud and misconduct, and credited with the discovery of the AIDS virus, set about to develop immune system ravaging, AIDS-like viruses, along with other Litton Bionetics researchers. You will learn that they took monkey viruses that were humanly benign, recombined them with DNA, RNA, and enzymes from other animal viruses that caused leukemias, lymphomas, and sarcomas, and then to get them to jump species, they cultured these new mutant viruses in human white blood cells in some studies, and human fetal tissue cells in other studies, to produce immune-system-destroying, cancer-causing viruses that could enter humans and produce virtually identical effects to what the AIDS virus is currently doing in people around the world."