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

01 Oct 2017


File List, RICO

1988 Steere says Lyme is like a B cell leukemia

Assoc Blogs-n-Webs:




Fungal Exosomes Inhibit Apoptosis

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


BlumenthalAntiTrust Lawsuit

Exosomes, Blebs


CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
Dearborn, 1994

Pathogenic Fungi

Bush's warcrimes, Oct 2000




HAMMERING THE LYME MAFIA - AN EMAIL to the Mob's Hired Goon, Alpert:




Subject: made *changes* to "Lyme" claims - the HLA-linked aspect
Date: Jan 31, 2013 6:46 AM

130129-130131  Answering Alpert’s (American Journal of Medicine) Latest Changes re “Lyme Disease”

Dear Mr. Alpert,

I can see what your problem is now: you apparently have no background in this science. You apparently went back to the people for whom you are debasing your profession and your journal in order to have them tell you how to respond to the scientific facts, citations and evidence of this crime we are revealing to you.   Here is the newer version of your video, which you modified and following that as far as I am told, here are your modifications:

ALPERT TRANSCRIPT II (January 28, 2013):
”Hello, I'm Joseph Alpert, editor-in-chief of the American Journal of Medicine, and I'm here today to call your attention to a very interesting article in the March issue of the journal. This article by [Halperin, who showed that “Lyme” caused ALS, and those ALS cases did not have the Dearborn antibody panel, so that is a murder charge
” …  And there's been a great debate as to why these individuals have these symptoms. ***It's still not totally clear, and there will continue to be research in this area, but it appears that these individuals have either an autoimmune activation, such as, for example, seen in patients with lupus,*** or that the symptoms are psychosomatic.”

Wrong.  These diseases are not about “immune activation.”  They are the opposite.  That is the persistent lie.  

LYMErix and “Lyme” bleb-exposure produced no antibodies and gave most people a disease we call “Chronic Lyme,” the name given to 1) the un-eradicable spirochetes, 2) the reactivation of latent herpesviruses, plus 3) TLR2 tolerance to mycoplasma in the blood in people without the acceptable HLAs. The model and the mechanisms are apparently the same in Gulf War Illness and in the brain damage in children commonly called “autism.”

Lupus is a condition of high antiphospholipid antibodies, and since Yale formerly had a “’Lyme’ and Lupus Clinic” that later became the RICO entity “L2 Diagnostics” (in formal, SEC-listed partnership with Corixa and Imugen), it would be hard for these criminals to suddenly start denying that “Lyme” caused all their former “New Great Imitators,” including the neurological outcomes.  That is why you mention only lupus in your corrected statements.  You did not mention the multiple sclerosis outcome of “Lyme” and LYMErix because the head of that NIH-NINDS department at the time, Roland Martin, quit and went home to his native Germany once he found out LYMErix of OspA was the cause of this MS outcome.  Apparently you and IDSA would like everyone to forget that there was an special division of the NINDS dedicated to understanding why Lyme caused multiple sclerosis.  You’d probably especially like everyone to forget that Roland Martin quit his NIH job when he found out LYMErix was the cause of the MS outcome of Lyme. 

As for persistence, I won’t go into that because at least 20 times these same criminals reported that treatment failed:

Please also see the history of the permanence and incurability of Relapsing Fever since 1911, here:  )
At the same time, when they weren’t deploying their RNA/DNA shell game with the primers to find spirochetes in ticks to patent, but also to find “Not ‘Lyme’” in humans:

Compare to their patents, here:

We know spirochetes are permanent and un-eradicable.  The problem is, Why did a recombinant antigen cause the same systemic disease?

Answer: LYMErix solved this crime for us.  If these IDSA/ALDF idiots had not tried to force a “Lyme” vaccine onto the market, and if they had not decided to perform medicine by slamming their victims with the scientifically invalid religion of psychiatry – which excuses psychopathic behavior like IDSA’s and Adam Lanza’s as “normal” and “common” because of the statistical frequency of your debauched behaviors -- we might not have ever solved the “Great Imitator” mystery or the Vaccines-Acquired-Autism crime, which is even bigger. 



1) SCIENTIFIC DATA ON IMMUNOSUPPRESSION from fungal antigens like OspA or LYMErix,
starting with Dattwyler in 1988.

2) THE FAILED TB and HIV VACCINES and WAYS THEY FAILED: Failed Tb and HIV vaccines 
& the HIV-LYMErix vaccine [Fauci and the new NIH grants to study why HIV-LYMErix failed (TLR2-agonist-induced immunosuppression)].   

NCI’s and the US Army’s Duray and the pre-cancerous EBV-transformed-like cells in Chronic "Lyme"
victims. (2 articles)

4) Fungal-Viral Synergy (FVS): FVS, in coordination with what was revealed by Paul Duray, is evidence
for exposure to fungal antigens causing immunosuppression and simultaneously activating latent Epstein-Barr. 

NOTE: There is a lot of overlap in these first 4 chapters, but the history of exposure to fungal antigens was warped due to
the fact that the ALDF/IDSA crooks did not even care what OspA was/did (structure being function) and lied about its results
to the public and to the FDA.

