Welcome to ActionLyme - the Lyme Cryme Whistleblower's Website

Borreliosis Basics (poster) USDOJ RICO Complaint The ALDF/IDSA RICO Patents Dattwyler on Seronegative Lyme Dearborn Booklet (pdf)
Lyme Facts (poster) Blumenthal Sues (AntiTrust) CDC's Patents with GSK Steere on Seronegative Neuro Lyme Dearborn Invitation (pdf)
Primers Shell Game (report
 your adverse events to FDA)
History of Relapsing Fever as a
 permanent brain infection
UConn Assaults Czech children
 with fake vaccine
Immunology Epstein-OspA-Borreliosis
 (tick acquired immune deficiency)
Imugen (Steere?) on Dearborn
 as 14% Accurate
Post-Lyme-Sepsis; 20 reports
 on relation to Autism Pandemic
IDSA Reports Lyme is a permanent
brain infection
Congenital Lyme, by Yale
 (autopsies)
Steere in Europe, falsifying the testing
 
for Dearborn
The Antics of Edward
 McSweegan and Durland Fish
Yale's Lyme Vaccine Scam IDSA's & CDC's Biomarkers JJ Halperin on Lyme & ALS Steere on Lyme causing Lupus Mark Klempner's Crymes
 


11/26/2014 23:20:57

Index/Home

"Khan Academy"; Lyme & LYMErix Activate Herpes,  Dearborn was performed to hide that fact :)


Cryme Trainer; Outline for Indictments and the OCCUPY the USDOJ




Follow the Lyme/LYMErix Scam in the order it occurred, below:

Older data on the incurability of Relapsing Fever

1986, McSweegan trashes Navy for $$$ for ALDF.com

1988, Dattwyler & about immune-suppressing, seronegative Lyme

1990, CDC: "Diagnose Lyme as if it was Relapsing Fever."

Allen Steere  "NeuroLyme won't test positive," 1990.

1992, CDC officer Allen Steere falsifies testing in Europe

1992, CDC patents with SmithKline show 2 kinds of Lyme

1993, Barbour and Fish slam Neurologic Lyme victims.

Compare the 2 kinds of Lyme in the RICO complaint

1994, FDA LYMErix Meeting

1994, CDC's Dearborn Booklet .pdf

CDC's invitation to participate in Dearborn .pdf

Dearborn, Who Said What?

Igenex, Harris, Dearborn .pdf

Evidence  Lyme criminals knew LYMErix produced the same "multisystem disease" as "Chronic Lyme"

LYMErix Damage Coverup (short)
 

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

ActionLyme/Kathleen Dickson predicts all of Bushie's outcomes in Oct 2000

ActionLyme/Kathleen Dickson predicts Bush will have us worshipping his bombs (Shock and Awe"), in Oct 2000 during the Gore Debates

 

"The fact that OspA vaccination caused all IDSociety.org's famous "New Great Imitator" outcomes like MS, Lupus, RA, Cancer, etc., as well as the Chronic Lyme/Chronic Fatigue/ME- Leukemia-like disease was the biggest medical discovery of the last 500 years. It was a huge breakthrough in medicine (fungal-viral synergy, now called "post-sepsis syndrome") that Yale, et al, can't now take credit for because they vehemently and viciously lied about this, even in numerous court cases." - The Future "Khan Academy" of Lyme Cryme & HLA-Negative Diseases


 

The Primers Shell Game, a version for the Facebook "Occupy the DOJ" group, a chapter of CRYME DISEASE and a lesson from the new “Khan Academy” of Lyme Cryme and HLA-Negative Diseases (includes all abused groups; CFIDS, ME, FM, Autism, medical rights, parents rights, psych rights, etc); 141031, KMD.


Okay, let me repeat, this is a chapter of “CRYME DISEASE.” Which means there is more than one chapter of CRIME DISEASE, and the primary chapter is Chapter One. Chapter One is about Scientifically Valid Testing for Lyme (which is not arbitrary but follows FDA rules), which includes this same information, below, that you need to understand about the genetic relatedness of these kinds of spirochetes.  Another chapter is 7 (BRAIN_PERMANENT.htm), where the crooks almost always use the OspA gene instead of the flagellin gene or a species-specific spacer gene to find "NO LYME," so you have to compare the following data to that, that is, if you want more examples than the following...

Flagellin is the species distinguisher.

All Borreliae are relapsing fever organisms, and the nature of the relapse is antigenic variation. Therefore you cannot use any DNA from plasmids – which is where the variable surface antigens are ordered manufactured and remanufactured – to assess for spirochetes. No one sane does this. No researchers outside the United States EVER uses plasmid DNA to assess for spirochetes. They only use species-specific spacer genes like 5, 16 and 23 S RNA or flagellin. That’s it.


 

Let’s start at the beginning because the moron “LLMDs” out there are killing me, really. I feel like I am in Beatrice’s World. (“That’s not how this works.”)

 

Now, let's side-step for a minute and talk about the FDA and what their rules are for the "Validation of an Analytical Method."  As you can see there is Accuracy (should detect 100% of the instances when the analyte in question is present), Specificity (only detects one thing), Linearity, Ruggedness, Precision (refers to instrumentation), Limit of Detection (this would be something like, "How low in concentration of the analyte in question can your method detect?"). 

This is from the new announcement July 31, 2014 regarding the FDA now about to ENFORCE their validation rules:
http://www.fda.gov/downloads/MedicalDevices/ProductsandMedicalProcedures/InVitroDiagnostics/ucm407409.pdf


 

 

 

Do you see the FDA wrote their words here?  I underlined them.

 

 




"Sensitivity" MEANS "Limit of Detection." The closest thing to that in the real VALIDITY requirements is Limit of Detection. 

FDA Rules on the VALIDATION of an Analytical Method
Specificity
(only detects one thing)
Accuracy (Should detect 100% of the instances where the analyte is present, and the concentration should be close to 100% of that known to be spiked in, and never should detect "none" as is the case with Lyme Western Blotting and the Lyme ELISA, especially)
Limit of Detection (means "What is the lowest concentration of the analyte in question does your method detect?")
Precision  (system has integrity in performance)
Ruggedness  (anyone can run the test with their own equipment and get the same results)
Linearity (concentration range of analyte for which the test is valid in and out of matrix or "inert ingredients")
 

But first, your test should detect all the cases in question, - or be 100% ACCURATE - and that means, in the case of Lyme, the only analyte that can be tested for is flagellin or anti-flagellar antibodies.  Anti-flagellar antibodies can be found in probably 95% of Lyme cases.  So, Yale went ahead and made that Specific (US patent 5,618,533) in 1991, here, next:


Says Yale:  "Molecular characterization of the humoral response to the 41-kilodalton flagellar antigen of Borrelia burgdorferi, the Lyme Disease spirochete."

"The earliest humoral response in patients infected with Borrelia burgdorferi, the agent of Lyme disease, is directed against the spirochete's 41-kDa flagellar antigen. In order to map the epitopes recognized on this antigen, 11 overlapping fragments spanning the flagellin gene were cloned by polymerase chain reaction and inserted into an Escherichia coli expression vector which directed their expression as fusion proteins containing glutathione S-transferase at the N terminus and a flagellin fragment at the C terminus. Affinity-purified fusion proteins were assayed for reactivity on Western blots (immunoblots) with sera from patients with late-stage Lyme disease. The same immunodominant domain was bound by sera from 17 of 18 patients. This domain (comprising amino acids 197 to 241) does not share significant homology with other bacterial flagellins and therefore may be useful in serological testing for Lyme disease."
http://www.ncbi.nlm.nih.gov/pubmed/1894359
 

Okay, so Yale says there, above, that their method (US patent 5, 618, 533) detects, early, late, neurological, and every other possible kind of Lyme outcome and that it detects 94.4% of the cases, which means it is the closest possible method we could possibly have to detect Lyme ("should be 100% of the cases," says the FDA, verbatim), and this method was made SPECIFIC, which means it does not detect any other flagellins.


When the FDA says "sensitivity," they really mean "LIMIT OF DETECTION" and refers to the METHOD and not the "CASES."  Accuracy addresses cases.  Yale took care of all that in 1991 and went ahead and patented it (but did not use this method to qualify LYMErix, their other patent, which is the essence of this False Claims Act case).


Okay, so in summary >> The only way to detect a spirochetal disease is to use recombinant specific flagellins from most of the specific borreliae - just like Yale did, above, only with the other borrelia - that we know to be at least in the United States.  THAT is what is "VALID," and the FDA and NIH agree with me.


 

Okay, so: DO NOT EVER listen to IDSA, the Lymedisease.org (LDA) or ILADS.org.  IDSA are criminals and the LDA/ILADS are retarded and have no real scientists in their camps.

ILADS and the LDA do not know what they are talking about and consistently come up with stupid, retarded announcements, giving everyone with Lyme-brainscramble and everyone who is an MD but has no science background... even more brainscramble.  It just is not fair. 

If you don't know what you are talking about, kindly do not talk.


 


Single Spirochete Infection and resultant MULTIPLE VARIANTS:

1951: Relapse Phenomena in Rats with a Single Spirochete
http://jb.asm.org/cgi/reprint/62/2/215?view=long&pmid=14861181

Oscar Felsenfeld and CDC officer Alan Barbour talking about/referencing this Single Spirochete Phenomena:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=link&linkname=pubmed_pubmed_citedin&uid=14861181
 

Oral Spirochetes infecting Alzheimer’s brains and traveling along inside nerves (this is not the only report that says this, you’ll find it in syphilis report too) (from BRAIN_PERMANENT.htm);  An independent study on spirochetes in the brain from dentists and they say:

Molecular and immunological evidence of oral Treponema in the human brain and their association with Alzheimer's disease.
Riviere GR, Riviere KH, Smith KS.
Department of Pediatric Dentistry, School of Dentistry, Oregon Health and Sciences University, Portland, OR 97201-3097, USA.
“The purpose of this investigation was to use molecular and immunological techniques to determine whether oral Treponema infected the human brain. Pieces of frontal lobe cortex from 34 subjects were analyzed with species-specific PCR and monoclonal antibodies. PCR detected Treponema in 14/16 Alzheimer's disease (AD) and 4/18 non-AD donors (P < 0.001), and AD specimens had more Treponema species than controls (P < 0.001). PCR also detected Treponema in trigeminal ganglia from three AD and two control donors. Cortex from 15/16 AD subjects and 6/18 controls contained Treponema pectinovorum and/or Treponema socranskii species-specific antigens (P < 0.01). T. pectinovorum and/or T. socranskii antigens were also found in trigeminal ganglia and pons from four embalmed cadavers, and 2/4 cadavers also had Treponema in the hippocampus. These findings suggest that oral Treponema may infect the brain via branches of the trigeminal nerve.”
http://www.ncbi.nlm.nih.gov/pubmed/11929559

 

Now, you will see why this "single-spirochete-becomes-multiple-strains" business is important later in this chapter, below, as regards Alan Barbour and Bioweapons, and how spirochetes creating multiple variants and all the individual spirochetes doing their own thing, varying their surface antigens on their own comes into play as far as ruining a person's immune system.  And a ruined immune system is the DAMAGE and is the ILLNESS and is the specific goal of a bioweapon:

           

"Methods of using antipersonnel agents undoubtedly wary so that no uniform pattern of employment or operation is evident [make sure it does not produce antibodies, so assess the HLAs in the population you intend to abuse like the defecting Russian scientists at NYMC have been doing, is the short version- KMD].  It is likely that agents will be used in combinations so that disease symptoms will confuse diagnosis and interfere with proper treatment.  It is also probable that biological agents would be used in heavy concentrations to insure a high percentage of infection [or just use the OspA vaccine- KMD] in the target area.  The use of such concentrations [or the multiple infections it causes, due to the immunosuppression like HIV, Lyme, or LYMErix as acquired immune deficiencies - KMD] could result in the breakdown of individual immunity because the large number of micro-organisms entering the body could overwhelm the natural body defenses [or just infect or inject people with an immune suppressor like OspA from a tick or a syringe, and the reverse will happen: people will acquire multiple infections because their immunity is trashed by fungal OspA- KMD].


 

 

Do you see the disease now? ▲▲▲  ??    It's fungal (shed borrelial antigens are TLR2/1-agonists or fungal).  It is about ovewhelming the immune system; it is about not producing identifiable antibodies; your bioweapons should be like a Trojan Horse, setting off other latent infections; your immune system now sucks (overwhelmed means turned off); you don't have "biofilms" at least of borrelia; Lyme was the "perfect stealth disabler;"... and then all of the CDC's ridiculous lies...  From the CDC's lies alone, you could call this an accidental release of a bioweapon.   But we have other circumstantial scientific evidence, as you will see...





Moron LLMDs Alert on “Biofilms”:

Use “Borrelia Staining” or “Borrelia Silver Staining” as search terms in PubMed and discover that Borrelia in vivo do not cluster at all, much less under a “Biofilm.”

Here is one. Look closely now, for the “clustered spirochetes hiding under a biofilm” (there is no such thing):
Demonstration of Spirochaetes in Patients with Lyme disease with a Modified Silver Stain
http://jmm.sgmjournals.org/content/23/3/261.long
 

Here is another one by Paul Duray (same guy who revealed that congenital Lyme brain damage kills babies and the same guy who revealed to us that Lyme and LYMErix diseases cause a leukemia like illness and that the cells in the CSF of Lyme patients "look like Epstein-Barr transformed (mutated, pre-cancerous) cells:
http://www.ncbi.nlm.nih.gov/pubmed/?term=Duray+and+borrelia+and+stain


PAUL DURAY >>> "Morphology of Borrelia burgdorferi: structural patterns of cultured borreliae in relation to staining methods.

"
The microscopic recognition of Borrelia burgdorferi in biologic fluids and tissues is difficult and challenging because of low numbers of organisms occurring as single isolated spirochetes, the apparent lack of colony formation in tissues, and differing lengths and structural morphologies."

http://www.ncbi.nlm.nih.gov/pubmed/1716264

 

Additionally, biofilms are covered in TLR2/1 agonists so the body does not even see them at all any more, if they are there, in this post-sepsis disease called Chronic Lyme, with the multiple reactivated herpes viruses, etc and the expansion of tolerance to other toll-like-receptor-managed antigen types.
 

Okay, so REVIEW:  Biofilms are NOT responsible for the persistent symptoms in Chronic Lyme Disease.  Spirochetes, while permanent - no one sane argues that they're not, since they always were known to be incurable infections, even with arsenic - (RICOCHRON.htm).  So, what is responsible?


Go to POST_LYME_SEPSIS_2014_SUMMER.htm and see the following, among others, FROM THE NIH!!!!
 

10) This is the NIH (NINDS’s MS-Lyme Group) group that discovered that *** OspA *** was the cause of the MS/New Great Imitator outcome of Lyme reporting in the New York Times in the summer of 2013 (Martin and Marques, 2006):

When Lyme Disease Lasts and Lasts – Jane Brody
"Complicating the picture is the fact that some people with PTLDS symptoms apparently never had Lyme disease in the first place, Dr. Marques said in an interview. There are other infectious organisms — Epstein-Barr virus, for example — that can produce similar symptoms and may be the real culprits."
http://well.blogs.nytimes.com/2013/07/08/when-lyme-disease-lasts-and-lasts/ 


Here are the NIH's 2 reports that say OspA (TLR2-agonist) is the cause of the MS/CFIDS/EBV-reactivated kind of Lyme (that also causes humoral immunosuppression),... and that as a result of exposure to OspA-like antigens (shed constantly in a process called blebbing, as revealed by CDC officer Alan "Stealth Bomber" Barbour), you might not even have anti-flagellar antibodies (TLR5-agonists):

Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.
http://www.ncbi.nlm.nih.gov/pubmed/16783164 

and

Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes.
http://www.ncbi.nlm.nih.gov/pubmed/16479520 


12) NCI and US Army Ft Detrick Pathologist Paul Duray on the CSF cells looking like "Epstein-Barr-like transformed cells" in IDSA's 1989 Reviews Supplement on Spirochetal Diseases:

Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Clinical pathologic correlations of Lyme disease.
"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." --
http://www.ncbi.nlm.nih.gov/pubmed/2814170 
Full Text:  http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm 
 


NEW, by the NIH:  "Surviving Sepsis: Detection and Treatment Advances"


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

13) Duray again in 1992, in Steve Schutzer's review of the 1992 Cold Spring Harbor Conference on Lyme:

"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. - book.


 



Yikes, I hope that is the end of THAT topic. God Save Us from stupid people who only will malpractice-treat rich people with long term antibiotics for post-sepsis immunosuppression, the reactivation of latent herpesviruses, and TL2/1 agonist (and expanded cross tolerance) tolerance, with their own little, “It must be babs, it must be bart, it must be today’s-flavor-of-whack-a-do coinfection number 467… and get a third mortgage, since the money from your second mortgage ran out, thanks, I love my new yacht….” abuse that you get from ILADS.org


===


BACK TO THE DNA SHELL GAME.....  DO NOT SKIP THESE 2 PARAGRAPHS:

So, when talking about the DNA and RNA shell game played by the crooks - where the crooks use the wrong DNA to find “NO-LYME HERE!” and the correct DNA when they want to run to the patent office to claim a new species…- we have to go back to Chapter One of Cryme Disease (CRYMEDISEASE_CHP1.htm is the extension) which is about Taxonomy
The very first thing you need to know about Lyme is that it is technically called Relapsing Fever.
Here is why:
http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=138 <<< Click on the larger texted heading, "Borrelia" in the above link. You will see that the taxonomic categorization of these organisms is based on differences in their flagellin, because that is the genetic species distinguisher - and not OspA or any of the plasmid DNA. [All Borrelia are arthropod-borne. That is why they are called borrelia. That is why they're distinct from other spirochetes. And if they are parasites, they cause disease in some way.]

One must understand how these spirochetes are related,… and the phylogeny,… and in the end “they’re all just Borreliae and you really can’t even talk about species ,” Oscar Felsenfeld… But if you must, use the flagellar genes, since those is the species distinguishers, taxonomically.



On second thought... I have decided to add the links and the graphics to Phylogeny Basics so you don’t have to bother going to the Taxonomy database.

Here we see as the key report from the NIH's NLM's Taxonomy (Fukunaga, et al) database showing Burgdorferi is closest to anserina, an African bird borreliosis. They just happen to do this kind of African-Diseases-With-North-American-Vectors-kind of "Research" on Plum Island (verifiably):
http://ijs.sgmjournals.org/content/46/4/898.long
 

 


Here we see the NIH Rocky Mountain Bioweapons Lab using anserina as an out-group, when in fact, it is the origin of the Plum Island burgdorferi group - African bird borreliosis - experimentally introduced to the microscopic bioweapony Ixodes, hard bodied tick: 
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC228430/pdf/332427.pdf

 




More on Evolution and Expansion of the anserina-come-burgdorferi-Plum-Island phenomenon:

SUNY-SB on Lyme/Plum Island as the original outbreak area:
Evolution of a focus of Lyme disease
http://www.ncbi.nlm.nih.gov/pubmed/3577493


UPenn on Lyme being evolutionarily unlikely:
UNCOORDINATED PHYLOGEOGRAPHY OF BORRELIA BURGDORFERI AND ITS TICK VECTOR, IXODES SCAPULARIS:
http://www.ncbi.nlm.nih.gov/pubmed/20394659

Despite the intimate association of B. burgdorferi and I. scapularis, the population structure, evolutionary history, and historical biogeography of the pathogen are all contrary to its arthropod vector.”


Durland Fish and his experiments with African diseases and vectors on Plum Island:
African Swine Fever Virus Infection in the Argasid Host, Ornithodoros porcinus porcinus

“ASFV isolates.

Chiredzi/83/1 (Ch1) was isolated from Ornithodoros spp. ticks collected near Chiredzi, Zimbabwe (26), and was obtained from the Plum Island Animal Disease Center reference collection. Pretoriuskop/96/4/1 (Pr4) and Crocodile/96/1 (Cr1) were isolated from O. porcinus porcinus ticks collected from warthog burrows in Kruger National Park, Republic of South Africa, in September 1996. Nooitverwacht/96/6 (No6) was isolated from O. porcinus porcinus ticks collected from a warthog burrow in the Northern Province, Republic of South Africa, in September 1996.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC109458/



CDC Lying about the viability of the cyst or spheroplast form of spirochetes,... and CDC lying about mycoplasma not being involved in Chronic Fatigue Syndrome: 
 

CDC: "How to Dessicate and Weaponize your Borrelia :) "
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC277387/pdf/jbacter00438-0287.pdf
 

CDC Throwing out the red blood cells (throwing out whole cells of any kind, including immune cells or white cells where the mycoplasma actually lived and used to be called epERYTHROzoa for that very reason:

"Absence of Mycoplasma species DNA in chronic fatigue syndrome"
"Plasma, the liquid portion of peripheral blood that is devoid of cells, is known to contain remnants of numerous physiological and disease processes. We used plasma DNA to detect and characterize bacterial 16S rDNA sequences in a group of individuals with CFS and a group of non-fatigued controls (Vernon et al., 2002). Whilst a variety of bacterial sequences were detected in both fatigued and non-fatigued groups, no Mycoplasma sp. 16S rDNA sequences were found."
http://jmm.sgmjournals.org/cgi/pmidlookup?view=long&pmid=14532349 

 

So, that's all obviously a lot of research fraud performed by CDC staff already, and next, in the DNA Shell game you will see it is almost entirely CDC officers committing this fraud.
 

========== Now on to where the crooks play the shell game with the DNA and RNA ========

 

ALAN BARBOUR playing the DNA/RNA shell game...

You will want to look at The Patents chapter of Cryme Disease (http://www.actionlyme.org/CENTRAL_LYME_RICO_PATENTS.htm ) to see that CDC officer and former head of the NIH’s Rocky Mountain Bioweapons Lab (where there are tons of Relapsing Fever but no “Lyme”) Alan Barbour reported that basically “antigenic variation in one spirochete, times all the spirochetes you have leaves the immune system ‘overwhelmed’ with “an infinite number of new antigens,” which is a bioweapons technique well described by the US Army when speaking to Congress and can be seen on the Bioweapons pages of ActionLyme.org (http://www.actionlyme.org/120702.htm and http://www.actionlyme.org/BIOWEAPONS_ATTRIBUTES.htm )


ALAN BARBOUR states clearly that OspA undergoes true antigenic variation and that you cannot use this as a vaccine, and certainly not for DNA diagnostics as Klempner did in his “BREAKING NEWS!!!” Bogus re-treatment "study" that is now the data used by IDSA for their "Guidelines" from the summer of 2001.

"Antibody-resistant mutants of Borrelia burgdorferi: in vitro selection and characterization."

Says Barbour above: “Second, previous studies had shown antigenic differences in outer membrane proteins, OspA and OspB, between strains (21-26) and also true antigenic variation of these proteins within a strain (25, 27-30).”
http://www.actionlyme.org/BARBOUR_MUTANTS_1992.htm
That’s PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/1339462

Mutants” is code language. They’re all mutants. Antigenic Variation is the nature of the relapse in Relapsing Fever, so to call them mutants is silly and redundant, and not the least bit correct as you will see in Barbour’s patents and in the older data re the Single Spirochete outcome.


Here is what Barbour says in one of his patents about antigenic variation and "overwhelming the immune system":
 

"2.1 Methods of Treatment

"An important aspect of the invention is the recognition that Borrelia VMP-like sequences recombine at the vls site, with the result that antigenic variation is virtually limitless. Multiclonal populations therefore can exist in an infected patient so that immunological defenses are severely tested if not totally overwhelmed."
http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6,719,983.PN.&OS=PN/6,719,983&RS=PN/6,719,983


So you can’t use OspA for a vaccine, for post-treatment DNA diagnostics, or for Lyme case detection in antibodies. The only thing you can do or say about OspA is remember it means little except that it helped the normally non-borreliae-bearing Ixodes (hard bodied) ticks acquire a ligand (OspA-B plasmid) with which to attach to and invade the hard bodies of hard bodied (Ixodes) ticks. So, Lyme spirochetes were adapted probably on Plum Island to local vectors. Genetically, the Lyme spirochete is closest to anserina, an African bird borreliosis. All the more better to spread it around, to use a bird strain  (see http://www.actionlyme.org/PIIB.htm and http://www.actionlyme.org/TRAINER_2012SUMMER.htm )


BARBOUR'S 1995 PATENT FOR SPECIFIC 16S RNA and Flagellin that GARY WORMSER DID NOT USE, WHILE
BARBOUR SAYS THIS IS IN LONE STAR TICKS IN MISSOURI (that study is below in this chapter):

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%2C932%2C220.PN.&OS=PN%2F5%2C932%2C220&RS=PN%2F5%2C932%2C220


 

MARK KLEMPNER, playing the DNA/RNA shell game...

You have previously seen that the OspA gene undergoes antigenic variation (Alan Barbour, owner of the ImmuLyme vaccine OspA patent, above), is not found in all Borreliae and you can't use this DNA for anything, especially not vaccines or detection.

We move on to the Klempner "Study" which resulted in the “Guidelines” and where he references which DNA he used to assess "NO LYME IN LYME VICTIMS" (he doesn’t actually and the peer reviewers never noticed he did not list his primers):

http://www.nejm.org/doi/full/10.1056/NEJM200107123450202#t=articleMethods


 

So, what was that mysterious REFERENCE 21 above ^^ DNA that Klempner failed to report and the so called peer-reviewers did not notice?

http://jid.oxfordjournals.org/content/174/3/623.full.pdf

WHICH SAYS:

 


 

So, the crooks – including Klempner in his bogus non-retreatment report that is now the basis of the IDSA “Guidelines” - say if the OspA gene is not there, there is no Lyme, right? Despite the fact that Lyme is a Relapsing Fever borrelia and OspA undergoes antigenic variation and not likely to be in the same form or produced by the exact same genetic code as one produced inside a tick, late in the disease in humans.


 

DURLAND FISH

And here is Durland Fish using the correct primers to look for new species of Borreliae to patent in 2001:

A relapsing fever group spirochete transmitted by Ixodes scapularis... - PubMed – NCBI

Vector Borne Zoonotic Dis. 2001 Spring;1(1):21-34. Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. NCBI.NLM.NIH.GOV|BY SCOLES GA , ET AL.

"A 1,347-bp portion of 16S rDNA was amplified from a pool of infected nymphs, sequenced, and compared with the homologous fragment from 26 other species of Borrelia. The analysis showed 4.6% pairwise difference from B. burgdorferi, with the closest relative being Borrelia miyamotoi (99.3% similarity) reported from Ixodes persulcatus in Japan. Phylogenetic analysis showed the unknown Borrelia to cluster with relapsing fever group spirochetes rather than with Lyme disease spirochetes. A 764-bp fragment of the flagellin gene was also compared with the homologous fragment from 24 other Borrelia species. The flagellin sequence of B. burgdorferi was 19.5% different from the unknown Borrelia and showed 98.6% similarity with B. miyamotoi."

http://www.ncbi.nlm.nih.gov/pubmed/12653133



 

Yet, here we see a year later, Durland Fish using the WRONG DNA (OspA gene again), to assess treated mice, to determine if there is any Borrelia, coming to the conclusion that there is pretty much no Borrelia:

http://jid.oxfordjournals.org/content/186/10/1430.long

Detection of Attenuated, Noninfectious Spirochetes in Borrelia...

"PCR of DNA.DNA was isolated from individual ethanol-fixed nymphs or pooled larvae by means of the Isoquick DNA isolation kit (ORCA Research) and was resuspended in 20 μL of double-distilled H2O. Primers used for amplification were as follows: *** ospA *** (GenBank accession no. M57248, product amplicon coordinates 80–781): forward, 5′-AAAACAGCGTTTCAGTAGATTTGCCTGGTG-3′, and reverse, 5′-CAACTGCTGACCCCTCTAATTTGGTGCC-3′; BBE21.1 (GenBank accession no. AE000785, product amplicon coordinates 14663–14921): forward, 5′-AGAATTATGTCGGTGGCGTTGT-3′, and reverse, 5′-ATTAAAGCCGCCTTTTCCTTGGT-3′; and p37-47 (GenBank accession no. AE000794, product amplicon coordinates 1309–1457): forward, 5′-TTCTGATGGCACTGAGCAAACCA-3′, and reverse, 5′-AACCCTTTACACTTTCTTCGATTGCGCT-3′. The primer set for p37–47 has 100% homology to sequences in both B. burgdorferi strains B31 and N40, and the gene has been localized to lp28-1 in both strains [26, 27]. The primer set for BBE21.1 amplifies a unique region in lp25 of B. burgdorferi strain B31 downstream of BBE21 (amplicon coordinates 13403–14530) [28]. BBE21 is located on a similar-size plasmid within B. burgdorferi strain N40 [29]. We have been able to amplify by PCR the region corresponding to GenBank accession number AE000785, product amplicon coordinates 14195–14921, indicating that BBE21 and BBE21.1 reside on the same plasmid in N40 (authors' unpublished data)"


^^^  Those are plasmids, those "lp... " things.  Plasmids are from where the variable surface protein antigens vary themselves.  So, that is a classical Durland Fish type "bogus article."



GARY WORMSER playing the DNA/RNA shell game....

Next we are going to look at Gary Wormser who is in 1992 using the correct primers:
Diagnosis of early Lyme disease by polymerase chain reaction amplification and culture of skin biopsies from erythema migrans lesions.

http://www.ncbi.nlm.nih.gov/pubmed/1452688
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC270592/pdf/jcm00036-0064.pdf

 

Here Gary Wormser in 1999 when using the CORRECT PRIMERS (16S) finds most people are infected with more than one species of Borrelia and that you can't really use Barbour-Kelly-Stoener culture media (the only one anyone sells in the USA):

Genetic diversity of Borrelia burgdorferi in lyme disease patients ... - PubMed – NCBI
J Clin Microbiol. 1999 Mar;37(3):565-9. Comparative Study; Research Support, U.S. Gov't, P.H.S.
NCBI.NLM.NIH.GOV|BY LIVERIS D , ET AL.
http://www.ncbi.nlm.nih.gov/pubmed/9986813


And yet here we have Gary Wormser not finding Lonestari in Missouri because *** he is using the wrong primers*** [he is not using Barbour's lonestari patent primers (1995), and his results conflict with Telford's, below, in 2001 report showing Missouri Relapsing Fever is closest to theileri a cow relapsing fever, and Wormser is using a general 16S primer not specific to Borreliae species at all]; Wormser is also using an OspA gene primer which Barbour determined in 1995 was not in his new theileri-like (cow relapsing fever) patented Borrelia:


2005: Microbiologic evaluation of patients from Missouri with erythema migrans.
http://www.ncbi.nlm.nih.gov/pubmed/15668867
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2773674/

“PCR amplifications were performed in a 50-μL reaction mixture containing 10 mmol/L Tris-HCl (pH 8.3); 1.5 mmol/L MgCl2; 50 mmol/L KCl, 0.1% (w/v) gelatin; 100 μmol/L each of dATP, dGTP, dCTP, and TTP; 1.25 units Taq polymerase; and 20 pmol of each primer. Detection of borrelial DNA in patient specimens and ticks was accomplished by the nested PCR amplification of flaB using primers FlaLL, FlaLS, FlaRL, and FlaRS as described by Barbour et al [11]. PCR of 16S rDNA was performed with broad-range eubacterial primers 8FPL and 1492RPL [26], which yields a product of ∼1.5 kbp. In cases in which no detectable product was obtained, second-round heminested PCR was performed with 8FPL and a reverse primer (519R: 5′-TTACCGCGGCTGCTGGC-3′) targeted at residues 535–518 (numbering corresponds to residues in the 16S RNA sequence of Escherichia coli) in 16S rDNA; this resulted in a fragment of ∼500 bp. Some specimens were also tested by PCR targeted at ospA (forward primer, 5′-CTGCAGCTTGGAATTCAGGCACTTC-3′; reverse primer, 5′-GTTTTGTAATTTCAACTGCTGACCCCTC-3′) and/or recA [27].”


WORMSER did not use the correct^^^ Borrelia-specific flagellin, or Borrelia-specific spacer genes as shown below by Telford and Barbour in his lonestari-like patent, and he did not use genus specific 16S RNA genes ("broad-range eubacteria"?), and he used a reverse primers for E coli ?? LOL.



SAM TELFORD's 2001 REPORT SAYING “Southern Lyme” is CLOSEST TO THEILERI OR BOVINE RELAPSING FEVER:
http://www.ncbi.nlm.nih.gov/pubmed/11158095

 


You can see that the ^^^ crooks have already sequenced the 4 similar strains of flagellar and genus specific 16S RNA spacer genes that are derived from a cow or bovine relapsing fever.

 

TO THIS DATE – from 1995 to 2015 - still, NO ONE IS USING BARBOUR'S RECOMBINANT LONESTARI FLAGELLIN OR 16S RNA GENE or any other of these gallblammed proper DNAs or RNAs TO DETECT HUMAN ILLNESS, NATURALLY.

 

They all know the only way to detect Lyme/Relapsing Fever is with specific recombinant flagellins from all the Borreliae, similar to Yale’s Lyme specific flagellin patented method, US 5,618,533.

 

ROBERT SCHOEN - 1995

J Immunol. 1995 Dec 15;155(12):5700-4.

An ospA frame shift, identified from DNA in Lyme arthritis synovial fluid, results in an outer surface protein A that does not bind protective antibodies.
Fikrig E1, Liu B, Fu LL, Das S, Smallwood JI, Flavell RA, Persing DH, Schoen RT, Barthold SW, Malawista SE.
http://www.ncbi.nlm.nih.gov/pubmed/7499856

 

Oh, you mean Lyme is a Relapsing Fever organism, so you can’t use the OspA gene for human treatment outcomes assessment, Huh Mr. Schoen, or to detect “Lyme” in EM rashes?


Here, next Yale's Robert Schoen (who says Lyme is not a real disease and needs no treatment) using 23S RNA primers to assure his RICO monopoly strain (and later patent with Dave Persing) is related to burgdorferi,...

Borrelia burgdorferi enzyme-linked immunosorbent assay for discrimination of OspA vaccination from spirochete infection.
http://www.ncbi.nlm.nih.gov/pubmed/8968914
http://jcm.asm.org/content/35/1/233.full.pdf


and also reveals there is "Lyme" in the Southern and Western states in 1996.
 


ANDREW PACHNER:


Another report of this type is "Borrelia burgdorferi infection of the brain: Characterization of the organism and immune sera in the mouse model"

"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. "


 

 

141113 The Lyme Vaccine Scam, Facebook "Occupy the USDOJ" Group version
 

You need to study this information in order to file your Adverse Event (AE) to the Dearborn Lyme case definition to the Food and Drug Administration.  Hopefully, when this cryme is prosecuted you can be compensated by the USDOJ in a similar manner to the other Vaccine Injury Compensation cases the USDOJ handles.  THAT is our ultimate goal.

Here is the FDA's AE reporting form re bogus medical testing:
https://www.accessdata.fda.gov/scripts/medwatch/index.cfm?action=consumer.reporting1

You need to study this report (in this yellow box) as well as the Primers Shell Game in order to see why you only ever needed antibody band 41 and the triad of Neurological, Cognitive, and Musculoskeletal signs after ruling out cancer, etc. for a diagnosis of borreliosis.
 

And if you already know about this cryme and are still wondering why the US "government" is so friggin stupid and incompetent, don't.  They just are.  It goes with the territory of government-employee-cults and government-employee union-cults.  Read about cults - they just protect themselves, their retirement funds and investments, and each other, you know, like cops.


First let’s examine the following 7 compelling reports from the “20 Reports that show the Lyme-and-LYMErix-Post-Sepsis Cover-up has to do with Hiding Autism Brain Damage from Vaccines
(http://www.actionlyme.org/POST_LYME_SEPSIS_2014_SUMMER.htm );”
 

These next 7 reports are basically by the NIH, especially the NINDS’s Lyme-And-MS group (Martin and Marques) which confirm and endorse the idea that the Lyme vaccine (OspA, which is a basic Pam3Cys molecule type and a TLR2/1-agonist) gave people the same New Great Imitator and especially Multiple Sclerosis outcomes as “Chronic Lyme” or Late Neurologic Lyme;

These reports are from the NIH, IDSA, the US ARMY, Ft. Detrick, the National Cancer Institute (NCI), and Washington University, St. Louis, MO (wustl.edu) about post-sepsis and the reactivation of the herpesviruses, et al (like AIDS) from exposure to Lyme. [This is how it appears anyway. If it is some other virus like a mouse herpesvirus from a tick bite, we don’t have that data yet. It’s something like that, that obviously no one at the Uncle Sam “government” seems too worried about, therefore, it must be a common thing like from the herpes family. There are easily 20 million of us with a CFIDS, Lyme, or Fibromyalgia etc junk-science diagnosis in America alone (NIH’s own published stats) and no one’s panicking like we got a new, slow Marburg, or contagious scrapie, or a new HIV or whatever going on.]
 

==================== The 7 Reports, 6 of NIH’s plus wustl.edu’s =================


1989 (this is in IDSA's own journal):

NCI and US Army Ft Detrick Pathologist Paul Duray on the CSF cells looking like "Epstein-Barr-like transformed cells" in IDSA's 1989 Reviews Supplement on Spirochetal Diseases:
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Clinical pathologic correlations of Lyme disease.

"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." --
http://www.ncbi.nlm.nih.gov/pubmed/2814170 

Full Text: http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm

=====

1992:

Duray again in 1992, in Steve Schutzer's review of the 1992 Cold Spring Harbor Conference on Lyme:

"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. - book.