5) Seronegative Epstein-Barr, currently known as chronic fatigue syndrome (CFS/fibromyalgia
syndrome (FMS) (4 articles)

“Lyme” and LYMErix, activating Epstein-Barr) and on pyridostigmine bromide..  Add immunosuppression also known to be caused by DEET.

7) The CDC’s “bogus article” on mycoplasma in chronic fatigue syndrome to which the eperythrozoons
adhere, causing CFS.

8) Childhood Immunizations and the brain damage that is called autism also fits this model: CDC’s and
BigPharma’s own data (5 reports), plus the NYT revelation that the thimerosal was intended to prevent mycoplasmal or fungal growth within the vials

9) CDC’s Patents with SmithKline in Europe that mention HLA-linked and non-HLA linked antibody outcomes
(5), with SmithKline, in Europe, 1992; The Dearborn stunt was for their own personal profit.

drugs (mabs), anti-virals -- Columbia and Johns Hopkins regarding the treatment of the pre-cancer condition of the immunosuppression diseases or the "no-antibody" diseases.  Rituximab and anti-virals for Chronic fatigue syndrome (anti-EBV/anti-CD20 mab).

11) Epstein-Barr’s Famous and well-known Chronic-, Autoimmune Disease- and Cancer Associations


Status:  While "Lyme,"  LYMErix, chronic fatigue syndrome and other immunosuppressing events/conditions are known to occur without antibodies and despite the crimes and idiocies of IDSA -- because TLR2-agonists turn off the antibody response -- the reactivation of Epstein-Barr/herpes is being addressed with anti-virals and rituximab, and is even being funded by the NIH. Yet nothing is being done about the return of mycoplasma, describing the relapse phenomenon in Brian Fallon’s long term Lyme treatment patients as [well as] the relapses seen in  chronic fatigue syndrome victims. 

We have no data on what would be a monoclonal antibody-type therapy to get rid of TLR2-tolerance.  We have no recent data on the current success of the Chinese with an anti-OspA/gp120 cationic defensin.  We just know we’re still trying to have the likes of you and the CDC/ID$A clowns indicted for performing the Dearborn $tunt for their VBD$ monopoly on grant$, patent$, test kit$, royaltie$, and the exclusive rights to test for all VBDs in America and Canada once LYMErix was on the market.

The No-HLA Diseases:  What happens to the other 85-70%?

There is a spectrum or a range, in common diseases, from what used to be called inflammatory (allergy) diseases to the immunosuppression outcomes like HIV and cancer.  The NIH’s stats on chronic fatigue syndrome (CFS) and fibromyalgia is 4 and 8 million, respectively (12 million).  We have no numbers on chronic “Lyme,” but we can extrapolate from the falsified Dearborn case definition (10 times under-reported times 15% reportable).  The frequency of the HLA’s for MS and lupus is approximately the same as the HLA representation in the general US population in RA (15-30 %).  So, what happens to the other 85-70% as a result of the same exposures?  

Note that at the CDC’s 1994, Dearborn, MI, “consensus” conference where the Steere-falsified testing for “Lyme” was “approved,” despite none of the participants agreeing with Steere’s research-fraud proposal for an antibody profile for a “positive” “case” for relapsing fever, the average approval rate of the attendees was only 15%.  That is, tested in the field, the participating, invited labs at the Dearborn conference, said this of Steere’s proposal for a “case”:

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

The above accuracy-rate of Steere’s bogus Dearborn panel matched the frequency of these arthritis and even MS/lupus HLAs in the general population (about 15%).  Eight-Five percent of us, upon the same infectious or hypervaccination or autovaccination (Osp blebbing by spirochetes) exposures, will not have an HLA-linked outcome that is detectable with antibody testing.  It’s the same number, 85, for the “safety and efficacy” of the falsified OspA vaccines outcomes, by the way, which is no coincidence (76 and 92%).



Dattwyler (again):

"Modulation of Natural Killer Cell Activity by Borrelia burgdorferi

"Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi.

Dattwyler’s references (please refer to the 1976 publication):

Harding and Radolf on OspA-induced Immunosuppression (no antibodies), J Immunol. 2001:
Toll-like receptor 2-dependent inhibition of macrophage class II MHC expression and antigen processing by 19-kDa lipoprotein of Mycobacterium tuberculosis
"Despite the ability of MTB 19-kDa lipoprotein to activate microbicidal and innate immune functions early in infection, TLR 2-dependent inhibition of MHC-II expression and Ag processing by MTB 19-kDa lipoprotein during later phases of macrophage infection may prevent presentation of MTB Ags and decrease recognition by T cells. This mechanism may allow intracellular MTB to evade immune surveillance and maintain chronic infection."

Clifford Harding, 2010, on the 35 year old mystery of "Steere's Bad Knees": 
”Mycobacterium tuberculosis synergizes with ATP to induce release of microvesicles and exosomes containing major histocompatibility complex class II molecules capable of antigen presentation.”

And the above mechanism of “shed HLA-antigen complex as a unique antigen” has had some follow up with Brucella (Pollak et al, PLoS One, 2012):

It also explains a lot of strange immunity like the anti-myelin oligodendrocyte basic protein (MOBP) antibodies produced from
exposure to OspA found in “Lyme”/LYMErix victims reported by Mark Klempner (Nature Medicine, 1999):

Pages of Huber and Klempner’s report scanned in showing autoimmunity in the CNS from OspA:
and the other well-known mechanisms of “mistaken self” as autoimmunity.  

If Lyme and LYMErix detonate EBV, then could the so-called HLA-antigen complex “autoimmunity” diseases of MS and Lupus as outcomes of Lyme and LYMErix be to [do] with EBV/other herpes antigens and not necessarily Lyme antigens?
Does the HLA-antigen complex theory explain Steere’s bizarre theory about OspA causing autoimmunity against lymphocytes that only attack the knee?
How much time should someone spend trying to unscramble what Allen Steere has had to say for the last 38 years?
Even SmithKline made fun of Allen Steere’s preposterous proposal at the 2001 FDA Meeting on LYMErix:

"- Identity of the auto-antigen

"− TRLA is observed in one (few) joint(s), while hLFA-1 is present on cells throughout the body” 

Biofilms are covered in SLYMErix (TLR2-agonists), but you can look that up for yourself on PubMed.  I personally find no reason to think small clusters of bacteria cause the systemic disease known as “Lyme” or CFS.  Instead, these diseases are undoubtedly about something in the blood plus some disordered immunity in the central nervous system, such as per NIH’s former employee, Roland Martin,…:

“We found that stimulation with B. burgdorferi lysate increased the expression of Toll-like receptors (TLRs) 1 and 2 in all cell types except neurons. However, despite similarities in global gene profiles of monocytes and microglia, only microglial cells responded to the stimulation with a robust increase in HLA-DR, HLA-DQ, and also coexpressed CD11-c, a dendritic cell marker. In contrast, a large number of HLA-related molecules were repressed at both the RNA and the protein levels in stimulated monocytes, whereas secretion of IL-10 and TNF-alpha was strongly induced. These results show that signaling through TLR1/2 in response to B. burgdorferi can elicit opposite immunoregulatory effects in blood and in brain immune cells, which could play a role in the different susceptibility of these compartments to infection." ),  

…plus the delirium/hypoxia signs detectable with PET and SPECT imaging.  The model of CFS-Lyme appears to be chronic
cerebrovascular dysimmunity and hypoxia without blatant anemia from mycoplasmally-disrupted erythrocyte membrane potential.




A)  Yeremeev VV et al (Russia), Clin Exp Immunol. 2000:

The 19-kD antigen and protective immunity in a murine model of tuberculosis
“These results are consistent with a model in which the presence of the 19-kD protein has a detrimental effect on the efficacy of vaccination with live mycobacteria. Targeted inactivation of genes encoding selected antigens represents a potential route towards development of improved vaccine candidates."


B)  Post et al (South Africa), Infect Immun. 2001:
Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits Mycobacterium smegmatis-induced cytokine production by
human macrophages in vitro
These results suggest that the diminished protection against challenge with M. tuberculosis seen in mice vaccinated with M. smegmatis expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha and IL-12 production, possibly leading to reduced induction of T-cell activation."


 C) Avi-Hai Hovav et al, Infect Immun. 2003: 
"The Mycobacterium tuberculosis recombinant 27-kilodalton lipoprotein induces a strong Th1-type immune response deleterious to protection ”
"Furthermore, the protection provided by BCG or other mycobacterial antigens was completely abolished once the 27-kDa antigen was added to the vaccine preparations. This study indicates that the 27-kDa antigen has an adverse effect on the protection afforded by recognized vaccines. We are currently studying how the 27-kDa antigen modulates the mouse immune response."


D) Anthony Fauci on the failed HIV-”LYME”rix vaccine, producing no antibodies, N Engl J Med 2008:

"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."


E) NIAID 2012 awarded grant (Bonaldo) re HIV-LYMErix vaccine making people sicker, like the failed Tuberculosis TLR2-agonist vaccines:

"After the failure of the merck STEP trial [which was OspA] that appears to have enhanced the rate of infection in vaccinees, ... "


F) NIAID 2012 awarded grant to Mark Klempner’s partner, Linden Hu, (together they performed the “retreatment” trial of people
who had never had ceftriaxone before as the basis of IDSA’s “guidelines”) to study this now well known phenomenon of TLR2-tolerance or immunosuppression caused by “Lyme” or LYMErix:
”PUBLIC HEALTH RELEVANCE: The innate immune system is one of the most important lines of host defense against microbial invaders, but it can also cause illness when stimulated inappropriately or too vigorously. In this proposal, we examine the mechanisms by which a specific component of the innate immune system, toll-like receptor 2, recognizes its targets and causes inflammation. A better understanding of the workings of innate immunity is important for developing therapies for diseases such as “Lyme” disease *** where either an ineffective*** or an over-exuberant immune response causes the symptoms of illness.



A), 1989, in Infectious Disease Reviews (IDSA’s former journal)
"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." --


B)  Paul Duray chapter (NCI, NIH, Ft. Detrick,) at the 1992 Cold Spring Harbor Crooks' Conference summary , published by
Steve Schutzer in Lyme Disease: Molecular and Immunologic Approaches.