=====

2006:

The NIH (NINDS’s MS-Lyme Group) group that discovered that *** OspA *** was the cause of the MS/New Great Imitator outcome of Lyme reporting in the New York Times in the summer of 2013 (Martin and Marques, 2006);
this article says these OspA like antigens constantly shed by Borreliae cause immunosuppression in the humoral immune system, but apparently a chronic inflammatory state in the central nervous system:

"Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression."
http://www.ncbi.nlm.nih.gov/pubmed/16783164


and this report means you might not even have anti-flagellar antibodies (flagellin is a TLR5-agonist) after being exposed to shed fungal OspA like antigens (TLR2/1-agonists):

"Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes.
http://www.ncbi.nlm.nih.gov/pubmed/16479520
 

2013 - Same NIH MS-Lyme Group as above, Martin and Marques:

"When Lyme Disease Lasts and Lasts" – Jane Brody

"Complicating the picture is the fact that some people with PTLDS symptoms apparently never had Lyme disease in the first place, Dr. Marques said in an interview. There are other infectious organisms — Epstein-Barr virus, for example — that can produce similar symptoms and may be the real culprits."
http://well.blogs.nytimes.com/2013/07/08/when-lyme-disease-lasts-and-lasts/

=====

2014:

Wustl.edu discovers that sepsis is like Lyme, in that the survivors of it are likely to have survived via the immunosuppression (TLR2-agonist tolerance/Endotoxin tolerance), but the result is the reactivation of latent viruses:

"Dormant viruses re-emerge in patients with lingering sepsis, signaling immune suppression"

"Patients with lingering sepsis had markedly higher levels of viruses detectable in the blood, compared with the healthy controls and critically ill patients without sepsis. Among the sepsis patients, for example, the researchers found that 53 percent had Epstein-Barr virus, 24 percent had cytomegalovirus, 14 percent had herpes-simplex virus, and 10 percent had human herpes simplex virus-7.

"These viruses generally don’t lead to significant illness in people who are healthy but can cause problems in patients who are immune-suppressed. "

http://news.wustl.edu/news/Pages/27015.aspx

FULL JOURNAL REPORT, snippet…

Reactivation of Multiple Viruses in Patients with Sepsis

“Sepsis is the host's non-resolving inflammatory response to infection that leads to organ dysfunction [1], [2]. A current controversial hypothesis postulates that if sepsis pursues a protracted course, it progresses from an initial primarily hyper-inflammatory phase to a predominantly immunosuppressive state [3]–[7]. Experimental therapeutic approaches in sepsis have almost exclusively focused on blocking early inflammation or host-pathogen interaction and failed [8]–[10]. Recently, immuno-adjuvant therapies that boost host immunity, e.g., GM-CSF and interferon-γ, have been successful in small clinical trials thereby supporting the concept that reversing immunosuppression in sepsis is a plausible strategy to improve outcome [11], [12]. However, several issues have limited this approach including lack of consensus that immunosuppression is a clinically important phenomenon [5], [6], [13]. Also, difficulty in identifying patients with impaired immunity as well as determining optimal timing for administration pose significant challenges to pursuing this approach [14]. While immuno-adjuvant therapies might improve sepsis survival if administered during the later immunosuppressive phase, these agents might worsen outcome if given during the early hyper-inflammatory phase [4], [14]. Thus, a means to distinguish these two contrasting phases of sepsis is needed not only to verify the hypothesis that sepsis progresses to an immunosuppressive state but also to guide use of potential agents which boost immunity.

“Latent viruses such as cytomegalovirus are normally held in abeyance by cellular and immune surveillance mechanisms which if impaired, for example by immunosuppressive medications, often result in viral reactivation, replication, and virally-mediated tissue injury [15]–[20]. Sepsis impairs innate and adaptive immunity by multiple mechanisms including apoptosis-induced depletion of immune effector cells and induction of T-cell exhaustion thereby possibly predisposing to viral reactivation and dissemination [21]–[23]. …”
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0098819 

=====

2014, Here the NIH confirms that they agree that post-sepsis, like wustl above describes, matches their own observations of what happens as a result of Chronic Lyme (EBV reactivated; ie, that being generally accepted as the main driver of MS and Lupus):

NEW, by the NIH: "Surviving Sepsis: Detection and Treatment Advances"

By Carolyn Beans for the National Institutes of Health | August 18, 2014 08:43am ET

http://www.livescience.com/47387-sepsis-diagnosis-treatment-research-nigms.html

"Preventing Secondary Infections

"Some people who survive sepsis can develop secondary infections days or even months later. A research team that included Richard Hotchkiss, Jonathan Green and Gregory Storch of Washington University School of Medicine in St. Louis suspected that this is because sepsis might cause lasting damage to the immune system. To test this hypothesis, the scientists compared viral activation in people with sepsis, other critically ill people and healthy individuals. The researchers looked for viruses like Epstein-Barr and herpes simplex that are often dormant in healthy people but can reactivate in those with suppressed immune systems. [Sepsis Has Long-Term Impact for Older Adults, Study Finds]"


======================== End 7 Reports =================

 

So, that data, those 7 reports are hard to argue with, and they also point to someone else potentially hypothesizing on what the treatment is for post-Lyme-post-sepsis, like wustl or the NIH and not me ☺

Importantly, everyone should go to PubMed and look at the data on medical school students and astronauts and see how the stress hormone cortisol is well-known to be activating mono or Epstein-Barr. If you are an astronaut or a medical school student or overworked resident, your chronic fatiguing disease is allowed to be real and not somatoformically produced with your magical brain ☺
 

Let's side step to show that LYMErix or OspA and OspA-like antigens constantly shed by borrelia in an immune-evasion-come-antigenic variation mechanism that can leave the immune system "completely overwhelmed," even if a mammal was infected with just one spirochete (see the Primers Shell Game).  We all have to know what these fungal OspA etc antigens are, that are shed by borreliae such that we know the pathology it causes.  OspA is or Pam3Cys or tripalmitoyl cysteine molecular type (see that this is confirmed by Ray Dattwyler in the "20 Reports that show the link between Lyme Cryme and Autism").  We have to know what these antigens are in order to know what they do (structure predicts function).  So, if you can't determine the structure, you can go by their function or biochemical properties and in this case, Pam3Cys type antigens are managed by TLR2/1 and that means they are fungal.
So what happens when the body is hyperexposed to fungal antigens?  In most cases, immunosuppression as shown by Justin Radolf and Clifford V. Harding, here, in the Plum Island chapter of Cryme Disease.  They cause the HLA molecules to fail to present antigen and thus, no more antibodies are made.  This is called tolerance.  Use PubMed to examine further what people like Medvedev and Harding have to say about what happens to the immune system after chronic exposure to fungal antigens.  Note in parallel, the data on the NO-TB-VACCINES, duh.  The Lyme criminals were too stupid to even try to discover if there had been any successful lipoprotein vaccines in the past. 



http://www3.interscience.wiley.com/cgi-bin/fulltext/120763430/PDFSTART

Use 141114_FUNGAL_FAILED_VACCINES.htm for about 12 reports that show you can't use this molecule type for a vaccine and that the Lyme criminals never gave a shit what it was or if it had been tried before as a vaccine.

 

 


Returning to what happened with LYMErix - the vaccine that gave people the very disease the ALDF-come-IDSA now deny exists and wrote out of the Dearborn serodiagnostic criteria specifically because of that ☺

[Repeat: The definitions of Lyme borreliosis excluded from the Dearborn case definition (falsified by Allen Steere in Europe in 1992) are the very ones caused by OspA vaccination. You just saw how in the above 7 reports, and there is much more data on that available on PubMed about the pathologies caused by chronic exposure to fungal antigens including cancer, and the similar outcomes of worse disease and immunosuppression from other experiments with fungal vaccines of this same TLR2/1 agonist type such as all the failed Tuberculosis vaccines ☺ ]

 

We back up to what was the original case definition serology the CDC published in 1990 such that we know it was falsified at Dearborn, and this data jives with what we know from the 7 reports by the NIH above:

1986, Allen Steere says:
“Antigens of Borrelia burgdorferi recognized during Lyme disease. Appearance of a new immunoglobulin M response and expansion of the immunoglobulin G response late in the illness.

“Using immunoblots, we identified proteins of Borrelia burgdorferi bound by IgM and IgG antibodies during Lyme disease. In 12 patients with early disease alone, both the IgM and IgG responses were restricted primarily to a 41-kD antigen. This limited response disappeared within several months. In contrast, among six patients with prolonged illness, the IgM response to the 41-kD protein sometimes persisted for months to years, and late in the illness during arthritis, a new IgM response sometimes developed to a 34-kD component of the organism. The IgG response in these patients appeared in a characteristic sequential pattern over months to years to as many as 11 spirochetal antigens. The appearance of a new IgM response and the expansion of the IgG response late in the illness, and the lack of such responses in patients with early disease alone, suggest that B. burgdorferi remains alive throughout the illness.”
http://www.ncbi.nlm.nih.gov/pubmed/3531237


1990, CDC publishes this case definition:
http://www.actionlyme.org/CDC_DOCUMENTS_1990.htm




The 1990 case definition standard (above) was basically based on the 1986 report (above that) by Allen Steere, which was that you have to merely show a person has a Relapsing Fever infection, with the “new IgM and changing bands emerging over time seen in repeat or serial Western Blots.” That meant, according to Allen Steere, “the bug is still alive.” New, IgM type bands meant the bug was still alive and you have not killed it with antibiotics. Steere also wrote in that same report that really all you need is band 41 to diagnose Lyme, just rule out Syphilis. That is important to remember. You only need band 41or the anti-flagellar antibody and the triad of symptoms to diagnose Lyme. The US patent 5,618,533 specific recombinant fragment of Borrelia burgdorferi flagellin of Yale’s is a better test and is an actual FDA-validation according to their criteria (as shown in the Primers Shell Game chapter of Cryme Disease).

I personally – and I am not a doctor – recommend everyone rule out all blood cancers since the symptoms of Chronic Lymphocytic Leukemia for example are identical to Chronic Lyme or MS, not to mention the fact that Lyme and LYMErix both are known to cause cancer as are the mycoplasma to which chronic late neurologic Lyme victims now are tolerized to (fungal).

 

And what is the current, 1994 CDC Dearborn case definition?
http://www.cdc.gov/mmwr/preview/mmwrhtml/00038469.htm

“It was recommended that an IgM immunoblot be considered positive if two of the following three bands are present: 24 kDa (OspC) * , 39 kDa (BmpA), and 41 kDa (Fla) (1).
“It was further recommended that an that IgG immunoblot be considered positive if five of the following 10 bands are present: 18 kDa, 21 kDa (OspC) *, 28 kDa, 30 kDa, 39 kDa (BmpA), 41 kDa (Fla), 45 kDa, 58 kDa (not GroEL), 66 kDa, and 93 kDa (2).”

 

That is very different criteria from the first criteria. First you only needed band 41, or test using repeat Western Blots to look for new IgM bands since Lyme is a relapsing fever organism, and the nature of the relapse is antigenic variation (producing new antigen and thus new IgM bands will be produced in a human), … and now all of a sudden you have to have all these bands showing up at once (indicative only of the hypersensitivity, HLA-linked response) and just ignore IgM bands, basically.
 

You can assume that the reason the IDSA/ALDF/CDC/Yale Lyme criminals do not want anyone treated for Lyme is because late in the disease it’s really about fungal antigen tolerance and cross tolerance, as well as reactivated herpesviruses. They don’t want Lyme victims being treated with antibiotics because that might help transfer antibiotic resistance genes between all the OTHER infections we have, like fungal, like Tuberculosis, Chlamydia, Candida, and whatever else … for which we are now carriers, … and you don’t treat the herpesviruses and subsequent B cell mutations with antibiotics.

IDSociety.org likes to say what diseases are not, but they never say what diseases are. It’s pretty strange but we got no Einsteins in that bunch. IDSA be like… an incomplete sentence. They’d be good screenwriters for American soap operas. The rest of MD-America does not even notice that IDSA’s is one funny script, even after these crooks lost their “vaccine,” Senator Richard Blumenthal (a former USDOJ prosecutor) sued them for Anti-Trust, and Edward McSweegan became America’s infamous NIH employee and America’s one and only “Man With No Work.”

 

So, Follow: First, Lyme was a regular old Relapsing Fever organism and a “New Great Imitator!” Later, it at the same time the crooks had a vaccine candidate in early phase trials, become nothing and a non-disease. We were then about to get “a vaccine for a disease that causes no illness.” That is still the current position of Yale, CDC, IDSA, and the ALDF/EUCALB. “Lyme patients are not sick, and OspA was a vaccine.” IDSA still makes that claim today. No one in the AMA or Mass Medical Society or NEJM or any other association or society of “doctors” even blinks at these contradictory notions. To me it looks like a case of Kraepelinian split-brain. We should wonder what other evidence there might be that medical school is a cult that produces schizophrenia.


 

Here is basically of the series of events that occurred in the process of redefining Lyme as a non-disease to pass off a bogus vaccine:

 

1986, Edward McSweegan trashes U.S. Navy for $$$ for his psycho buddies at the ALDF.com cabal in a letter to Senator Barry Goldwater. See the Navy’s furious response. Sweeg thinks there can be a vaccine for Relapsing Fever, confirming the paraphysical theory that arrogance is the seed corn or germinal element in true, genuine stupidity and/or the development of a criminal mind.
http://www.actionlyme.org/GOLDWATER_LETTER.htm


1988, Raymond Dattwyler & immune-suppressing, seronegative Lyme; supernatant (lipid layer) of borrelia mash causes NK cell anergy or a blunted immune response. Later Dattwyler tells the FDA Vaccine committee that the seronegative patients are the sickest (now we know why, as shown above where Lyme and LYMErix are the Great Detonators of the latent herpesviruses and expanded or cross tolerance to other than TLR2/1-agonist bearing antigens; in short, they’re double-fatigued and neurologically damaged):
http://actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm




1990, CDC: "Diagnose Lyme as if it was Relapsing Fever."
http://www.actionlyme.org/CDC_DOCUMENTS_1990.htm


1990, Allen Steere reports that "NeuroLyme won't test positive," uses Dattwyler and Volkman’s Seronegative Lyme T Cell Assay
http://www.actionlyme.org/STEERES_SERONEG_LYME_ASSAY.htm
http://www.actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm

CHRONIC NEUROLOGIC MANIFESTATIONS OF LYME DISEASE (NEJM, Nov 1990)
http://www.nejm.org/doi/pdf/10.1056/NEJM199011223232102
Says Steere:




“If the patient was seronegative according to these methods, the serum was further tested by immunoblotting (25) and peripheral blood mononuclear cells were tested for reactivity with borrelial antigens by proliferative assay.(26)"

And what was reference number 26?


 


Pretty amazing, huh?


1990, ALDF.com founded, self- proclaimed “entrepreneurial quartet” is McSweegan, Fish, Wormser and Connolly. (You will want to look at who are their sponsors and on their board, seriously.)
http://www.actionlyme.org/CONNOLLY_FISH_WEINSTEIN.htm
http://www.actionlyme.org/ALDF_BOARD.htm

 

1992, CDC officer Allen Steere falsifies testing in Europe:
http://www.actionlyme.org/STEERE_IN_EUROPE.htm
The PubMed links to those 2 reports – no full text available, that is why I got them out of the Yale Medical Library in 2002 and scanned them in are:
“Antibody responses to the three genomic groups of Borrelia burgdorferi in European Lyme borreliosis.”
http://www.ncbi.nlm.nih.gov/pubmed/8106763
“Western blotting in the serodiagnosis of Lyme disease.”
http://www.ncbi.nlm.nih.gov/pubmed/8380611

Of those 2 reports of Steere’s shenanigans in Europe, only the second one is made a part of CDC’s Dearborn booklet but the first one is where you can see how he falsified the testing.

Steere in Europe used bogus high passage strains that drop plasmids helping leave OspA and B out of the diagnostic standard  (by using the recombinant protein end only- you need the lipids to be immune stimulatory) for his later monopoly on post-LYMErix-approval North America, with Corixa, Yale’s L2 Diagnostics and Imugen, officially listed on the Securities and Exchange Commission (SEC) as “partners” in sharing licensing of the RICO Monopoly patent with the strain of Borrelia that had dropped an OspA-B plasmid US Patent 6,045,804 (we will come to this later, it is critical to the whole scam and shows the intent of their entire enterprise);



Here is a transcript of what is in the first report on exactly how Steere defrauded Uncle Sam:

“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 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 -"




Here is what it says in the Persing/Schoen/Steere or Imugen RICO Monopoly patent, that shows the intended monopoly:

“Method for detecting B. burgdorferi infection”

"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 or diagnostic applications where only part of the subject population has been vaccinated or where the vaccination status of the population is unknown. "
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


The monopoly on post-LYMErix-FDA-approval testing for all vector borne diseases in America and Canada was their stated intention.  Once LYMErix was on the market, you had to use a strain of borrelia that did not have the vaccine antigens in them, because you never test for vaccine efficacy with the very same antigen as the vaccine antigen (you would not know if the person has the actual virus or whatever, or that antibody came from the vaccine). So, their monopoly depended on LYMErix being on the market.  That way, Corixa, L2 Diagnostics and Imugen would be the only labs in the country licensed to use this RICO strain.  They, at the same time would have access to all the human blood to pharm all sorts of DNA data from humans as well as any new and emerging infectious diseases... meaning even more vaccine patents. 

So, they falsified the case definition to leave out neurologic Lyme cases, and they left OspA and B out for a later monopoly on testing and future patents.  And there, you just read that in a patent developed by Schoen and Persing in 1995.
 

1992, CDC staff, Barbara Johnson and Joe Piesman, own patents with SmithKline that show 2 kinds of Lyme, HLA-linked and non-HLA-linked antigens:
http://www.google.com/patents/CA2135800A1?cl=en

“Summary of the Invention
“In one aspect, the invention provides isolated --B. burgdorferi antigens which are regulated and differentiated by growth of the B. burdorferi in a tick vector. Novel antigens of the invention are listed below in Table I.

“Certain of these antigens are characterized as being B. burgdorferi B31 strain specific and major histocompatibility complex (MHC) nonrestricted. Certain other of these antigens are characterized as being MHC-restricted.”

 

So, what the hell is the CDC talking about ”MHC-restricted and MHC non-restricted?” What we know that to mean is for instance, classic autoimmune diseases tend to be MHC-restricted, or the antigens, due to intermolecular forces, bind in the HLA groove too strongly causing a hypersensitivity response. That is the new definition Steere claimed in these 1992 reports and at the CDC’s 1994 Dearborn conference.
The very re-definition of “Lyme Disease” at Dearborn became “HLA-restricted,” “just the arthritis,” “too-many-antibodies-HLA-associated response.” In short, Steere and the CDC claim Lyme Disease is just an HLA-restricted disease. Here in their 5 1992 patents with SmithKline, the CDC mentions the other outcome? The no- or fewer antibody result?


1993, Barbour and Fish slam Neurologic Lyme victims:
The SOCIAL Phenomenon of Lyme Disease or what the hell ever… where they admit Phase I and Phase II trials of OspA vaccines are underway. Therefore, as is shown in the Persing RICO Monopoly patent from 1995 shown and linked above (US 6,045,804), they already knew the OspA vaccines were causing a disease indistinguishable from vaccine failure, or CHRONIC LYME:
http://actionlyme.org/BarbourFishpdf.pdf

 

Compare the 2 kinds of Lyme in the RICO complaint filed with the USDOJ in July 2003– compare the blots. On the left is neurological Lyme (the sickest, according to Ray Dattwyler) and on the right is the HLA-linked outcomes of arthritis and acrodermatitis:
http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm


 

So, these assholes left out the left-sided, neurological outcomes in their Dearborn scam. The whole point of the redefinition of Lyme at Dearborn was to narrow it to just the HLA-linked hypersensitivity cases. This is how and why they get away with perjury. When the IDSA/Yale Lyme crooks say “Lyme Disease” that means HLA-linked arthritis AND NO OTHER SYMPTOMS.