1992-  "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." - 


New, re “immature immune cells” in chronic TLR2 exposure (Seeboth et al, Vet Res. 2012):

The fungal T-2 toxin alters the activation of primary macrophages induced by TLR-agonists resulting in a decrease
of the inflammatory response in the pig

"By contrast, the activation of TLR7 by ssRNA was not modulated by T-2 toxin pre-treatment. In conclusion, our results suggest that ingestion of low concentrations of T-2 toxin affects the TLR activation by decreasing pattern recognition of pathogens and thus interferes with initiation of inflammatory immune response against bacteria andviruses. Consequently, mycotoxins [OspA exposure, either thru blebbing or vaccination-KMD] could increase the susceptibility of humans and animals to infectious diseases." 

“Furthermore, T-2 toxin reduces lymphocyte proliferative response [8,9] and ***disturbs the maturation process of dendritic cells [10]*** suggesting its immunosuppressant potency [7,11]”

”Indeed Li et al. [15] showed that systemic T-2 exposure increases the severity of respiratory ***reovirus***infection with marked exacerbation of bronchopneumonia and modulation of cytokine responses in mice alveolar macrophages.

NOTE: The above sounds quite a bit like how to make a pandemic flu, don’t it?  Sounds quite a bit like, to me, that Lyme
Cryme victims, rather than becoming walking canisters of tick disinfectant (according to the alleged modality of Lyme
“prevention” by the Yale criminals with their OspA vaccines), instead will become the next Pandemic Flu/Other Typhoid
Marys.  We’re the Hostesses with the Mostesses and we are also quite certain the antics of Yale and IDSA will backfire in a
bigger way than the 10 lost years of the HIV-LYMErix vaccine.


ARTICLE CONTINUES: ”Moreover, similar distribution of TLR on human and swine cells, unlike rodents, has been previously
described [48]

And this, above, is why all mouse studies of “Lyme” where the molecular mice are not transfected with human TLR2 can be thrown out.  All infectious diseases studies where mouse TLR2 was used to measure the antibody response can be thrown out.  All antibody-associations to all diseases data can be thrown out.  Only non-Primershellgame DNA/RNA and properly defined biomarkers are acceptable for correlations.




SECTION 4: FUNGAL-VIRAL SYNERGY (FVS) -- FVS, in coordination with what was revealed by Paul Duray, is evidence for exposure to fungal antigens causing immunosuppression and simultaneously activating latent Epstein-Barr.   


This is from the 1950s, where we see that fungal antigens like LYMErix or OspA or Borrelial outer surface proteins are known to activate viruses via immunosuppression:

"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."

NOTE: Later we see the CDC throw out the red blood cells to which mycoplasma adhere when determining whether or
not mycoplasma is involved in Chronic fatigue syndrome.  It’s cute.  It’s cute what the CDC does. Which is why DARPA
now wants nothing to do with the CDC.

OspA Inhibits Apoptosis in “Lyme”-infected cells (and there are many more besides the following report by Power et al, J Immunol. 2004):
Bacterial lipoprotein [OspA] delays apoptosis in human neutrophils through inhibition of caspase-3 activity: regulatory
roles for CD14 and TLR-2.

“In this study, we demonstrate that BLP inhibits neutrophil mitochondrial membrane depolarization with a subsequent reduction in caspase-3 processing, ultimately leading to a significant delay in PMN apoptosis.”

Here are 130 more PubMed entries on this:


You’ve heard of BCL2-analogs and the fact that some organisms have their own such genes to help with their parasitic and disease activities?  OspA behaves like a BCL2-analog in that the end result is the same. OspA is not a program like BCL2, it’s just that the result is the same.  OspA is associated with the porin P66, so its function is apparently to help spirochetes attach to and suck membranes.  One can assume OspA might have the same function as a free antigen inside a cell, attaching to membranes and perhaps depolarizing the internal  structures/membranes/cell machinery, like mycoplasma do to red blood cells.  OspA is “sticky” says CDC officer  and OspA patent owner, Alan Barbour.


More on gumming-up the immunity process by, again, Harding (J Immunol. 2012):    
TLR2 signaling depletes IRAK1 and inhibits induction of type I IFN by TLR7/9
"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."


Older published works in this area:

de Waal Malefy et al, J Exp Med. 1991. [LYMErix/ OspA and IL-10 perhaps independently inhibiting apoptosis in EBV infected cells
as the main mechanism of induction of the New Great Imitators With Or Without HLAs -], cited over 100 times:
“Interleukin 10 (IL-10) and viral IL-10 strongly reduce antigen-specific human T cell proliferation by diminishing the antigen-presenting capacity of monocytes via downregulation of class II major histocompatibility complex expression.”

“… Collectively, our data indicate that IL-10 and v-IL-10 can completely prevent antigen-specific T cell proliferation by inhibition of the antigen-presenting capacity of monocytes through downregulation of class II MHC antigens on monocytes.


IN BETWEEN (besides Paul Duray’s observation of EBV-transformed-like cells in chronic “Lyme”):

Hulínská D et al, Folia Biol (Praha), 2003:

Interaction of Borrelia burgdorferi sensu lato with Epstein-Barr virus in lymphoblastoid cells

“Since the possibility of interruption of latent EBV infection has been suggested by the induction of the lytic virus cycle with chemical substances, other viruses, and by immunosuppression, we hypothesized that the same effect might happen in B. burgdorferi sensu lato infection as happens in Lyme disease patients with positive serology for both agents. We have observed EBV replication in lymphoblastoid cells after superinfection with B. garinii and B. afzelii strains after 1 and 4 h of their interaction. We found that viral and borrelial antigens persisted in the lymphoblasts for 3 and 4 days. Morphological and functional transformation of both agents facilitate their transfer to daughter cells. Association with lymphoblasts and internalization of B. garinii by tube phagocytosis increased replication of viruses more successfully than B. afzelii and chemical inductors. Demonstration of such findings must be interpreted cautiously, but may prove a mixed borrelial and viral cause of severe neurological disease. 

And here is Gary Wormser, again, in 2000, while LYMErix was still on the market, on immunosuppression from OspA exposure:
Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA)
”OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression.”


And here is Dave Persing, one of the “Lyme” crooks and owner of the Corixa RICO (No-OspA-B in the spirochete)  patent:
Molecular evidence and clinical significance of herpesvirus coinfection in the central nervous system


By the way, Persing is not the only “Lyme” crook  who apparently has only two areas of interest -- “Lyme” and Epstein-Barr:

This also holds true for Paul “I don’t know what OspA is” Auwaerter, Adrianna Marques (NINDS, former partner of Roland Martin’s), and Brigitte Huber (former partner of Steere’s who now agrees with us and not Steere).  Auwaerter, I guess is interested in nf-kappa events – immunosuppression:

Epstein-Barr virus BGLF4 kinase downregulates NF-κB transactivation through phosphorylation of coactivator UXT


Much like “Lyme” and LYMErix exposure:


"Induction of in vitro reprogramming by Toll-like receptor (TLR)2 and TLR4 agonists in murine macrophages: effects of
TLR "homotolerance" versus "heterotolerance" on NF-kappa B signaling pathway components.

“LPS-induced NF-κB DNA binding, c-jun N-terminal kinase (JNK) kinase activity, and TNF-α secretion were significantly
inhibited in murine macrophages pre-exposed to a mycoplasma lipopeptide, macrophage-activating lipopeptide (MALP)-2, which signals through TLR2 (19).”


Synergy and Cross-Tolerance Between Toll-Like Receptor (TLR) 2- and TLR4-Mediated Signaling Pathways

“A family of Toll-like receptor (TLR) mediates the cellular response to bacterial cell wall components; murine TLR2 and TLR4
recognize mycoplasmal lipopeptides (macrophage-activating lipopeptides, 2 kDa (MALP-2)) and LPS, respectively. Costimulation of mouse peritoneal macrophages with MALP-2 and LPS results in a marked increase in TNF-α production, showing the synergy between TLR2- and TLR4-mediated signaling pathways. Macrophages pretreated with LPS show hyporesponsiveness to the second LPS stimulation, termed LPS tolerance. The LPS tolerance has recently been shown to be primarily due to the down-regulation of surface expression of the TLR4-MD2 complex. When macrophages were treated with MALP-2, the cells showed hyporesponsiveness to the second MALP-2 stimulation, like LPS tolerance. Furthermore, macrophages pretreated with MALP-2 showed reduced production of TNF-α in response to LPS. LPS-induced activation of both NF-κB and c-Jun NH2-terminal kinase was severely impaired in MALP-2-pretreated cells. However, MALP-2-pretreated macrophages did not show any reduction in surface expression of the TLR4-MD2 complex. These findings indicate that LPS-induced LPS tolerance mainly occurs through the down-regulation of surface expression of the TLR4-MD2 complex;
in contrast, MALP-2-induced LPS tolerance is due to modulation of the downstream cytoplasmic signaling pathways.”


2005, re the two sides of the same fungal/viral coin -- cancer and its opposite -- diseases with antibodies:

”Phosphorylation of NF-kappaB and IkappaB proteins: *** implications in cancer and inflammation. ***”
“Nuclear factor-kappaB (NF-kappaB) is a transcription factor that has crucial roles in inflammation, immunity, cell proliferation and apoptosis. Activation of NF-kappaB mainly occurs via IkappaB kinase (IKK)-mediated phosphorylation of inhibitory molecules, including IkappaBalpha. Optimal induction of NF-kappaB target genes also requires phosphorylation of NF-kappaB proteins, such as p65, within their transactivation domain by a variety of kinases in response to distinct stimuli. Whether, and how, phosphorylation modulates the function of other NF-kappaB and IkappaB proteins, such as B-cell lymphoma 3, remains unclear. The identification and characterization of all the kinases known to phosphorylate NF-kappaB and IkappaB proteins are described here. Because deregulation of NF-kappaB and IkappaB phosphorylations is a hallmark of chronic inflammatory diseases and cancer, newly designed drugs targeting these constitutively activated signalling pathways represent promising therapeutic tools.