 

Here next, in 2005, Klempner and Wormser re-revealed that “Lyme Disease” is just one thing. There are 2 things, and the controversial thing really does not have a name right now, but “Lyme Disease” is JUST a bad knee and no other illness signs. THAT is the definition. It’s a legal one and a criminal one, and based on bullshit and no consensus, but here is what it is again (2005):

“A Case-Control Study to Examine HLA Haplotype Associations in Patients with Posttreatment Chronic Lyme Disease”


 

People with ONLY the HLA-linked arthritis (the falsified Dearborn case definition)…“Patients generally feel well aside from their arthritis symptoms,” Say Wormser and Klempner. Pretty amazing right? That the people with the falsified Dearborn case definition of “only an HLA-linked arthritis in a knee” have only an HLA-linked arthritis in a knee and no other symptoms?
http://jid.oxfordjournals.org/content/192/6/1010.full

I love it when that happens ☺
You falsify the case definition and say “ONLY the HLA-linked hypersensitivity response can be a ‘case’ of ‘Lyme Disease,’" and then 11 years later say, “Oh, how amazing for us to find only the HLA-linked case definition is HLA-linked and is only a bad knee. Maybe someone can promote me to the head of a CDC bioweapons lab in Boston on accountta my astuteness.”



 

1994, June FDA LYMErix Meeting (note that June precedes October, so the FDA never approved of the Dearborn method, not to mention it was research fraud and not a consensus):
http://www.actionlyme.org/1994_FDA_MEETING_LYMERIX.htm

Transcript of June 1994 FDA Meeting Minutes:

“So, individuals with a poor immune response tend to have worse disease.”

 

We know why now ☺ Borrelial fungal antigens cause immunosuppression and… a classic “post-sepsis” like result with chronic active EBV, et al.

 

The CDC recently made a big ta-do over the Blumenthal et al letter to the Office of Policy and Management, where the Senators are forcing the FDA to do their jobs and assure that the testing for Lyme is validated according to their own FDA rules (See the Primers Shell Game for more on that). The CDC is trying to say the Dearborn method was FDA validated.

False. The FDA had nothing to do with the Dearborn stunt.



1994, CDC's invitation to participate in Dearborn .pdf   Labs were invited, they said the Steere proposal sucked, CDC blew off these labs recommendations:
http://www.actionlyme.org/DEARBORNINVITATION.pdf

 

1994, October CDC's Dearborn Booklet .pdf
http://www.actionlyme.org/DEARBORN_PDF.pdf

 

Dearborn, Who Said What?
http://www.actionlyme.org/DEARBORN_WHO_SAID_WHAT.htm

1) Gary Wormser at New York Medical College reports that Steere’s Dearborn proposal method detected 9/59 of IgG cases (which, most very sick people being detected too late are obviously not going to have this Early Lyme profile, especially considering Steere’s Late Lyme Arthritis Dearborn falsified definition was intended to be for early Lyme, regardless of his lab shenanigans with the strains and the phony recombinant OspA and B in Europe):
Serodiagnosis in Early Lyme Disease


 

So, Wormser says only 9 of the 59 meet Steere’s Late Lyme Arthritis case definition. That’s 15% accurate.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC266355/pdf/jcm00024-0026.pdf


2) Igenex- Steere’s IgG detected 8% of the cases

3) Imugen – Steere’s method detected 14% of the cases:

4) Wisconsin - Steere’s method was 15% accurate

5) UCONN- Larry Zemel was referring to Lyme as comparable to juvenile rheumatoid arthritis. Recommended adding band 50 for children’s blots.

6) Roche—28% were positive for 5 of 10 Steere IgG bands.

7) Wadsworth – had some different scoring system. Did not report on accuracy of Steere

8) Ontario Ministry of Health

9) Lutheran Hospital— 22 % were accurate by Steere’s IgG

10) MarDx Labs – recommended adding bands 31 and 34, but were given CDC positive arthritis positive blood to falsely qualify their test strips. Theirs were used in both vaccine trials. MarDx was later sold to an Irish company, Trinity Biotech, Dublin, so presumably all they know about the crime was taken out of the country.

11) CDC Atlanta – talked about mice, not humans. The mouse criteria was 2 out of three from OspC, 16 kD, 17.9 kD, for the mice. Wonderful. Everyone is concerned about Western Blotting the poor little mice. Such a tragedy that they have to run around sick. We read about this tragedy at least once a week in the New York Times. People say each other all the time, “Oh, what wonderful weather we’re having, too bad the mice are too sick with Lyme Disease to enjoy it. “ You see those little collection tins at all the supermarket check-outs: “Please Donate One Dollar for the Poor Mice with Lyme Disease!”


 

So, we got this standard anyway, even though none of the invited participants agreed - not by a long shot.  See the Primers Shell Game reports here or at this link:
http://www.actionlyme.org/PRIMERSHELLGAME.htm
for an explanation of how VALID testing is performed according to the FDA rules and how Yale knows all about how to validate a method, validated one (Bb specific flagellar antigen) and patented it (US 5,618,533).  So that's all obvious criminal fraud.


Who was involved with approving the bogus Dearborn method at Dearborn when all the invited labs said it sucked??  Why, none other than the CDC vaccine patent  owners and all the scammers you see here:
http://www.actionlyme.org/Dearborn_Who_Approved.htm





Alan Barbour, Edward McSweegan, Allen Steere. Arthur Weinstein, "The CDC Lyme Disease Group" (Barbara Johnson)

Kind of amazing. The same people involved in the OspA vaccines scam were involved in falsifying the testing.

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



Igenex, Harris’ view of the Dearborn event .pdf published in the Lyme Disease Foundation’s journal:
http://www.actionlyme.org/HARRIS_IGENEX_DEARBORN.pdf


 

1998 FDA Meeting where Luft says LYMErix produces a multi-system disease just like chronic Lyme:
http://www.fda.gov/ohrms/dockets/ac/98/transcpt/3422t1.rtf

BEN LUFT: "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 [means not limited to "bad knees”- KMD]. 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 sero positive, you can start to have a different take on when someone has an adverse event of 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. I can only say from my own ..."


 

Evidence Lyme criminals knew LYMErix produced the same "multisystem disease" as "Chronic Lyme"

1) Ben Luft said it at the 1998 FDA meeting (above), 2) Dave Persing said it in his RICO patent (above), 3) Fish and Barbour started trashing us with their “Social Aspects” bullshit in 1993 (above) paving the way, claiming we’re all nuts and hysterics for when the vaccine produced the same result so they’d have a ready made derogatory slander/libel answer and propaganda,…

... 4) Dave Persing and his company Corixa wanted to sell vaccine adjuvants but they had to drop OspA as a candidate adjuvant because, he said… in another patent (applied for May, 2001 while LYMErix was still on the market, harming people and he never said anything to the FDA about it)…
“Prophylactic and therapeutic treatment of infectious and other diseases with mono- and disaccharide-based compounds”
"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

5) In 1998 Robert Schoen (involved in developing the RICO monopoly patent - US 6,045,804 - with Dave Persing, 1995) wrote this, once again, paving the way for when the vaccine came on the market and caused the same systemic, seronegative disease damage…

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



========

Next, how these crooks lied about their vaccine results, and what happened after LYMErix was approved and on the market.

 

The 1998 Vaccines Reports (ImmuLyme and LYMErix):

LYMErix results (76% "safe and effective"):
http://content.nejm.org/cgi/content/abstract/339/4/209

ImmuLyme results (92% "safe and effective"):
http://content.nejm.org/cgi/content/abstract/339/4/216 

From the LYMErix trial, "categories of outcomes:"
http://content.nejm.org/cgi/content-nw/full/339/4/209/T1


 

Here the crooks claim "we can't read our OspA vaccine results" reports, which means the lied in their OspA vaccine safety and efficacy reports, since they both claimed to be using the Dearborn method and MarDx's Western Blot test strips:

1) SCHOEN and PERSING, with JOHN ANDERSON,1996 - the RICO report:
http://jcm.asm.org/cgi/reprint/35/1/233?view=long&pmid=8968914

2) SCHOEN AND PERSING IN THEIR 1996 RICO METHOD PATENT:
The Dave Persing, Mayo Clinic FRAUD Patent-6,045,804 
3) PERSING WITH SIGAL EXPLAINING THAT THE WESTERN BLOTS WERE UNREADABLE, 2000:
http://www.journals.uchicago.edu/doi/pdf/10.1086/313920

4) Yale's ROBERT SCHOEN in the 1998 Munchausen's Book, instructing MDs to blow off LYMErix systemically injured people ("but send the post-vaccination blood to the Yale L2 Diagnostics RICO lab if you must bother to be a physician").

This ▲ is obviously a FALSE CLAIM or a QUI TAM or FRAUD on the GOVERNMENT since they're declaring to the FDA, in the LYMErix case, saying they had a vaccine.
http://www.usdoj.gov/usao/eousa/foia_reading_room/usam/title9/crm00921.htm


 

I'll just plagiarize myself here and just use the text from the reports below on "Lyme Facts" and "Borreliosis Basics":

So in the Fall of 1998, the LYMErix vaccine was approved, anyway, by the FDA (the FDA panel being loaded with people like Allen Steere, Robert Schoen, and Vijay Sikand – the very people who ran the OspA trials) and came on to the market in late 1998 despite numerous “provisos.” More than 1,000 systemic adverse events were reported through the VAERS from September 1999 to November 2000, whereupon the FDA granted a public hearing, January 31, 2001:

http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2.htm

Whereupon I blew the whistle on Dearborn and how LYMErix actually caused immunosuppression (the FDA did not scan in the last 19 pages of this booklet, which were 19 pages out of the Dearborn booklet, proving no one agreed with Steere's proposal for an antibody panel for a "case definition":
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf

 
Several months later, in the fall of 2001, Karen Forschner of the Hartford, CT based Lyme Disease Foundation (Lyme.org) delivered to the FDA – in person -, a patent owned by Bridgitte Huber at Tufts where it was declared that OspA was technically a “toxin,” right in the abstract (US Patent 6,689,384). The FDA then gave SmithKline and Yale (the assignee of the LYMErix patent), an ultimatum: “Either you remove LYMErix voluntarily or we will order it off the market.” SmithKline chose to avoid the embarrassment and pulled their own non-vaccine.

We’re still stuck with this bogus Dearborn case definition, despite numerous attempts at lawsuits against IDSA, SmithKline, and filing complaints to the U. S. Department of Justice. It is still very dangerous for the public to be unaware that the average person, or 85% of us – who are the “seronegative patients are the sickest ,“ according to Raymond Dattwyler at the 1994 FDA meeting on Lyme and LYMErix (which preceded Dearborn) - have no chance of testing positive to this criminal CDC’-Dearborn standard, because the actual disease is one of immunosuppression, or is an Acquired Immune Deficiency,… or is similar to AIDS with all the opportunistic infections that the Lyme and LYMErix victims cannot control.

It was said at the time LYMErix was still on the market that this vaccine, via its claimed mechanism of disinfecting ticks with human antibodies (yes, if you can believe it), that LYMErix would turn humans into walking cannisters of tick disinfectant, when in fact, LYMErix turned people into walking “cesspools of disease.” The same is true for Chronic Lyme. Chronic Lyme victims’ immune systems are “overwhelmed”- a term used by CDC officer Alan Barbour, when describing what antigenic variation in spirochetes does to humans (US Patent 6,719,983). This is a term you want to remember in case you hear it again: “overwhelmed” immune system means: “turned off.” “Turned off” is the complete opposite of an “inflammatory” or “autoimmune disease.”

 

That's all for now, folks.... KMD

 

 

 

 

141122:  SUBMITTED IN COMMENTS FOR THE NIH RULE PROPOSAL RE FDA VALIDATED TESTING FOR CLINICAL TRIALS (see link at the end):

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

We in the Lyme Cryme Victim community would like to know if any of these rules related to FDA validations requirements (see "Guidelines on the Validation of Bioanalytical Methods," by the FDA; ie., specificity, linearity, accuracy, limit of detection, precision, ruggedness, where Yale's patented flagellin method, US Patent 5, 618, 533 is the only method that meets the FDA's criteria for a Validation) will be retroactively applicable to previous bogus Clinical Trials such as Mark Klempner's 2001 research fraud report on the non-retreatment of 2/3rds of his victims with IV ceftriaxone (2/3rds never had IV ceftriaxone before, yet this was called a re-treatment study); the criteria [for Klempner’s bogus clinical trial] was the falsified CDC Dearborn case definition:
http://content.nejm.org/cgi/reprint/345/2/85.pdf 


or [will it apply to] the 2 bogus Lyme vaccine trials:

LYMErix results (76% "safe and effective"):
http://content.nejm.org/cgi/content/abstract/339/4/209 

ImmuLyme results (92% "safe and effective"):
http://content.nejm.org/cgi/content/abstract/339/4/216 

Dearborn Falsified case definition (as you can see, there was no consensus, and nowhere will you find evidence that the FDA approved this new criteria, since at the FDA meetings in 1994 and 1998, participants objected the entire time and said "HLA-linked Lyme arthritis was the exception rather than the rule," and that "seronegative patients were the sickest (Dattwyler).
http://www.actionlyme.org/DEARBORN_PDF.pdf

The seronegative and neurological cases were excluded by Allen Steere in Europe and also at the 1994 CDC Dearborn meeting where the average consensus from all the invited labs was 15% accuracy. The FDA says your testing should detect ALL the cases or be 100% accurate. The current case definition for Lyme Disease was not valid and it was far from a consensus.

Recently Senators Blumenthal, Gibson, et al requested that the OBM.gov ask the FDA to enforce their Guidelines on Validations regarding the Lyme Disease testing schema falsified by Allen Steere in Europe in 1992
http://www.actionlyme.org/STEERE_IN_EUROPE.htm 

where he fraudulently left OspA and B out of the case definition to satisfy a later intended monopoly on post-FDA "approval" of the Yale OspA vaccine, in grants, national testing for vector borne diseases, patents for new vector borne diseases vaccines and test kits, and for all the HLA-related disease susceptibility data from the human population... intended to OWN all personal, private, proprietary data exclusively by the 3 labs who orchestrated the scam: Corixa (later purchased by SmithKline to take evidence of the LYMErix/Dearborn cryme out of the country), Yale's L2 Diagnostics, and Imugen (Norwood, Mass), and never approved by anyone at the CDC's bogus Dearborn Meeting on the "standardization of testing" for Lyme, as previously mentioned.

The 3 RICO monopoly labs who intended to use this patent (you can see it is related to the Dearborn case definition because there is no OspA-B plasmid, which interferes with the reading of Western Blots)

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

No one knows the exact relationship between Allen Steere and Imugen but it was whispered that he was part-owner of Imugen. I myself cannot find that information to confirm. Here is what was posted by Corixa years ago demonstrating that Yale's L2 Diagnostics and Imugen were officially listed as "partners" (even with the SEC). (Yale's and L2 Diagnostics Robert Schoen worked on the development of the OspA-B-plasmid-absent strain as a method to test for post-LYMErix victims. That fact does not come up in that US # 6,405, 804 RICO patent):
https://groups.google.com/forum/?hl=en#!original/sci.med.diseases.lyme/D6v-QHQdMbc/WupHjKwFilIJ 

So, the whole thing was total corruption for personal gain by CDC officers, many of whom own multiple patents, in particular Alan Barbour and Barbara Johnson - the same people who "approved" this falsified Dearborn case definition. We're also wondering how we all will be compensated for this crime, that mainly seemed to have the intention of benefiting Yale since they owned the LYMErix patent, and were conspiring with Corixa and Imugen for a later monopoly on testing of people who had been unfortunately vaccinated with this Pam3Cys vaccine which of course was never a vaccine since it is a fungal antigen and TLR2/1-agonist, well known to be of the fungal type, causing T cell anergy.

Thank you. We all want to know when this will be prosecuted. We won't be backing down until it is. This was an international cryme affecting thousands of our personal friends in Europe as well. We look bad. We look like the Germans during the NAZI regime... it looks like we aren't standing up to these war criminals.

Kathleen M. Dickson
Analytical Chemist, formerly with Pfizer
Whistleblower for Dearborn and OspA as immunosuppressive:
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
RICO Complaint filed with the USDOJ July, 2003
http://www.actionlyme.org/index.htm


Clinical Trials Registration and Results Submission
http://www.regulations.gov/#!documentDetail;D=NIH-2011-0003-0003


 

141119;  For People Interested in what the NIH thinks about treatments for Chronic Active Lyme/Epstein-Barr Etc/Chronic Fatigue Syndrome, which are all basically reactivated herpesviruses with fungal antigen-induced immunosuppression...

MEANWHILE, if it is the CDC reporting, you can NOT believe the data. CDC has been caught lying about
1) what Lyme is;
2) changing the definition of Lyme "Disease" to exclude neurologic cases (Dearborn);
3) the CDC continually lies to the public about the Senators’ (Gibson, Blumenthal et al) activity regarding asking the OBM.gov to FORCE the FDA to do their jobs and assure Lyme testing meets their own definition of “valid,” and they lied to the public about the FDA validating Dearborn.  The FDA did no such thing.  In fact, they objected and said the seronegative patients were the sickest, and said to continue to use the old standard of repeat Western Blots and NO ELISAs (Dattwyler, below);
4) CDC denies the viability of the cyst or spheroplast form of Lyme, while earlier (1964) having been the authors of exactly how to weaponize Borreliae,
5) the CDC was caught throwing out the red and white blood cells to which the mycoplasma or epERTHROzoons as they were formerly called, to which the mycoplasma adhere and invade, when trying to prove Chronic Fatigue Syndrome is not due to mycoplasma (in addition to some combination of herpesviruses);
6) the CDC are lying about the HPV vaccine, giving women a false sense of security against cervical cancer, when the other STDs like chlamydia and mycoplasma cause endometriosis and subsequent infertility. [”Here, take this vaccine and go ahead and be a whore (Secret: Just don’t expect to ever be a mother).”] 
7) This is all not to mention all the lies they tell about childhood immunizations (MMR) and how it is the vaccine viruses themselves causing the brain damage we call Autism.  SEVEN HUGE LIES like that affecting millions of people worldwide is quite enough to be convinced. You can also assume they know Lyme and LYMErix are the Great Detonators of cancer, MS, ALS, (indirectly thru the other microbes activated by OspA/Borrelia) and everything else because they have been lying about it since Day One, as demonstrated by their deployment of that true moron Allen Steere, originally, to Old Lyme.- KMDickson


 

1)   "Chronic active Epstein-Barr virus infection (CAEBV) is characterised by chronic or recurrent infectious mononucleosis-like symptoms, such as fever, hepatosplenomegaly, persistent hepatitis and extensive lymphadenopathy. Patients with CAEBV have high viral loads in their peripheral blood and/or an unusual pattern of EBV-related antibodies. This disease is rare but severe with high morbidity and mortality. Nearly three decades have passed since this disease was first identified, and recent advances in technology have increased our understanding of CAEBV pathophysiology. There is accumulating evidence that the clonal expansion of EBV-infected T or natural killer (NK) cells plays a central role in the pathogenesis of CAEBV. However, it remains unclear whether CAEBV is truly a monoclonal lymphoproliferative disorder. EBV-infected T or NK cells are able to evade the host cellular immune system due to the limited expression of viral proteins of reduced antigenicity. Recent studies suggest that infection of T or NK cells is a common event during primary EBV infection. A defect or single nucleotide polymorphism in host immune-modulating genes may allow for the expansion of virus infected cells giving rise to CAEBV. In this review, I summarise our current understanding of the pathogenesis of CAEBV and propose a model of CAEBV pathogenicity.
http://www.ncbi.nlm.nih.gov/pubmed/16791843

 

2)    RELATED ARTICLES:
http://www.ncbi.nlm.nih.gov/pubmed?linkname=pubmed_pubmed_citedin&from_uid=16791843


 

3)   NIH >> "Optimal Treatment for Chronic Active Epstein-Barr Virus Disease"

"Epstein-Barr virus (EBV) is a ubiquitous virus that infects...