Fungal Antigen Effect on Caspases:

”Bacterial lipoprotein delays apoptosis in human neutrophils through inhibition of caspase-3 activity: regulatory roles for CD14 and TLR-2.”

You should be sure to read that one, the full text link, above, through thoroughly and study all the citations, too.

And you can follow up on what causes EBV’s and OspA’s inhibition of apoptosis, IL-10 induced changes and TLR2 agonist “TOXINS’” changes to immune cells on your own. 



SECTION 5: SERONEGATIVE EPSTEIN-BARR, currently known as chronic fatigue
syndrome (CFS)/fibromyalgia syndrome (FMS) (4 articles)

1) Down-regulation of MHC class II expression through inhibition of CIITA transcription by lytic transactivator Zta during
Epstein-Barr virus reactivation


2) Innate immune modulation in EBV infection

3) The lytic cycle of Epstein-Barr virus is associated with decreased expression of cell surface major histocompatibility complex class I and class II molecules

4) Epstein-Barr virus evasion of CD8(+) and CD4(+) T cell immunity via concerted actions of multiple gene products

“Synthesis of new MHC class I molecules is blocked by BGLF5. Viral-IL10 causes a reduction in mRNA levels of TAP1 and bli/LMP2, a subunit of the immunoproteasome. MHC class I molecules present at the cell surface are downregulated by BILF1. Also the antigen presenting capacity of MHC class II molecules is severely compromised by multiple EBV lytic gene products, including gp42/gH/gL, BGLF5, and vIL-10. In this review, we discuss how concerted actions of these EBV lytic proteins result in highly effective interference with CD8(+) and CD4(+) T cell surveillance, thereby providing the virus with a window for undisturbed generation of viral progeny.”


None of this is new.  We could keep going.  The point is that Epstein-Barr-antibody and mycoplasmal-antibody studies in CFS, ”Lyme” - and everything else - can all be thrown out. 

We can call these sick people who have been both abandoned and tortured by the so-called medical community,  “The Pre-
cancerous-, Non-HLA-linked-, Non-antibody-linked-, MS-Related Diseases,” for short.  We can even suggest that the
lack of progress in tuberculosis, “Lyme,” HIV, and these other “waste basket" diagnoses that typically have the stigma of
somatization attached to them thanks to the medical elites (and thus this incorrect information trickles down to even the smallest of country doctors' practices), was deliberate, even so far as to assume that the failed HIV-LYMErix vaccine trial was deliberate.  We are talking about the CDC, various other US government departments, and we are talking about Yale -- all well-known purveyors of prevarications, be it weapons of mass destruction (WMDs) in Iraq, the Gulf of Tonkin, the 3-for-2 airplane episode in NYC with the 7 second (acceleration of gravity) collapse of Building 7, or the fake Yellowcake Letter and the subsequent persecution of Joe Wilson.

In truth, we’re actually not the Dahmer-Lanzas of the world.  That’s you and your,.. what is a non-slang word for “handlers?”  That’s the so-called professionals, rife with conflicts of interest, who project onto us some psychic ability to cause ourselves all the scientifically valid and verifiable illness signs, particularly all of IDSA’s own published valid biomarkers of disease:

With no scientific talent, monotonous, transparent skits and stunts, and now bankrolled yet bankrupt, to trust a US  (dot)gov at this juncture one would have to be severely lacking in IQ.



 (act like “Lyme” and LYMErix, activating Epstein-Barr) and on pyridostigmine bromide.

Recently Knighted professor of psychiatry at the Institute of Psychiatry, King's College London, and director of the King's Centre for Military Health Research, Simon Wessely seemingly has the world in the palm of this hand. Now if we could just get him to start telling the truth.

Wessely reports with the Pentagon that vaccination in the Gulf is associated with Gulf War Illness (GWI)/fatigue:

Wessely, 2000:
"Role of vaccinations as risk factors for ill health in veterans of the Gulf war: cross sectional study
CONCLUSION (Wessley’s): “There was a specific association between the timing of multiple vaccines and ill health: personnel who received multiple vaccines before deployment were not at increased risk, whereas those who had received them during deployment were.”

Wessely later reported that he threw out such data to invent the theory that one can later throw out the same data, and instead blame the victims, and thus everyone will admire him and crown him King.  Or at least, Knight:

”Something old, something new, something borrowed, something blue: The true story of Gulf War Syndrome”    Wednesday,
25 January 2006

SAYS WESSELY: "One other thing that many people told us was that they had received a lot of vaccines in a short space of time. Of course this was because it was a bit of a rush, as these things always are, and we had not just the biological vaccines, we had the other, more routine, vaccines that had to be given as well. There is no particular reason to suspect that that would be associated with ill health.”

What Knight Wessely fails to mention here is his own former data with the Pentagon where he showed that there was an association with vaccines and the GWI outcome. "King-Me!!"

CONTINUES WESSELY: “We did, however, also look at the central nervous system - that’s the brain, basically. One way of doing that is through neuro-imaging, but we didn’t get the money to do that, so instead we have used sophisticated neuro-psychological testing, which has been largely normal in this group as well.”