"Most patients with CAEBV present with fever, liver dysfunction, and splenomegaly. About half of patients have lymphadenopathy, thrombocytopenia, and anemia (3). Other frequent symptoms (occurring in 20–40% of patients) include hypersensitivity to mosquito bites, rash, hemophagocytic syndrome, and coronary artery aneurysms. Less common features are calcification of basal ganglia, oral ulcers, lymphoma, interstitial pneumonia, and central nervous system disease. The presence of thromobocytopenia, onset at age 8 or older, and infection of T cells with EBV was associated with a poorer prognosis (5). Death is frequently due to liver failure, malignant lymphoma, or opportunitistic infections.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2776035/ 


 

4)    "Characterization and treatment of chronic active Epstein-Barr virus disease: a 28-year experience in the United States."
NIH AGAIN >>
http://www.ncbi.nlm.nih.gov/pubmed/21454450

Although patients with CAEBV from Japan have normal or increased numbers of NK cells, many of our patients had reduced NK-cell numbers. Although immunosuppressive agents, rituximab, autologous cytotoxic T cells, or cytotoxic chemotherapy often resulted in short-term remissions, they were not curative. Hematopoietic stem cell transplantation was often curative for CAEBV, even in patients with active lymphoproliferative disease that was unresponsive to chemotherapy. These studies are registered at http://www.clinicaltrials.gov as NCT00032513 for CAEBV, NCT00062868 and NCT00058812 for EBV-specific T-cell studies, and NCT00578539 for the hematopoietic stem cell transplantation protocol.


 

5)    NIH AGAIN >>>   "Altered antibody profiles against common infectious agents in chronic disease"

“Despite the important diagnostic value of evaluating antibody responses to individual human pathogens, antibody profiles against multiple infectious agents have not been used to explore health and disease mainly for technical reasons. We hypothesized that the interplay between infection and chronic disease might be revealed by profiling antibodies against multiple agents. Here, the levels of antibodies against a panel of 13 common infectious agents were evaluated with the quantitative Luciferase Immunoprecipitation Systems (LIPS) in patients from three disease cohorts including those with pathogenic anti-interferon-γ autoantibodies (IFN-γ AAB), HIV and Sjögren's syndrome (SjS) to determine if their antibody profiles differed from control subjects. The IFN-γ AAB patients compared to controls demonstrated statistically higher levels of antibodies against VZV (p=0.0003), EBV (p=0.002), CMV (p=0.003), and C. albicans (p=0.03), but lower antibody levels against poliovirus (p=0.04). Comparison of HIV patients with blood donor controls revealed that the patients had higher levels of antibodies against CMV (p=0.0008), HSV-2 (p=0.0008), EBV (p=0.001), and C. albicans (p=0.01), but showed decreased levels of antibodies against coxsackievirus B4 (p=0.0008), poliovirus (p=0.0005), and HHV-6B (p=0.002). Lastly, SjS patients had higher levels of anti-EBV antibodies (p=0.03), but lower antibody levels against several enteroviruses including a newly identified picornavirus, HCoSV-A (p=0.004), coxsackievirus B4 (p=0.04), and poliovirus (p=0.02). For the IFN-γ AAB and HIV cohorts, principal component analysis revealed unique antibody clusters that showed the potential to discriminate patients from controls. The results suggest that antibody profiles against these and likely other common infectious agents may yield insight into the interplay between exposure to infectious agents, dysbiosis, adaptive immunity and disease activity.

http://www.ncbi.nlm.nih.gov/pubmed/24312567

PLoS One. 2013 Dec 2;8(12):e81635. doi: 10.1371/journal.pone.0081635. eCollection 2013.

NIH >>> (Same report, full text):

Altered Antibody Profiles against Common Infectious Agents in Chronic Disease

"Moreover, a major gap exists regarding our understanding of whether microbes and viruses, which are not generally recognized to cause chronic illnesses, show more complex interactions in chronic diseases."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847058/



Fungal-Viral Synergy,anyone?? (referring to the above report) >> "To potentially characterize the interplay between additional infectious agents in these patients compared to controls, we employed LIPS to profile antibodies against 13 different infectious agents including viral and fungal agents." -- yup.

Like LYMErix-like shed Borrelial TLR2/1 agonists activating EBV, ya mean??


Same report, Number 5 above, Authors, participants:


1Clinical Dental Research Core, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, United States of America
2Western Regional Research Center, U.S. Department of Agriculture, Albany, California, United States of America
3Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, Maryland, United States of America
4Sjögren Syndrome Clinic, Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, United States of America
5Department of Perioperative Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland, United States of America
6Medical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America
7Center for Infection and Immunity, Columbia University, New York, New York, United States of America
8Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America
Charité-University Medicine Berlin, Germany

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847058/


 

6)    PubMed Search, all “ EBV DNA and altered immunity “
http://www.ncbi.nlm.nih.gov/pubmed/?term=EBV+DNA+and+altered+immunity


 

7)    "Detection of viral DNA and immune responses to the human herpesvirus 6 101-kilodalton virion protein in patients with multiple sclerosis and in controls."

"Human herpesvirus 6 (HHV-6), a latent lymphotropic and neurotropic virus, has been suspected as an etiologic agent in multiple sclerosis (MS). The study was undertaken to correlate virologic evidence for HHV-6 activity with the state of host immunity to HHV-6 in MS patients and control subjects. The study revealed that cell-free DNA of HHV-6 was detected more frequently in both serum and cerebrospinal fluid of MS patients than in those of control subjects. T cells recognizing the recombinant 101-kDa protein (101K) corresponding to the major immunoreactive region unique to HHV-6 occurred at significantly lower precursor frequency in MS patients than in control subjects. The resulting HHV-6-specific T-cell lines obtained from MS patients exhibited skewed cytokine profiles characterized by the inability to produce interleukin-4 (IL-4) and IL-10. The decreased T-cell responses to HHV-6 and the altered cytokine profile were consistent with significantly declined serum immunoglobulin G (IgG) titers for HHV-6 of MS patients compared to those of control subjects. In contrast, elevated serum IgM titers for HHV-6 were detected in the majority of MS patients, which may reflect frequent exposure of B cells to HHV-6. The findings suggest that the decreased immune responses to HHV-6 may be responsible for ineffective clearance of HHV-6 in MS patients."

http://www.ncbi.nlm.nih.gov/pubmed/?term=HHV-6+DNA+and+altered+immunity


 

8) 2012   "Association of active human herpesvirus-6, -7 and parvovirus b19 infection with clinical outcomes in patients with myalgic encephalomyelitis/chronic fatigue syndrome."

1August Kirchenstein Institute of Microbiology and Virology, Riga Stradins University, Ratsupites Street 5, LV-1067 Riga, Latvia.

“Frequency of active human herpesvirus-6, -7 (HHV-6, HHV-7) and parvovirus B19 (B19) infection/coinfection and its association with clinical course of ME/CFS was evaluated. 108 ME/CFS patients and 90 practically healthy persons were enrolled in the study. Viral genomic sequences were detected by PCR, virus-specific antibodies and cytokine levels-by ELISA, HHV-6 variants-by restriction analysis. Active viral infection including concurrent infection was found in 64.8% (70/108) of patients and in 13.3% (12/90) of practically healthy persons. Increase in peripheral blood leukocyte DNA HHV-6 load as well as in proinflammatory cytokines' levels was detected in patients during active viral infection.

" Definite relationship was observed between active betaherpesvirus infection and subfebrility, lymphadenopathy and malaise after exertion, and between active B19 infection and multijoint pain. Neuropsychological disturbances were detected in all patients. The manifestation of symptoms was of more frequent occurrence in patients with concurrent infection. The high rate of active HHV-6, HHV-7 and B19 infection/coinfection with the simultaneous increase in plasma proinflammatory cytokines' level as well as the association between active viral infection and distinctive types of clinical symptoms shows necessity of simultaneous study of these viral infections for identification of possible subsets of ME/CFS."
http://www.ncbi.nlm.nih.gov/pubmed/22927850

 

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

https://www.facebook.com/download/804792629578566/141119_NIH_TREATMENT_CAEBV.docx


 


OKay, this keeps coming up, so we can start over at the beginning - the Issue of the 15% vs the 85% and HLA positive (15%, associated with Lyme arthritis or RA) vs HLA-negative (85% NORMAL people who won't make antibodies against most OspA-like antigens shed all the time by spirochetes, which first behaves like flak, and later turns off the immune response in an outcome called tolerance or immunosuppression).

There are 3 different things you have to look at (with your *eyeballs* - there is no way around this, science is 3D) and they are: the USDOJ Lyme RICO complaint, the PacMan Guys, and the real Khan Academy video on "Professional Antigen Presenting Cells."

So, where does HLA vs non-HLA come from? It started back in the day when they were beginning to transplant organs and tissue and found you have to have compatibility between the donor and the recipient - or histo (tissue) compatibility.

So they had to categorize tissue types, and they found, for instance a tendency towards rheumatoid arthritis or allergies were genetic and heritable. And what was that heritable immune thing?

It was determined to be the HLA molecules or the "Human Leukocyte Antigens" (antigen is a bad word for this, because it confuses people with real antigens, which means foreign material; a transplanted tissue with HLAs from an incompatible source, you get it, would be rejected like an antigen).

So, like I tell everyone, go to the real Khan Academy and watch at least the video on "Professional Antigen Presenting Cells." You will find that what the HLA molecules do (clam shaped), is "present" antigen (the real kind, usually), against which the B cells will make antibodies... that is the normal or typical case.

Then look at the 2 PacMan graphics and READ THE TEXT ASSOCIATED with the graphics. The first one shows what the Khan Academy shows. The second one shows what happens if you have Steere's HLAs or Rheumatoid Arthritis HLAs or the HLAs associated with some other "autoimmune" or hypersensitibty (allergy) response-- the 15%. And then I say THIS DOES NOT HAPPEN (antigen is presented - does not happen) in late Lyme in the 85%

Then look at the RICO complaint and see WITH YOUR EYEBALLS the 2 Western Blot outcomes: the 85% or neurological Lyme is on the LEFT, and the Steere's HLA's is on the RIGHT. You will SEE WITH YOUR EYEBALLS a big difference in antibody concentration (the one on the right, arthritis makes a lot of antibodies so the WB bands are darker and there are more of them).

So, what happened was the OspA vaccine was making people sick with a disease like we have - and not so much arthritis, it was a systemic disease outcome, contrary to what is in the popular literature) - in Phase I and Phase II trials, prior to 1994 and Dearborn... Get it?

Dearborn was intended to throw out those systemic adverse events, and they did. Just like us. The expensive kind of Lyme, that is a CNS disease, and we later found out was due to something else - probably EBV reactivated, and EBV is obviously a neurological infection - was thrown out. Kaiser Permanente and The Blues did not want to pay for this, so THEY were the ones screaming for a vaccine, and not us, again, as falsely claimed.

Think about it - the sick people are already sick, so what good is a vaccine going to do them? *We* were not the ones asking for a vaccine, we wanted a cure... Just like today, we have the same trouble: People are less interested in getting this thing STOPPED and the crooks BUSTED, and they say so all the time. They say, "I only want to get better, I am not interested in all the bullshit," not thinking of course, that *WE* would like to get better too, duh.

So, now, look at the following for items you need to review.
 

Khan Academy on Professional Antigen Presenting Cells (does not happen after a while if the antigen is fungal like OspA oe like shed Borrelial antigen or TLR2/1 agonists:
https://www.khanacademy.org/science/biology/immunology/v/professional-antigen-presenting-cells-apc-and-mhc-ii-complexes



Compare to the 2 Pac Man guys, graphics.


 


 


 

http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm  <<  See the Western Blots – but it’s 15% not 30% who have the Steere/Rheumatoid Arthritis HLAs.



http://actionlyme.org/141113_1994_DATTWYLERMINUTES.jpg

^^^ That is related. It shows the CDC is lying about Dearborn being FDA approved. The FDA never approved this, in fact, they never looked to see if Dearborn was validated. I know because I asked them, and their answer was that they are not FORCED to assure the testing used was validated, Now they are being FORCED to as re Lyme, per Senator Blumenthal et al. Follow? ILADS and the LDA are totally clueless and are giving out the WRONG information.


The 85% are normal people who do not have Steere's rheumatoid arthritis predisposition or HLAs. So, they're "negative to Steere's arthritis HLAs."

Steere and the CDC say you are not allowed to have "Lyme Disease" unless you have the rheumatoid arthritis-associated HLAs or the high antibody response.

The CDC and their associated ALDF.com/IDSA/Yale/NYMC Lyme crooks also say those people only have arthritis in one or two joints, but no fatigue or neurological signs (Klempner and Wormser, as shown below)). It was said at the 1998 FDA meeting by Vijay Sikand that the people with Lyme arthritis make enough antibodies to fight off the disease (and are not as sick).

The Lyme crooks don’t care if NYMC gets sued because that’s a Catholic Hospital and most of the Lyme crooks are Israelis.


 


 



PREVIOUS HOMEPAGE 2014_JAN_NOV.htm

 

 

141117; Biomarkers of Real Illness Discovered and Described by Yale and IDSA.

The Entire Lyme scam as you know by now was performed by CDC officers (Allen Steere, Alan Barbour, Barbara Johnson, Mark Klempner) with the assistance of self-alleged smart people like Edward McSweegan and Durland Fish. The latter 2 see themselves as Double-Oh Secret Bioweaponeers. The CDC officers admire themselves as clever business people, beating everyone else to the patent office. They claimed that vector borne diseases were a "rich vein of gold" from which to mine patent royalties.

However, in addition to attempring to profiteer off the calamity, the Lyme scam was performed for 2 reasons. The first reason has to do with the Autism pandemic. The association between Lyme and Autism is OspA, not necessarily spirochetes. OspA causes imunosuppression and the reactivation of latent herpesviruses and also tolerance-spreading from TLR2/1-agonist tolerance to viral and bacterial tolerance (other TLR2-agonists, like TLR4 and TLR7 and TLR9 - See Medvedev and Harding). Now it appears that the NIH has endorsed the description by Washington University St Louis this summer of 2014 and we are calling this post-sepsis. It implies ongoing active infections, and not just post-septic schock damage.

They (wustl and the NIH) refer to the herpesviruses, especially Epstein-Barr. This is in parallel with what happens when a child is immunosuppressed, has a concurrent active bacterial infection and is vaccinated anyway, or the vaccine vial has been contaminated with mycoplasma, which is myco, which is fungal, which is like OspA: causes immunosuppression and the lack of antibody production. The child will get the virus instead of the protection. Congenital Rubella causes Autism - that was the reason they decided to vaccinate against it in the first place.

Use this report for that data, much of it by the CDC, BigPharma and the NIH:
http://actionlyme.org/POST_LYME_SEPSIS_2014_SUMMER.htm 

The second reason the CDC does not want anyone to know about the mechanisms of illness from spirochetes constantly shedding outer surface proteins in a process called blebbing-plus-antigenic variation ("multi-clonal populations overwhelm the immune system," (Barbour), "even if infected with just one spirochete" (Barbour, et al), is that the description of a bioweapon happens to match Alan Barbours "multiclonal populations... overwhelm the immune system." And have no antibodies that identify the original detonator infection...

http://www.actionlyme.org/120702.htm 

However, others are leaking this information. And Russia knows the NYMC associated Russians were HLA-datapharming (this means they were looking at HLAs all over the world; one does not design a bioweapon against a population that will make strong, robust, healthly antibodies. No. You go for the reverse - populations where there is NO association to HLA groups that will produce many antibodies and identify the original infections. See Ethnic Bioweapons in Wikipedia where the Russian Duma kicked all Americans out in 2007 for this reason.

 

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


On Biomarkers, let's look at the present view (due to Mark Klempner's "Re-treatment study" scam) and the work backwards.

In 1997 Mark Klempner took a 4.7 million dollar grant to perform research fraud and then declare that more treatment does not help Lyme victims. This is the link to that report: http://content.nejm.org/cgi/reprint/345/2/85.pdf

He reported his "results" in the July 13, 2001 NEJM. There were numerous aspects of fraud committed in the protocol including using the falsified Dearborn case defition, and that 2/3 of his victims never had ceftraixone before, yet he claimed he was retreating with the standard of care at the time, which was 30 days of ceftriaxone. So, those patents, the 2/3ds, were not "re-treated." He also did not report which primers he used to detect NO LYME in the spinal fluid of his victims (this is written up in the new Primers Shell Game report), when in fact, whenever he did find such people, he rejected them from the study. Not inly did he say this in the write up of the report protocol - if they were positive for Bb DNA in the spinal fluid, they would be rejected from the study -, this actually happened. We know of at least one person who had Bb DNA in her spinal fluid that Klempner rejected from the study, yet he did not report this.

In 2005 Klempner wrote 2 important reports; one with a man maned Kaplan at UConn and another with Gary Wormser. The one with Wormser we already talked about. It was the one where he revealed there were 2 kinds of Lyme: The Dearborn, HLA-linked arthritis in a knee kind,... and the other, the 85%, the neurological, seronegative kind, which we learned about in the new report called "The Lyme Vaccine Scam": The patients with arthritis feel fine except for their arthritis signs. The report with Kaplan, Klempner reported that these people had no neurological compromise and therefore their symptoms were psychiatric:

"Cognitive function in post-treatment Lyme disease: do additional antibiotics help?"

"CONCLUSION:

"Patients with post-treatment chronic Lyme disease who have symptoms but show no evidence of persisting Borrelia infection do not show objective evidence of cognitive impairment. Additional antibiotic therapy was not more beneficial than administering placebo."
http://www.ncbi.nlm.nih.gov/pubmed/?term=klempner+and+kaplan+Lyme

Everyone knows that's false. Cognitive impairment and biomarkers of the central nervous system degradation even Mark Klempner wrote about and reported extensively. Klempner in addition to finding the Lyme was not curable with IV ceftriaxone - that is, it does not kill all lthe spirochetes, even without cells to hide within -, he found that the majority (79%) of Lyme victims have a unique sign or biomarker of a nerve and brain degrading enzyme called matrix-metalloproteinase-130.

Here are those 2 reports:

"Matrix metalloproteinases in the cerebrospinal fluid of patients with Lyme neuroborreliosis."

"Neurologic manifestations of Lyme disease include meningitis, encephalopathy, and cranial and peripheral neuropathy. There are no sensitive markers for neuroborreliosis, and diagnosis is often based on clinical presentation and cerebrospinal fluid (CSF) abnormalities, including intrathecal antibody production. Matrix metalloproteinase (MMP) activity in CSF was compared in patients with neuroborreliosis, patients with diverse neurologic disorders, and healthy controls. The CSF of 17 of 18 healthy subjects and 33 of 37 patients with neurologic symptoms and normal CSF and imaging studies contained only MMP2. The CSF of several patients with neurologic disorders contained MMP2, MMP9, and gelatinolytic activity at 130 and 250 kDa. The 130-kDa MMP was found without the 92-kDa MMP9 in the CSF of 11 (79%) of 14 patients with neuroborreliosis and only 7 (6%) of 118 control patients (P < .001). This pattern of CSF gelatinase activity may be a useful marker for neuroborreliosis.
http://www.ncbi.nlm.nih.gov/pubmed/?term=klempner+and+MMP-130

FULL TEXT: http://www.actionlyme.org/Retro_Klempnerization.htm

  and

"Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro.""The Lyme disease spirochete, Borrelia burgdorferi, can be recovered long after initial infection, even from antibiotic-treated patients, indicating that it resists eradication by host defense mechanisms and antibiotics. Since B. burgdorferi first infects skin, the possible protective effect of skin fibroblasts from an antibiotic commonly used to treat Lyme disease, ceftriaxone, was examined. Human foreskin fibroblasts protected B. burgdorferi from the lethal action of a 2-day exposure to ceftriaxone at 1 microgram/mL, 10-20 x MBC. In the absence of fibroblasts, organisms did not survive. Spirochetes were not protected from ceftriaxone by glutaraldehyde-fixed fibroblasts or fibroblast lysate, suggesting that a living cell was required. The ability of the organism to survive in the presence of fibroblasts was not related to its infectivity. Fibroblasts protected B. burgdorferi for at least 14 days of exposure to ceftriaxone. Mouse keratinocytes, HEp-2 cells, and Vero cells but not Caco-2 cells showed the same protective effect. Thus, several eukaryotic cell types provide the Lyme disease spirochete with a protective environment contributing to its long-term survival."
http://www.ncbi.nlm.nih.gov/pubmed/?term=klempner+and+ceftriaxone+and+1992

FULL TEXT:

http://actionlyme.org/Mark_Klempner_Fibroblasts.htm 


REPEAT: Mark Klempner also wrote in 1998 that OspA was the cause of anti-myelin antibodies or probably contributed to the MS form of Lyme. I think he may have meant OspC, since that was my reading of Roland Martin's 1988 "Lyme causes Multiple Sclerosis" report, but regardless, MS is not a personality or anxiety disorder:
http://actionlyme.org/KFORSCHNER_DISCOVERS_LYME_TOXIN.htm

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

So, obviously that guy Klempner is lying about everything. Lyme is incurable and causes nerve and brain degrading enzymes as a marker of this terrible disease... that is not a disease and people are inventing their symptoms?

.

Next, what are the other biomarkers discovered byt the Same-Crooks-Who-Now-Call-Us-Psychiatric or Poisoners-of-Our-Children (Munchausen's, yes, straight up Munchausen's accusations; this was meant for what happened after the fake vaccines were on the market- they intended to blame the parnts for poisoning their children should they become sick from the OspA vaccines)??


A) MMP-130 - Klempner as shown above.


B) GFAp, or glial-fibrillary acidic protein - ROBERT SCHOEN, - and this one you are really going to love perhaps even more than Klempner, as you will later see, re what Schoen says to the press about us - found in the CNS as a biomarker of glial cell degradation. Now what is a glial cell?

To surround neurons and hold them in place

To supply nutrients and oxygen to neurons

To insulate one neuron from another

To destroy pathogens and remove dead neurons.

From http://en.wikipedia.org/wiki/Neuroglia

When trying to push the Yale LYMErix vaccine, Schoen mentions this biomarker, when trying to show how devastating Lyme is, and that you'd better get that vaccine (2000, while LYMErix was still on the market), mentioning the destruction of these cells, the sign of which is GFAp in the spinal fluid:

"The Lyme Disease Vaccine: Conception, Development, and Implementation"
"Other peripheral neuropathies and Lyme meningitis are also seen at this stage. In late-stage disease, the central nervous system may be involved. A new diagnostic test measuring glial fibrillary acidic protein in cerebrospinal fluid may prove to be a useful tool for measuring such involvement (20)."
http://annals.org/article.aspx?articleid=713400

 

C) Anti-heat-shock antibodies (Sigal and Barbour, re anti-flagellar antibodies)

"H9724, a monoclonal antibody to Borrelia burgdorferi's flagellin, binds to heat shock protein 60 (HSP60) within live neuroblastoma cells: a potential role for HSP60 in peptide hormone signaling and in an autoimmune pathogenesis of the neuropathy of Lyme disease."

"Although Borrelia burgdorferi, the causative agent of Lyme disease, is found at the site of many disease manifestations, local infection may not explain all its features. B. burgdorferi's flagellin cross-reacts with a component of human peripheral nerve axon, previously identified as heat shock protein 60 (HSP60). The cross-reacting epitopes are bound by a monoclonal antibody to B. burgdorferi's flagellin, H9724. Addition of H9724 to neuroblastoma cell cultures blocks in vitro spontaneous and peptide growth-factor-stimulated neuritogenesis. Withdrawal of H9724 allows return to normal growth and differentiation. Using electron microscopy, immunoprecipitation and immunoblotting, and FACS analysis we sought to identify the site of binding of H9724, with the starting hypotheses that the binding was intracellular and not identical to the binding site of II-13, a monoclonal anti-HSP60 antibody. The current studies show that H9724 binds to an intracellular target in cultured cells with negligible, if any, surface binding. We previously showed that sera from patients with neurological manifestations of Lyme disease bound to human axons in a pattern identical to H9724's binding; these same sera also bind to an intracellular neuroblastoma cell target. II-13 binds to a different HSP60 epitope than H9724: II-13 does not modify cellular function in vitro. As predicted, II-13 bound to mitochondria, in a pattern of cellular binding very different from H9724, which bound in a scattered cytoplasmic, nonorganelle-related pattern. H9724's effect is the first evidence that HSP60 may play a role in peptide-hormone-receptor function and demonstrates the modulatory potential of a monoclonal antibody on living cells."
http://www.ncbi.nlm.nih.gov/pubmed/11860186


So they're saying antibodies against flagellin causes some pathology, while at the same time saying band 41 means nothing and you have a non-disease. It happens to be for the very reason - says Barbour - that antibodioes against flagellin cause cross-reactove antibodies against human heat shock protein-60 that there is no flagellin vaccine. So, because the anti-flagellar antibody causes harm and damage, the crooks say of you HAVE that antibody, if means you're psychiatric and don't have a real disease :)

 

D) QEEG or electroencephalograms (Sigal, primary Munchausen's accuser)

QEEG and evoked potentials in central nervous system Lyme disease.

"Quantitative EEG, flash visual evoked potentials, auditory evoked potentials to common and rare tones, and median nerve somatosensory evoked potentials were obtained from 12 patients with active CNS Lyme disease and from 11 patients previously treated for active CNS Lyme disease. Abnormal QEEG and/or EPs were found in 75% of the active Lyme disease patients and in 54% of the post CNS Lyme disease patients. Three different types of neurophysiological abnormality were observed in these patients includingQEEG slowing, possible signs of cortical hyperexcitability, and focal patterns indicating disturbed interhemispheric relationships. In patients tested before and after treatment QEEG and EP normalization was associated with clinical improvement.
http://www.ncbi.nlm.nih.gov/pubmed/?term=sigal+and+qeeg 

 

E) SPECT (Steere)

"Reversible cerebral hypoperfusion in Lyme encephalopathy."

"Lyme encephalopathy (LE) presents with subtle neuropsychiatric symptoms months to years after onset of infection with Borrelia burgdorferi. Brain magnetic resonance images are usually normal. We asked whether quantitative single photon emission computed tomography (SPECT) is a useful method to diagnose LE, to measure the response to antibiotic therapy, and to determine its neuroanatomic basis. In 13 patients with objective evidence of LE, SPECT demonstrated reduced cerebral perfusion (mean perfusion defect index [PDI] = 255), particularly in frontal subcortical and cortical regions. Six months after treatment with 1 month of intravenous ceftriaxone, perfusion significantly improved in all 13 patients (mean PDI = 188). In nine patients with neuropsychiatric symptoms following Lyme disease, but without objective abnormalities (e.g., possible LE), perfusion was similar to that of the treated LE group (mean PDI = 198); six possible LE patients (67%) had already received ceftriaxone prior to our evaluation. Perfusion was significantly lower in patients with LE and possible LE than in 26 normal subjects (mean PDI = 136), but 4 normal subjects (15%) had low perfusion in the LE range. We conclude that LE patients have hypoperfusion of frontal subcortical and cortical structures that is partially reversed after ceftriaxone therapy. However, SPECT cannot be used alone to diagnose LE or determine the presence of active CNS infection."
http://www.ncbi.nlm.nih.gov/pubmed/9409364 

 

F) Antiphospholipid antibodies (Steere and Yale claiming Lyme caused Lupus - probably more likely to be due to the reactivated EBV, but we will look more closely later)

"Reactivity of neuroborreliosis patients (Lyme disease) to cardiolipin and gangliosides."

"A subset of patients (50%) with neuroborreliosis (Lyme disease) showed IgG reactivity to cardiolipin in solid phase ELISA. In addition, a subset of patients with neuroborreliosis (29%) and syphilis (59%) had IgM reactivity to gangliosides with a Gal(beta 1-3) GalNac terminal sequence (GM1, GD1b, and asialo GM1). Anti-ganglioside IgM antibodies were significantly more frequent in these two groups of patients compared to patients with cutaneous and articular Lyme disease, primary antiphospholipid syndrome, systemic lupus erythematosus and normal controls. Correlative evidence and adsorption experiments indicated that antibodies to cardiolipin had separate specificities from those directed against the gangliosides. IgM antibodies to Gal(beta 1-3) GalNac gangliosides appeared to have similar specificities since these were positively correlated and inhibitable by cross adsorption assays. Given the clinical associations of patients with neuroborreliosis and syphilis with IgM reactivity to gangliosides sharing the Gal(beta 1-3) GalNac terminus, we suggest that these antibodies could represent a response to injury in neurological disease or a cross reactive event caused by spirochetes."
http://www.ncbi.nlm.nih.gov/pubmed/?term=steere+and+anti-phospholipid+antibodies

FULL TEXT:
http://www.actionlyme.org/STEERE_AND_LUPUS_LYME.htm

 

G) Quin or quinolinic acid found in the central nervous system, which is a produce of the immune response against a bacterial infection (JJ Halperin)

Now all of these fellows, remember, say Lyme disease does not cause a disease at all. but is a mental illness similar to a somatoform illness, the definition of which is that you can have valid, scientifically detectable outlier markers signs of a real illness, but that you don't have a real illness. Somatoform means "magic" or done with your brain like a paranormal event. That is the technical definition; Magic.

"Neuroactive kynurenines in Lyme borreliosis."

"In patients with encephalopathy, serum QUIN was elevated with corresponding increments in CSF QUIN. Lymphokine concentrations were not consistently elevated. We conclude that CSF QUIN is significantly elevated in B burgdorferi infection--dramatically in patients with CNS inflammation, less in encephalopathy. The presence of this known agonist of NMDA synaptic function--a receptor involved in learning, memory, and synaptic plasticity--may contribute to the neurologic and cognitive deficits seen in many Lyme disease patients...."
http://www.ncbi.nlm.nih.gov/pubmed/1531156 

 

H) Lyme Is associated with  ALS (Halperin, Dattwyler):

"Immunologic reactivity against Borrelia burgdorferi in patients with motor neuron disease."

"Of 19 unselected patients with the diagnosis of amyotrophic lateral sclerosis (ALS) living in Suffolk County, New York (an area of high Lyme disease prevalence), 9 had serologic evidence of exposure to Borrelia burgdorferi; 4 of 38 matched controls were seropositive. Eight of 9 seropositive patients were male (8 of 12 male patients vs 2 of 24 controls). Rates of seropositivity were lower among patients with ALS from nonendemic areas. All patients had typical ALS; none had typical Lyme disease. Cerebrospinal fluid was examined in 24ALS patients--3 (all with severe bulbar involvement) appeared to have intrathecal synthesis of anti-B burgdorferi antibody. Following therapy with antibiotics, 3 patients with predominantly lower motor neuron abnormalities appeared to improve, 3 with severe bulbar dysfunction deteriorated rapidly, and all others appeared unaffected. There appears to be a statistically significant association betweenALS and immunoreactivity to B burgdorferi, at least among men living in hyperendemic areas."
http://www.ncbi.nlm.nih.gov/pubmed/?term=halperin+and+als+and+borrelia 

FULL TEXT:
http://www.actionlyme.org/ALSLYME47.htm 


 

I) NO in the brain (Steere):

"Borrelia burgdorferi and Escherichia coli lipopolysaccharides induce nitric oxide and interleukin-6 production in cultured rat brain cells."
http://www.ncbi.nlm.nih.gov/pubmed/7513330 

(Remember now, the definition of "Lyme Disease" refers to "only the bad knee or arthritis," so brains are not knees unless Steere has finally made that fantastic discovery he's always longed for.)



J) Anti-ganglioside antibodies (Benach)


"Experimental immunization with Borrelia burgdorferi induces development of antibodies to gangliosides."

"Patients with neuroborreliosis produce antibodies, mostly of the immunoglobulin M (IgM) class, to gangliosides, particularly to those with Gal(beta 1-3)GalNac terminal sequences. Lewis rats were immunized with a nonpathogenic strain of Borrelia burgdorferi and with a chloroform-methanol extract (nonprotein) of this organism (CM) to determine whether antibodies to B. burgdorferi also recognized gangliosides. Rats were also immunized with asialo-GM1 to determine whether the elicited antibodies recognized antigens in B. burgdorferi. Rats immunized with B. burgdorferi produced low levels of IgM antibodies that cross-reacted with asialo-GM1 and GM1. Rats immunized with CM had marked IgM reactivity to asialo-GM1 and GM1. Immunization with asialo-GM1 resulted in antibodies that cross-reacted with B. burgdorferi antigens. Although antibodies to B. burgdorferi were of both the IgM and IgG classes, those to CM and to asialo-GM1 and GM1 were predominantly in the IgM fraction. Reactivity of the IgM antibodies decreased after adsorption with the heterologous and the homologous antigens, indicating bidirectional cross-reactivity between CM, asialo-GM1, and GM1 and that immunization with one produces antibodies to the other. There was no in vivo deposition of Ig in peripheral nerves, nor was there nerve pathology as a result of immunizations, but IgM antibodies to asialo-GM1 and CM recognized homologous antigens in the nodes of Ranvier of peripheral nerves from nonimmunized rats. This immunization model suggests that antibodies to gangliosides in Lyme disease have a microbial origin and are potentially relevant in pathogenesis."
http://iai.asm.org/content/63/10/4130.full.pdf+html?view=long&pmid=7558329 


 

K) And Last but Not Least, Paul Duray in IDSA's journal with the most important biomarker of all,..... published in IDSA's journal!!!! (How can they deny this?)...   The 7 Reports, 6 of NIH’s plus wustl.edu’s....

1989 (this is in IDSA's own journal):NCI and US Army Ft Detrick Pathologist Paul Duray on the CSF cells looking like "Epstein-Barr-like transformed cells" in IDSA's 1989 Reviews Supplement on Spirochetal Diseases:Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.

"Clinical pathologic correlations of Lyme disease."

"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." -- http://www.ncbi.nlm.nih.gov/pubmed/2814170 

Full Text: http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm

=====

1992:

Duray again in 1992, in Steve Schutzer's review of the 1992 Cold Spring Harbor Conference on Lyme:

"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. - book.

=====

2006:

The NIH (NINDS’s MS-Lyme Group) group that discovered that *** OspA *** was the cause of the MS/New Great Imitator outcome of Lyme reporting in the New York Times in the summer of 2013 (Martin and Marques, 2006); this article says these OspA like antigens constantly shed by Borreliae cause immunosuppression in the humoral immune system, but apparently a chronic inflammatory state in the central nervous system:

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

http://www.ncbi.nlm.nih.gov/pubmed/16783164 

and this report means you might not even have anti-flagellar antibodies (flagellin is a TLR5-agonist) after being exposed to shed fungal OspA like antigens (TLR2/1-agonists):

"Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes."

http://www.ncbi.nlm.nih.gov/pubmed/16479520

.

2013 - Same NIH MS-Lyme Group as above, Martin and Marques:

"When Lyme Disease Lasts and Lasts" – Jane Brody, NYTimes

"Complicating the picture is the fact that some people with PTLDS symptoms apparently never had Lyme disease in the first place, Dr. Marques said in an interview. There are other infectious organisms — Epstein-Barr virus, for example — that can produce similar symptoms and may be the real culprits."
http://well.blogs.nytimes.com/2013/07/08/when-lyme-disease-lasts-and-lasts/

====

2014:

Wustl.edu discovers that sepsis is like Lyme, in that the survivors of it are likely to have survived via the immunosuppression (TLR2-agonist tolerance/Endotoxin tolerance), but the result is the reactivation of latent viruses:

"Dormant viruses re-emerge in patients with lingering sepsis, signaling immune suppression"

"Patients with lingering sepsis had markedly higher levels of viruses detectable in the blood, compared with the healthy controls and critically ill patients without sepsis. Among the sepsis patients, for example, the researchers found that 53 percent had Epstein-Barr virus, 24 percent had cytomegalovirus, 14 percent had herpes-simplex virus, and 10 percent had human herpes simplex virus-7.