There happens to be no such thing as "sophisticated psychological testing."  There is the only scientifically valid testing, as per the FDA’s rules on the validation of an analytical METHOD used to determine scientifically valid OUTLIERS in human biochemistry and physiology parameters, such as IDSA’s Biomarkers of Chronic Lyme and the New Great Imitators: SPECT scans, spinal fluid analyses for the likes of signs of degradation of the central nervous system found by Mark Klempner (MMP-130) and Robert Schoen (Gfap), QEEG (Sigal), etc.  These valid illness signs would be considered Organic brain compromise.  And there is B), a verifiable history of Trauma, and there C) is cognitive testing which, for example, can pick up the Genetic likes of VIQ>>> PIQ in high-functioning autism like Einstein’s, or its reverse, Asperger’s.  The only valid axes are Genetic, Organic, and Traumatic, but there is no “psychological” testing because psychology is not real:

Here is why:

New York Times (Tierney, 2008):
Deep Down, We Can’t Even Fool Ourselves
”But as useful as hypocrisy can be, it’s apparently not quite as basic as the human instinct to do unto others as you would have them do unto you. Your mind can justify double standards, it seems, but in your heart you know you’re wrong.”

New York Times (Carey and Hartocollis): Psychiatry admits they do not identify evil, re the Sandy Hook Massacre
Warning Signs of Violent Acts Often Unclear
"The sort of young, troubled males who seem to psychiatrists most likely to commit school shootings — identified because they have made credible threats — often do not qualify for any diagnosis, experts said. They might have elements of paranoia, of deep resentment, or of narcissism, a grandiose self-regard, that are noticeable but do not add up to any specific “disorder” according to strict criteria."

Self-worship is "not a disorder," according to psychiatry, which, many fail to realize, is a belief system and not science.  Putting yourself above others is “normal,” says psychiatry. 

But you know it in your heart when you do something wrong, they also claim, above, using actual analytical methods. The so-called courts also agree that there is some element of the human Will at work in human behavior (let’s call that, Organic, Traumatic, Genetic, the human Will…as the verifiable axes).  But at the same time, these psychiatrists claim “wrong” is so common that it is “normal,” and therefore acceptable.  Can we suppose there is yet a fifth element or force at work?  One that explains a cumulative history of decisions to harm people making it easier and easier to continue to do so on a daily basis and even with “MD” after one’s name?  Does psychopath describe “walking Evil?”  Can a psychopath more easily pass a lie detector test?   There is other evidence that Evil is as verifiable as Robert Schoen’s Gfap – or Glial Fibrillary acidic protein in the CSF of “Lyme” victims.  

More on stress-activated Epstein-Barr, which is clearly an outcome of the reversed placebo effect of Wessely’s now obviously criminally fraudulent accusations against Gulf War Illness Veterans (2 reports, one on heart disease):

Stowe et al, Psychosom Med. 2001:
Elevated stress hormone levels relate to Epstein-Barr virus reactivation in astronauts

Uchakin et al, Interdiscip Perspect Infect Dis. 2011:
Fatigue in medical residents leads to reactivation of herpes virus latency

Yang et al, Brain Behav Immun. 2010:
Glucocorticoids activate Epstein Barr virus lytic replication through the upregulation of immediate early BZLF1 gene expression

Science Daily, 2013:
Viral [EBV] Reactivation a Likely Link Between Stress and Heart Disease

Back to Wessely and how nerve agent antidote causes immunosuppression:

Peden-Adams et al, Immunopharmacol Immunotoxicol. 2004:
Pyridostigmine bromide (PYR) alters immune function in B6C3F1 mice

”Exposure to PYR did not alter splenic and thymus weight or splenic cellularity. However, 20 mg PYR/kg/day decreased thymic cellularity with decreases in both CD4+/CD8+ (20 mg/kg/day) and CD4-/CD8- (10 and 20 mg/kg/day) cell types. Functional immune assays indicated that lymphocyte proliferative responses and natural killer cell activity were normal; whereas exposure to PYR significantly decreased primary IgM antibody responses to a T-cell dependent antigen at the 1, 5, 10 and 20 mg/kg treatment levels for 14 days. This is the first study to examine the immunotoxicological effects of PYR and demonstrate that this compound selectively suppresses humoral antibody responses.”


There are other reports regarding the toxicity of PYR on MedLine.

I am claiming, since it is already claimed by these labs, that immunosuppression-plus-hypervaccination in the Gulf could be contributing factors in Gulf War Illness.  And Simon Wessely is a tool deployed against both GWI and CFS/myalgic encephalomyelitis (ME) victims in the UK, much like the Munchausen’s and Shaken Baby false accusations have been flung at the parental victims of vaccines that cause encephalitis and hemorrhage and death.  I propose that these outcomes, GWI and “autism,” mimic both the HLA(strange immunity)-  and non-HLA- models of LYMErix disease.


SECTION 7: The CDC’s “bogus article” on mycoplasma in chronic fatigue syndrome; CDC throws out the red blood cells, to which the eperythrozoons adhere, causing CFS:

”Absence of Mycoplasma species DNA in chronic fatigue syndrome.”
CDC centrifuges the blood, throws out the erythrocytes to which the eperythrozoons adhere, mentions that these patients have no antibodies which is to be expected after chronic exposure to fungal antigens as shown by Harding and Radolf, above, and subsequent related studies like the no-antibodies from the HIV-”LYME”rix exposure, as explained by Anthony Fauci (above).