"These viruses generally don’t lead to significant illness in people who are healthy but can cause problems in patients who are immune-suppressed. "
http://news.wustl.edu/news/Pages/27015.aspx


FULL JOURNAL REPORT, snippet…

"Reactivation of Multiple Viruses in Patients with Sepsis"

“Sepsis is the host's non-resolving inflammatory response to infection that leads to organ dysfunction [1], [2]. A current controversial hypothesis postulates that if sepsis pursues a protracted course, it progresses from an initial primarily hyper-inflammatory phase to a predominantly immunosuppressive state [3]–[7]. Experimental therapeutic approaches in sepsis have almost exclusively focused on blocking early inflammation or host-pathogen interaction and failed [8]–[10]. Recently, immuno-adjuvant therapies that boost host immunity, e.g., GM-CSF and interferon-γ, have been successful in small clinical trials thereby supporting the concept that reversing immunosuppression in sepsis is a plausible strategy to improve outcome [11], [12]. However, several issues have limited this approach including lack of consensus that immunosuppression is a clinically important phenomenon [5], [6], [13]. Also, difficulty in identifying patients with impaired immunity as well as determining optimal timing for administration pose significant challenges to pursuing this approach [14]. While immuno-adjuvant therapies might improve sepsis survival if administered during the later immunosuppressive phase, these agents might worsen outcome if given during the early hyper-inflammatory phase [4], [14]. Thus, a means to distinguish these two contrasting phases of sepsis is needed not only to verify the hypothesis that sepsis progresses to an immunosuppressive state but also to guide use of potential agents which boost immunity.

“Latent viruses such as cytomegalovirus are normally held in abeyance by cellular and immune surveillance mechanisms which if impaired, for example by immunosuppressive medications, often result in viral reactivation, replication, and virally-mediated tissue injury [15]–[20]. Sepsis impairs innate and adaptive immunity by multiple mechanisms including apoptosis-induced depletion of immune effector cells and induction of T-cell exhaustion thereby possibly predisposing to viral reactivation and dissemination [21]–[23]. …”

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0098819 

=====

2014, Here the NIH confirms that they agree that post-sepsis, like wustl above describes, matches their own observations of what happens as a result of Chronic Lyme (EBV reactivated; ie, that being generally accepted as the main driver of MS and Lupus):

NEW, by the NIH: "Surviving Sepsis: Detection and Treatment Advances"

By Carolyn Beans for the National Institutes of Health | August 18, 2014 08:43am ET

http://www.livescience.com/47387-sepsis-diagnosis-treatment-research-nigms.html 

"Preventing Secondary Infections

"Some people who survive sepsis can develop secondary infections days or even months later. A research team that included Richard Hotchkiss, Jonathan Green and Gregory Storch of Washington University School of Medicine in St. Louis suspected that this is because sepsis might cause lasting damage to the immune system. To test this hypothesis, the scientists compared viral activation in people with sepsis, other critically ill people and healthy individuals. The researchers looked for viruses like Epstein-Barr and herpes simplex that are often dormant in healthy people but can reactivate in those with suppressed immune systems. [Sepsis Has Long-Term Impact for Older Adults, Study Finds]"

============= End 7 Reports =================

 

So, one is allowed to wonder how IDSA gets off saying Lyme has no illness signs or is a somatoform disorder.

 


 

20+ REPORTS for Doctor Competency Evaluations - Show OspA and the 2 kinds of Autism are linked (and not spirochetes):
 

Raymond Dattwyler in his European patent for an inhalation form of OspA says OspA is Pam3Cys and a TLR2-agonist (everyone else like NIH, CDC, even Yale say they don't know what OspA is, but ILADS and the LDA would not even ask, duh, "Cause Known"); it means OspA could never have been a human injectable vaccine because it is fungal and causes immunosuppression as you will see:

" A lipidation/processing reaction has been described for the intact OspA gene of B. burgdorferi. The p...
rimary translation product of the full-length B. burgdorferi OspA gene contains a hydrophobic N-terminal sequence, of 16 amino acids, which is a substrate for the attachment of a diacyl glyceryl to the sulflhydryl side chain of the adjacent cysteine (Cys) residue (at position 17). Following this attachment, cleavage by signal peptidase II and the attachment of a third fatty acid to the N-terminus occurs. The completed lipid moiety, a tripalmitoyl-S-glycerylcysteine modification, is termed Pam3Cys (or is sometimes referred to herein as Pam(3)Cys or Pam3Cys). It has been suggested that the lipid modification allows membrane localization of proteins, with polypeptide portions exposed as immune targets. In addition to serving as targets for the immune response, Pam3Cys-modified proteins, such as OspA, have been reported to act as potent inflammatory stimulants though the toll-like 2 receptor mechanism (TLR2).

http://patentscope.wipo.int/search/en/detail.jsf?docId=US42934470&recNum=9&maxRec=30&office=&prevFilter=&sortOption=Pub+Date+Desc&queryString=tripalmitoyl+
cysteine+or+Pam3Cys+and+Epstein-Barr&tab=NationalBibliohttp://patentscope.wipo.int/search/en/detail.jsf?docId=US42934470&recNum=9&maxRec=30&office=&prevFilter=&sortOption=Pub+Date+Desc&queryString=tripalmitoyl+
cysteine+or+Pam3Cys+and+Epstein-Barr&tab=NationalBiblio



All data here was also moved to the "Khan Academy" of Lyme

The 20+ REPORTS that show OspA/fungal antigens act like BCL2 class genes and are the causes of the 2 kinds of Autism (and cancer, MS, ALS, etc);

History: Use the following page and search for the term apoptosis, http://www.actionlyme.org/101016.htm  to see how well known it is that fungal antigens inhibit apoptosis. Additionally, go to PubMed and search for P38 and apoptosis and p53 and apoptosis and find that these are the apoptosis enzymes whose functions are inhibited by bacterial lipoproteins like OspA (re the report here, on reprogamming Watson, below).

One kind of Autism is ***Genetic [reverse duplication of a BCL2-class gene, resulting in inhibition of apoptosis and resultant inhibition of "normal synaptic pruning" (see Einstein, Grandin, Tesla)],*** … and the other, the Brain-Damage kind, results from contaminated vaccines (with mycoplasma/fungi), and the subsequent immunosuppression and reactivation of the live, attenuated viruses in the vaccine vial. Both are related to LYMErix (fungal / acts like BCL2, inhibiting apoptosis), or shed Lyme/spirochetal fungal antigens and not spirochetes, per say.

Herpesviruses also have a human BCL2 analog, and that is the main cause of leukemias, including childhood leukemias. BCL means B Cell Lymphoma (Clue).
 

1) MARCH 2002: Organisation of the pericentromeric region of chromosome 15: at least four partial gene copies are amplified in patients with a proximal duplication of 15q.

"We identified a fourth pseudogene, BCL8A [a BCL-2 class molecule, which inhibits apoptosis is reverse-duplicated and therefore overexpressed- KMD], which maps to the pericentromeric region and is coamplified along with the NF1 sequences. Interphase FISH ordering experiments show that IgH D lies closest to the centromere, while BCL8A is the most distal locus in this pseudogene array;"   http://www.ncbi.nlm.nih.gov/pubmed/11897815 

Reversed duplications imply the anti-apoptosis gene is probably over-expressed. The New York Times recently (summer, 2014) ran an article about another mechanism of inhibition of apoptosis leading to the genetic kind of autism, as if that was news, given what we know about the co-occurance of Einstein kind of Autism in Neurofibromatosis. This connection was written up in all the older books on “psychiatry,” duh.

Compare to:
http://www.nytimes.com/2014/08/22/health/brains-of-autistic-children-have-too-many-synapses-study-suggests.html?_r=0

Duh.

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

2) – BigPharma: Patent, US # 7,632,510

Methods of inducing flavivirus immune responses through the administration of recombinant flaviviruses comprising an engineered japanese encephalitis virus signal sequence

"Finally, there is the risk that the virus may not be fully or completely inactivated or attenuated and thus, the vaccine may actually cause disease."

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=7%2C632%2C510.PN.&OS=PN%2F7%2C632%2C510&RS=PN%2F7%2C632%2C510 

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


3) CDC: Measles, Mumps, and Rubella -- Vaccine Use and Strategies for Elimination of Measles, Rubella, and Congenital Rubella Syndrome and Control of Mumps: Recommendations of the Advisory Committee on Immunization Practices (ACIP)

"Updated information on adverse events and contraindications, particularly for persons with severe HIV infection, persons with a egg allergy or gelatin allergy, persons with a history of thrombocytopenia, and persons receiving steroid therapy [are immunosuppressed - KMD]." 
http://www.cdc.gov/mmwr/preview/mmwrhtml/00053391.htm 
 

Fauci just announced (Sep, 2014) huge new funding for adjuvants for vaccines for immunosuppressed children, duh, why would he do that if this was not a problem.

"NIH awards seven new vaccine adjuvant discovery contracts"
"The goal of this research is to identify novel adjuvant candidates that safely and selectively boost vaccine-induced immune responses,” said NIAID Director Anthony S. Fauci, M.D. “Such adjuvants could be used to improve current vaccines, extend the vaccine supply or enhance vaccine efficacy in people with immature or weakened immune systems, such as infants and the elderly.”
http://www.nih.gov/news/health/sep2014/niaid-29.htm

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

4) CDC: Human Exposure to Brucella abortus Strain RB51 -- Kansas, 1997

http://www.cdc.gov/mmwr/preview/mmwrhtml/00051495.htm 

In the above, an immunosuppressed pregnant cow was given a Brucella (“LYME”rix-like) "live attenuated" vaccine and the baby cow ended up with the disease, which then was transferred to the humans handling the cow and her dead baby. This parallels what is happening to children who are vaccinated while immunosuppressed, or who receive mycoplasmally (“LYME”rix-like) contaminated vaccines.

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


5) In the case of pandemic MRSA, as we have seen, the vaccine didn't work because TLR2 agonists (lipoproteins) suppress the immune system. We also learned from the MRSA vaccine patent, that (US patent 7,771,728)

Method for identification, isolation and production of antigens to a specific pathogen

"Several established vaccines consist of live attenuated organisms where the risk of reversion to the virulent wild-type strain exists. In particular in immunocompromised hosts this can be a live threatening scenario. Alternatively, vaccines are administered as a combination of pathogen-derived antigens together with compounds that induce or enhance immune responses against these antigens (these compounds are commonly termed adjuvant), since these subunit vaccines on their own are generally not effective."

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=7%2C771%2C728.PN.&OS=PN%2F7%2C771%2C728&RS=PN%2F7%2C771%2C728

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

6) The effect of exogenous corticosterone on West Nile virus infection in Northern Cardinals (Cardinalis cardinalis)

Corticosterone was administered at levels that individuals enduring chronic stressors (i.e ., long-term inclement weather, food shortage, anthropogenic pollution) might experience in the wild. Corticosterone greatly impacted mortality: half of the corticosterone-implanted cardinals died between five - 11 days post-inoculation whereas only one of nine sham-implanted (control) birds died.

No differences were found in viral titer between corticosterone- and sham-implanted birds. However, cardinals that survived infections had significantly higher average body temperatures during peak infection than individuals that died.

In sum, this study indicates that elevated corticosterone could affect the survival of WNV-infected wild birds, suggesting that populations may be disproportionately at-risk to disease in stressful environments.”

http://7thspace.com/headlines/410671/the_effect_of_exogenous_corticosterone_on_west_nile_virus_infection_in_northern_cardinals_cardinalis_cardinalis.html

The same is true for humans and cortisol and the activation of latent herpesviruses, therefore it’s not “psychiatric” or “psychosomatic,” it’s EBV due to cortisol, meaning real and not due to having the powers of a witch. (Later we add this data, in this project, and you can see it now in the next section.)

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

7) NYTimes; Doctors admit Thimerosal is put in vaccines to prevent fungi:

Vaccine Rule Is Said to Hurt Health Efforts (Dec, 2012)

They say:

"But a proposal that the ban include thimerosal, which has been used since the 1930s to prevent bacterial and fungal contamination in multidose vials of vaccines, has drawn strong criticism from pediatricians.

"They say that the ethyl-mercury compound is critical for vaccine use in the developing world, where multidose vials are a mainstay.

"'Banning it would require switching to single-dose vials for vaccines, which would cost far more and require new networks of cold storage facilities and additional capacity for waste disposal, the authors of the articles said.'"

http://www.nytimes.com/2012/12/17/health/experts-say-thimerosal-ban-would-imperil-global-health-efforts.html?_r=2& 

^^ They are revealing why so few doctors' own kids get vaccines-acquired brain damage. Their kids probably get the first shot out of the vial.

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

8) Fungi Activate Viruses, Rockefeller, 1953 [Go back to the 1950s to see Rockefeller Bioweapons Inc experimenting with mycoplasma antigens like OspA - Enhancing Mouse Leukemia Virus, just like fungally-contaminated vaccines do, which was the reason they put Thimerosal in vaccines, to prevent fungi from doing this (Clue: HIV and "Lyme" bearing the same immunosuppressing triacyl lipopeptide fungal antigen, OspA]:

ACUTE HEPATITIS ASSOCIATED WITH MOUSE LEUKEMIA

IV. THE RELATIONSHIP OF EPERYTHROZOON COCCOIDES TO THE HEPATITIS VIRUS OF PRINCETON MICE

"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."

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

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

9) OspA acts like BCL2, inhibiting apoptosis reactivating EBV/Similars:

Targeting proteins computationally

"Apoptosis is regulated by both pro- and anti-apoptotic members of the B cell lymphoma-2 (Bcl-2) family of proteins. Epstein Barr virus (EBV), the causative agent of Burkitt’s lymphoma, encodes a pro-survival mimic of these Bcl-2 proteins called BHRF1 that inhibits cellular apoptosis during infection and is thought to contribute to lymphomagenesis."
http://www.fredhutch.org/en/news/spotlight/imports/targeting-proteins-computationally.html 

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

10) This is the NIH (NINDS’s MS-Lyme Group) group that discovered that *** OspA *** was the cause of the MS/New Great Imitator outcome of Lyme reporting in the New York Times in the summer of 2013 (Martin and Marques, 2006):

When Lyme Disease Lasts and Lasts – Jane Brody

"Complicating the picture is the fact that some people with PTLDS symptoms apparently never had Lyme disease in the first place, Dr. Marques said in an interview. There are other infectious organisms — Epstein-Barr virus, for example — that can produce similar symptoms and may be the real culprits."

http://well.blogs.nytimes.com/2013/07/08/when-lyme-disease-lasts-and-lasts/ 


Here are the NIH's 2 reports that say OspA (TLR2-agonist) is the cause of the MS/CFIDS/EBV-reactivated kind of Lyme (that also causes humoral immunosuppression),... and that as a result of exposure to OspA-like antigens (shed constantly in a process called blebbing, as revealed by CDC officer Alan "Stealth Bomber" Barbour), you might not even have anti-flagellar antibodies (TLR5-agonists):

Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.
http://www.ncbi.nlm.nih.gov/pubmed/16783164 

and

Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes.
http://www.ncbi.nlm.nih.gov/pubmed/16479520 

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

11) Wustl.edu discover (?- wow, thanks) that sepsis is lyke Lyme, in that the survivors of it are likely to have survived via the immunosuppression (TLR2-agonist tolerance/Endotoxin tolerance), but the result is the reactivation of latent viruses:

Dormant viruses re-emerge in patients with lingering sepsis, signaling immune suppression

"Patients with lingering sepsis had markedly higher levels of viruses detectable in the blood, compared with the healthy controls and critically ill patients without sepsis. Among the sepsis patients, for example, the researchers found that 53 percent had Epstein-Barr virus, 24 percent had cytomegalovirus, 14 percent had herpes-simplex virus, and 10 percent had human herpes simplex virus-7.

"These viruses generally don’t lead to significant illness in people who are healthy but can cause problems in patients who are immune-suppressed. "

http://news.wustl.edu/news/Pages/27015.aspx 


FULL JOURNAL REPORT, snippet…

Reactivation of Multiple Viruses in Patients with Sepsis

Sepsis is the host's non-resolving inflammatory response to infection that leads to organ dysfunction [1], [2]. A current controversial hypothesis postulates that if sepsis pursues a protracted course, it progresses from an initial primarily hyper-inflammatory phase to a predominantly immunosuppressive state [3]–[7]. Experimental therapeutic approaches in sepsis have almost exclusively focused on blocking early inflammation or host-pathogen interaction and failed [8]–[10]. Recently, immuno-adjuvant therapies that boost host immunity, e.g., GM-CSF and interferon-γ, have been successful in small clinical trials thereby supporting the concept that reversing immunosuppression in sepsis is a plausible strategy to improve outcome [11], [12]. However, several issues have limited this approach including lack of consensus that immunosuppression is a clinically important phenomenon [5], [6], [13]. Also, difficulty in identifying patients with impaired immunity as well as determining optimal timing for administration pose significant challenges to pursuing this approach [14]. While immuno-adjuvant therapies might improve sepsis survival if administered during the later immunosuppressive phase, these agents might worsen outcome if given during the early hyper-inflammatory phase [4], [14]. Thus, a means to distinguish these two contrasting phases of sepsis is needed not only to verify the hypothesis that sepsis progresses to an immunosuppressive state but also to guide use of potential agents which boost immunity.

Latent viruses such as cytomegalovirus are normally held in abeyance by cellular and immune surveillance mechanisms which if impaired, for example by immunosuppressive medications, often result in viral reactivation, replication, and virally-mediated tissue injury [15]–[20]. Sepsis impairs innate and adaptive immunity by multiple mechanisms including apoptosis-induced depletion of immune effector cells and induction of T-cell exhaustion thereby possibly predisposing to viral reactivation and dissemination [21]–[23]. …”
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0098819 

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

12) NCI and US Army Ft Detrick Pathologist Paul Duray on the CSF cells looking like "Epstein-Barr-like transformed cells" in IDSA's 1989 Reviews Supplement on Spirochetal Diseases:

Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Clinical pathologic correlations of Lyme disease.
"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." --
http://www.ncbi.nlm.nih.gov/pubmed/2814170 
Full Text:  http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm 


NEW, by the NIH:  "Surviving Sepsis: Detection and Treatment Advances"


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

13) Duray again in 1992, in Steve Schutzer's review of the 1992 Cold Spring Harbor Conference on Lyme:

"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. - book.


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


14) Anthony Fauci on how the LYMErix vaccine (Pam3Cys) was apparently (?) used as an HIV vaccine failed in the same way LYMErix failed, causing immunosuppression and greater susceptibility to disease (HIV's gp120 is Pam3Cys in triplicate at least in the vaccine attempt, apparently - DeFoort):

An HIV Vaccine — Challenges and Prospects

"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"

"Unexpectedly, post hoc analyses of the STEP trial also found a trend toward a greater number of new infections among vaccine recipients than among placebo recipients."

http://www.nejm.org/doi/full/10.1056/NEJMp0806162#t=article 

[DEFOORT Pam3Cys Quadrivalent OspA-HIV, see]

AND, ODDLY…

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

Böltz T1, Hummel RP, Tröger W, Rübsamen-Waigmann H, Biesert L, Müller-Lantzsch N, Koch P, Bessler W, Jung G.

"A novel immunoassay technique using synthetic lipopeptide (Pam3Cys-Ser) linked to immunodominant peptide domains of HIV-1 and HIV-2 envelope proteins as an antigen adsorbent has been developed. Attachment of peptides to microtiter plates can be considerably improved with this method by employing the hydrophobic properties of lipopeptide. From the sera of 121 HIV-1 infected patients 117 reacted with Pam3Cys-Ser-[HIV-1(598-609)cyclic disulfide]. Five of 5 HIV-2 positive sera were positive with Pam3Cys-Ser-[HIV-2(593-603)cyclic disulfide]. Control sera failed to react with these conjugates.
http://www.ncbi.nlm.nih.gov/pubmed/?term=2464607 
 

So, what does that mean? They made an HIV vaccine out of the same structure as the fungal OspA- LYMErix?,... and did not know this would not work because Yale lied to the FDA and the journals about the outcome of LYMErix? How did these patients test positive to the new Pam3Cys antigen while everyone with Lyme does not, especially later in the disease.  Were these HIV patients all NEW HIV patients?  No way to know at present, since there is no available structure of HIV's gp120 that we can find.

The Koreans found Pam3Cys sticks to itself? >> http://newjournal.kcsnet.or.kr/main/j_search/j_download.htm?code=B961118 

That OspA sticks to itself explains why the Western Blots in LYMErix-and ImmuLyme-vaccinated people had unreadable Western Blots with the Blot-Smudging?

PERSING WITH SIGAL EXPLAINING THAT THE WESTERN BLOTS WERE UNREADABLE due to the blot smudging (probably due to OspA sticking to itself, which Alan Barbour reported a long time ago, yet he is the owner of the ImmuLyme OspA vaccine patent), 2000:
Detection of Multiple Reactive Protein Species by Immunoblotting after Recombinant Outer Surface Protein A Lyme Disease Vaccination
http://www.journals.uchicago.edu/doi/pdf/10.1086/313920 
 

Anthony Fauci's patent for the treatment of immune suppression outcomes of bacterial, viral, and fungal infections:
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=5,696,079.PN.&OS=PN/5,696,079&RS=PN/5,696,079

"FIELD OF THE INVENTION

"The present invention pertains to a method for activating the immune system of a patient by intermittently administering interleukin-2 (IL-2) to that patient. Such administration of IL-2 can optionally be combined with other therapies, such as anti-retroviral, anti-bacterial or anti-fungal therapies, suitable for treatment of the patient's condition. This invention also relates to an approach to gene therapy that entails administering IL-2 to a patient so as to facilitate in situ lymphocyte transduction by a retroviral vector also administered to the patient.

"BACKGROUND OF THE INVENTION

"....Illustrative of specific disease states in treatment of which the present invention can be applied are HIV infection and other diseases characterized by a decrease of T-cell immunity, for example, mycobacterial infections like tuberculosis and fungal infections such as cryptococcal disease. This method also can be used in the treatment of secondary infections that occur in patients with suppressed immune systems, such as the opportunistic infections that occur in AIDS patients. ..."
 

You can't make this stuff up.

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

15) EVERYONE READ THIS, AND THE RELATED ARTICLES ON THE PLOS WEBSITE LINKED ON THE RIGHT in this article; THIS IS LYMERIX-DISEASE (TLR2-agonist, or bacterial lipoprotein and NOT LPS) OR POST-LYME SEPSIS,

MicrRNA-146a Is Upregulated by and Negatively Regulates TLR2 Signalling

"Pre-exposure of monocytes/macrophages (in vitro) or the host (in vivo) to LPS or endotoxin induces a transient state of cellular hyporesponsiveness to a secondary LPS challenge with diminished production of proinflammatory cytokines, thereby conferring protection against LPS-induced lethality and resulting in a significant survival advantage [8]–[10]. This phenomenon is well established and termed endotoxin tolerance. Furthermore, emerging evidence has revealed that modulation of the TLR4-mediated signal transduction pathway is involved in the development of endotoxin tolerance [9], [10]. For example, down-regulated cell-surface expression of TLR4, reduced interleukin-1 receptor-associated kinase 1 (IRAK-1) expression and myeloid differentiation factor 88 (MyD88)-IRAK immunocomplex formation, and attenuated nuclear factor (NF)-κB activation and mitogen-activated protein kinase (MAPK) phosphorylation are all considered as significant markers for endotoxin tolerance. Therefore, endotoxin tolerance may represent a protective mechanism, whose primary function is to prevent excessive inflammatory response induced by overactivation of the TLR4 signaling pathway. It has been shown that endotoxin tolerance occurs in several disease settings including sepsis, trauma, surgery and pancreatitis [9]; however, acquisition of endotoxin tolerance may contribute to an increased incidence of secondary bacterial infection in hospitalized patients due to development of an immunesuppressed state [9], [10]."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3639252/ 

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

16) THIS IS UCONN's Medvedev (fiormerly with Duke?) talking about Immunosuppression from Post-Lyme and Post-LYMErix Sepsis (TLR2-agonists or Pam3Cys is OspA or shed borrelial antigens)

IRAK4 kinase activity is not required for induction of endotoxin tolerance but contributes to TLR2-mediated tolerance

"Development of endotoxin tolerance following the initial “cytokine storm” phase of sepsis is thought to protect the host from an overexuberant immune response and tissue damage but at the same time, may render the host immunocompromised and more susceptible to secondary infection [18,–20]. ...

"Reprogramming [21] of TLR4 signaling in endotoxin-tolerant monocytes and macrophages does not occur as a result of decreased TLR4 expression but involves altered recruitment, tyrosine phosphorylation, and K63-linked polyubiquitination of proximal receptor-adapter-kinase complexes [22,–27] and induction of negative regulators IRAK-M, SHIP1, and A20 [24, 25, 28]. Although a few studies have sought to dissociate kinase and adapter functions of IRAK4 in IL-1R/TLR signaling, albeit with conflicting results [13,–16, 29,–31], it is unclear how IRAK4 kinase activity affects induction of TLR2 and TLR4 homo- and heterotolerance. To address these questions, we used IRAK4KDKI mice to determine the impact of kinase deficiency of IRAK4 on the induction of TLR tolerance. Our data showed comparable induction of endotoxin tolerance in WT or IRAK4KDKI PMs and BMDMs, as judged by attenuated MAPK phosphorylation, inhibited expression of proinflammatory cytokines and chemokines, and up-regulation of negative TLR regulators, A20 and IRAK-M. Notably, IRAK4 kinase activity was found to be a prerequisite for conferring inhibition of LPS-inducible JNK and p38 MAPK activation following prior exposure to Pam3Cys. These results represent the first systematic analyses of the role of IRAK4 kinase activity in TLR homo- and heterotolerance and pave the way for improved understanding of how IRAK4 kinase dysregulation may underlie immunocompromised states in late sepsis."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714565/ 

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

17) RE-PROGRAMMING WATSON - with the OspA data, LOL; This is funny. p53 is the apoptosis generator/enzyme/kinase, that is inhibited in the first step of nearly all disease, and the very thing I am screaming about for what 10 years? OspA stops the normal activity of p53/p38, LOL. Then read this and the lead-in into it. Yer gonna laff:

IBM Watson Ushers in a New Era of Data-Driven Discoveries

"In a retrospective, peer reviewed study released this week by Baylor College of Medicine and IBM, scientists demonstrated a possible new path for generating scientific questions that may be helpful in the long term development of new, effective treatments for disease. In a matter of weeks, biologists and data scientists using the Baylor Knowledge Integration Toolkit (KnIT), based on Watson technology, accurately identified proteins that modify p53, an important protein related to many cancers, which can eventually lead to better efficacy of drugs and other treatments. A feat that would have taken researchers years to accomplish without Watson's cognitive capabilities, Watson analyzed 70,000 scientific articles on p53 to predict proteins that turn on or off p53's activity. This automated analysis led the Baylor cancer researchers to identify six potential proteins to target for new research. These results are notable, considering that over the last 30 years, scientists averaged one similar target protein discovery per year.

"On average, a scientist might read between one and five research papers on a good day," said Dr. Olivier Lichtarge, the principal investigator and professor of molecular and human genetics, biochemistry and molecular biology at Baylor College of Medicine. "To put this in perspective with p53, there are over 70,000 papers published on this protein. Even if I'm reading five papers a day, it could take me nearly 38 years to completely understand all of the research already available today on this protein. Watson has demonstrated the potential to accelerate the rate and the quality of breakthrough discoveries."

http://www.stockhouse.com/news/press-releases/2014/08/28/ibm-watson-ushers-in-a-new-era-of-data-driven-discoveries#F16SfxTHczjPCGJ4.99 

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

18) This is a Chinese group trying to figger out how to reverse the well-known phenomenon of OspA-, fungal-antigen- induced immunosuppression or OspA-induced fungal antigen tolerance

A20 is critical for the induction of Pam3CSK4-tolerance in monocytic THP-1 cells.

"A20 functions to terminate Toll-like receptor (TLR)-induced immune response, and play important roles in the induction of lipopolysacchride (LPS)-tolerance. However, the molecular mechanism for Pam3CSK4-tolerance is uncertain. Here we report that TLR1/2 ligand Pam3CSK4 induced tolerance in monocytic THP-1 cells. The pre-treatment of THP-1 cells with Pam3CSK4 down-regulated the induction of pro-inflammatory cytokines induced by Pam3CSK4 re-stimulation. Pam3CSK4 pre-treatment also down-regulated the signaling transduction of JNK, p38 and NF-κB induced by Pam3CSK4 re-stimulation. The activation of TLR1/2 induced a rapid and robust up-regulation of A20, suggesting that A20 may contribute to the induction of Pam3CSK4-tolerance. This hypothesis was proved by the observation that the over-expression of A20 by gene transfer down-regulated Pam3CSK4-induced inflammatory responses, and the down-regulation of A20 by RNA interference inhibited the induction of tolerance. Moreover, LPS induced a significant up-regulation of A20, which contributed to the induction of cross-tolerance between LPS and Pam3CSK4. A20 was also induced by the treatment of THP-1 cells with TNF-α and IL-1β. The pre-treatment with TNF-α and IL-1β partly down-regulated Pam3CSK4-induced activation of MAPKs. Furthermore, pharmacologic inhibition of GSK3 signaling down-regulated Pam3CSK4-induced A20 expression, up-regulated Pam3CSK4-induced inflammatory responses, and partly reversed Pam3CSK4 pre-treatment-induced tolerance, suggesting that GSK3 is involved in TLR1/2-induced tolerance by up-regulation of A20 expression. Taken together, these results indicated that A20 is a critical regulator for TLR1/2-induced pro-inflammatory responses."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3905037/ 

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

19) 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): http://actionlyme.org/TRAINER_2012SUMMER.htm 

Modulation of natural killer cell activity by Borrelia burgdorferi. - 1988

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.

"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)."

http://www.ncbi.nlm.nih.gov/pubmed/?term=3056196 

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

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

Gary Wormser's peer-reviewed article about how OspA was immunosuppressive

http://www.ncbi.nlm.nih.gov/pubmed/10865170 

Gary Wormser's peer reviewed article about how Dearborn "case definition" detected only 15% of the cases in IgG (9 out of 59):

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=266355&blobtype=pdf 

It's pretty obvious why the majority of the participants at the 1994 Dearborn conference (see below) said Steere's testing proposal that said Lyme was only an HLA-linked arthritis, SUCKED!!!

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

20) Here is Clifford Harding, the discoverer of the mechanisms of both outcomes of OspA Disease or Lyme Disease [immunosuppression and no antbodies, and the other one, where the HLA-molecule together with the antigen is released as an entirely new antigen called an exosome or a vessicle, but is really a complex against which partial auto-/self- antibodies will be made; and in the case of alyme, particularly Allen Steere's version of autoimmunity against Human Leukocyte antigen (I assume)] talking about how if you have been exposed to Borrelial lipid TLR2-liktigens, you will end up with a null or non-response to other TLR agonists, such as viruses:

TLR2 signaling depletes IRAK1 and inhibits induction of type I IFN by TLR7/9.
J Immunol. 2012 Feb 1;188(3):1019-26. doi: 10.4049/jimmunol.1102181. Epub 2012 Jan 6.
Liu YC1, Simmons DP, Li X, Abbott DW, Boom WH, Harding CV.
Author information
1Department of Pathology, Case Western Reserve University/University Hospitals Case Medical Center, Cleveland, OH 44106, USA.

Abstract

"Pathogens may signal through multiple TLRs with synergistic or antagonistic effects on the induction of cytokines, including type I IFN (IFN-I). IFN-I is typically induced by TLR9, but not TLR2. Moreover, we previously reported that TLR2 signaling by Mycobacterium tuberculosis or other TLR2 agonists inhibited TLR9 induction of IFN-I and IFN-I-dependent MHC-I Ag cross processing. The current studies revealed that lipopeptide-induced TLR2 signaling inhibited induction of first-wave IFN-α and IFN-β mRNA by TLR9, whereas induction of second-wave IFN-I mRNA was not inhibited. TLR2 also inhibited induction of IFN-I by TLR7, another MyD88-dependent IFN-I-inducing receptor, but did not inhibit IFN-I induction by TLR3 or TLR4 (both Toll/IL-1R domain-containing adapter-inducing IFN-β dependent, MyD88 independent). The inhibitory effect of TLR2 was not dependent on new protein synthesis or intercellular signaling. IL-1R-associated kinase 1 (IRAK1) was depleted rapidly (within 10 min) by TLR2 agonist, but not until later (e.g., 2 h) by TLR9 agonist. Because IRAK1 is required for TLR7/9-induced IFN-I production, we propose that TLR2 signaling induces rapid depletion of IRAK1, which impairs IFN-I induction by TLR7/9. This novel mechanism, whereby TLR2 inhibits IFN-I induction by TLR7/9, may shape immune responses to microbes that express ligands for both TLR2 and TLR7/TLR9, or responses to bacteria/virus coinfection."

http://www.ncbi.nlm.nih.gov/pubmed/22227568

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21) Poland 2013 The influence of toll-like receptor stimulation on expression of EBV lytic genes.

Abstract
Epstein-Barr virus (EBV) establishes latency in the resting memory B-cell compartment. It has been recently suggested that maintenance of chronic infection is dependent on periodic reactivation. Although the stimuli for EBV reactivation in vivo during natural infections are largely unknown, there is evidence indicating that heterologous infections could trigger herpesviruses reactivation. The purpose of this work was to identify the influence of Toll-like receptors stimulation on EBV replication in EBV latently infected Burkitt lymphoma cells (P3HR-1, Raji and Namalwa). The cells were stimulated with Pam3CSK4 (synthetic triacylated lipoprotein), PolyI:C (synthetic analog of dsRNA), LPS (lipopolysaccharide from E.coli), measles virus (MeV) and PMA (phorbol myristate acetate). Non-stimulated cells (NS) served as control. EBV expression was investigated at mRNA level for three viral lytic genes: BZLF1 (immediate early, ZEBRA), BALF2 (early, EA) and BcLF1 (late, VCA). Additionally, the effect of stimulation on NF-kBp65 and inflammatory cytokines (IL-lb, IL-6, IL-8, IL-10, IL-12p70, and TNF) was investigated. Stimulation of TLRs led to limited changes in EBV expression manifesting as increase of ZEBRA at mRNA level in cells treated with PolyI:C and Pam3CSK4. Stimulation with PolyI:C, Pam3CSK4 and LPS also lead to considerable increase of NF-kBp65, while increased levels of inflammatory cytokines were observed for IL-8, TNF and IL-6 in cells treated with PMA and MeV. In conclusion, the results of our experiments support the suggestion that TLRs stimulation with microbial ligands influences EBV virus replication.

http://www.ncbi.nlm.nih.gov/pubmed/24459828
Full text pdf  : http://www.pjm.microbiology.pl/archive/vol6232013237.pdf  <<< Get the full text, seriously, it clarifies much


 

 

Einstein, Telsa, Duray, CDC's BIG Secret, and the Witches of Chronic Fatigee; It's about BCL2

Subtitle:  If you suck at science like Yale University does, and have only a money-based-model of medicine and not a science-based-model, you will miss the Unified Theory of Health and Unhealth.
(Clue: It helps to give a crap about human suffering.)


By Kathleen Dickson on Monday, November 24, 2014 at 11:59pm


The NIH agrees with me (ActionLyme.org) that Lyme is like "post-sepsis syndrome" with the severe PTSD ("I felt like I was gonna die"), the reactivated herpesviruses, the fungal antigen (TLR2-agonist) tolerance and cross tolerance (the inability of the immune system to react to OTHER antigens besides fungi), and that it is caused by OspA vaccination too, since they, the NIH, are the authors of those reports:

1) Paul Duray (NCI, US Army, Yale Dept of Pathology) found that Lyme produced EBV-like transformed cells in the CNS of Lyme victims in 1989. 2) NIH's Martin and Marques found that Osp-A type antigens caused the MS kind of Lyme (reactivated EB/Similars) *and* the seronegative kind of Lyme (reactivated EBV/Similars), ***with chronic inflammation in the BRAIN (sound familiar?).***

Both OspA or fungal antigens shed by borrelia or injected with mycoplasma-contaminated vaccines (or other mold exposures) inhibit the auto-kill or apoptosis kinases. Inhibition of the auto-kill kinases is also a feature of the genetic kind of AUTISM, where there is a duplication of the BCL2-type genes (BCL2- means B Cell Lymphoma and what they do is inhibit auto-kill kinases). EBV does the same thing - they have their own version of a human BCL2-type gene. Acquired Autistic children (from vaccines) for the most part have brain damage from the viruses in the vaccine vials which are reactivated when co-injected with mycoplasma contamination,... or the children are vaccinated while in a state of immunosuppression. The kids are getting the viruses. The viruses do the brain damage.

The genetic kind of Autism comes with the large brains like Einstein, Tesla and Temple Grandin. Since the BCL2-genes inhibit the auto-kill kinases, there is a lack of "normal synaptic pruning" in these children. The kids all have large heads/brains at birth etc, and tend to have reverse-hemispheric dominance. Reversed hemispheric dominance means: since 95% of right-handed people are controlled by left-brain, and 70% of left-handed people are controlled by right-brain, you get right-handed, right-brain dominance in Genetic Autistics, or as the Autistics say, "I think in pictures." These people are all well known to be "engineers and scientists." (There is no explanation yet for Asperger's, which is defined as left-brain dominance with a performance IQ or right-brain deficit or the complete opposite of Autism. And no, I do not know why it was left out of the new DSM. Asperger's could be due to the same phenomenon, since there is no explanation at present for why the right-brain lopsidedness as a result of too much BCL2 in High Functioning Autistics; who knows, it could be something simple like how you lie in the uterus...)

Now you see the relatedness between vaccines-acquired Autism (brain damage from the viruses), the genetic kind of not-exactly-brain-damage kind of Autism, and the Waste-Basket Diagnoses of Fibro, Lyme, CFIDS, ME. The CDC does not want to reveal they know why 1:50 kids are brain damaged for life (Fungal-Viral Synergy), so they trash us and call us the 21st century term for witches... Somatoformers. Magick People. Poorly developed Wiccans who are only able to cast spells on themselves and not other people. VooDoo-Boomerangers... whatever you want to call bad paranormallers...

HOW DID I FIND THAT LINK? Neurofibromatosis and High Functioning Autism co-occur at 150 times the rate they would if they were independent genetic events, and NF-Autism share that feature in "Nerve and Brain Overgrowth Syndromes" - reversed duplications of BCL2-class genes.

And we know what BCL2- is, and we know OspA does the same thing... inhibits the auto-kill kinases.