1992; “[The effect of Eperythrozoon suis infection on the osmotic fragility of erythrocytes]”
"Osmotic fragility of erythrocytes was tested in weaned pigs experimentally infected with Eperythrozoon (E.) suis. Acute
eperythrozoonosis of splenectomized pigs ***led to an increase of osmotic fragility.*** It is supposed that E. suis infection
causes a structural change in erythrocyte membrane. Possible mechanisms of this cell membrane injury are discussed.

And you can follow up on ^^^ that.  Do the RBC-zoons or the mycoplasma cause fatigue in animals?  The PubMed crystal
ball says yes:

No longer can anyone claim that “no antibodies means no organism,” or “no disease,” nor can they claim “mycoplasma are absent from the erythrocytes of CFS victims.” 



8) Childhood Immunizations and the brain damage that is currently called autism also fits this model – CDC’s and
BigPharma’s own data (5 reports), plus the NYT revelation that the thimerosal was intended to prevent mycoplasmal or fungal
growth within the vials (you can’t autoclave a vial with a rubber septum, obviously).

A) – BigPharma: "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."

”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 g allergy or gelatin allergy, persons with a history of thrombocytopenia, and persons receiving steroid therapy [are
immunosuppressed- KMD]."

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

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.

D) 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:

"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.",771,728.PN.&OS=PN/7,771,728&RS=PN/7,771,728


E) "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.”



SECTION 9: CDC’s PATENTS WITH SMITHKLINE IN EUROPE, discussing the 2 kinds of "Lyme," A) the HLA-linked kind which is the Dearborn kind and which is the Clifford-Harding-Solves-Steere’s-Bad-Knees kind, which produces antibodies, and B) the non-HLA-linked kind which is now called hypochondria, Munchausens, a “pattern of protection,” Fibro-Viagra-Deficit
(instead of a sexually transmitted disease, fibromyalgia is the opposite) or whatever is the next permutation of cowardly witch hunts and victim-blaming.

Which will boomerang.

The 5 European Patents owned by CDC staff:

In the descriptions of these 5, 1992 CDC's staff's patents with SmithKline in Europe, CDC staff admits that Lyme arthritis is not the only kind of Lyme:

"Summary of the Invention

"In one aspect, the invention provides isolated B. burgdorferi antigens which are regulated and differentiated by growth of the B. burgdorferi 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...." 

The Dearborn stunt excluded these non-HLA-linked cases via research fraud performed by Allen Steere in Europe, where he fooled around with strains and raised the cut-off for a positive ELISA to 5 std and deliberately left out the neurologic or meningitis cases. 
These were the 2 reports:
Antigens in Europe and Dressler/Steere:

The research fraud committed by Steere playing a game with the strains and the non-lipidated recombinant antigens to leave out OspA and B for a monopoly on post-LYMErix testing with Imugen, Corixa and Yale’s L2-Diagnostics:

In 1992 Allen Steere went to Germany, with, as he claimed,

“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 -"

-- illegal, plasmid-dropping, antigen-and-antibody dropping, “high passage strains” and OspA and B with no lipids attached (not likely to produce antibodies), resulting in the new, 1994, Centers for Disease Control (CDC), “case definition” of “Lyme Disease (8, 9)."

See the rest of the above report and the graphic snippet of Steere’s research fraud here:

The intended monopoly is described in the Corixa’s advertisements and in the Corixa-Yale RICO patent:

Posted to the Lyme Newsgroup in 1999:
“Imugen, a lab in Norwood, MA, is in a partnership with CORIXA another growing biotech company...Here's why: 
”Target Product:   Reference diagnostic for detection of certain tick-borne diseases   
”Status: Development 
”Partner:  IMUGEN, Inc. 
[Corixa and others are looking for markers of infection; to patent other commercially viable diagnostic test kit antibodies/ biomolecules- KMDickson]

”From a Corixa press release,  April 7, 1998: 
"...The agreement provides Imugen with an exclusive license, including the right to sub-license these recombinant antigens for reference laboratory testing in the US and Canada in exchange for a share of revenues from any diagnostics kits or blood screening tests that are developed as a result of this collaboration..."!topic/


Corixa's RICO Patent Claims:

Note the date on the patent:  May, 1996.

"Additional uncertainty may arise if the vaccines are not completely protective; vaccinated patients with multisystem c
omplaints 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. "

Or maybe they mean, “appropriate for a monopoly on vaccines and testing.”  The entire Dearborn/Fake-Vaccine stunt was
about a monopoly on vector borne diseases grants, patents, and commercial products like test kits and vaccines.  But Lyme is Relapsing Fever, antigenic variation is the nature of the relapse, and so none of this, scientifically, could ever happen unless we are talking about the genus/species determinant, flagellin, for testing.


The entire crime is about the falsified Dearborn testing.  This is the reason the IDSA cronies keep insisting on Klempner’s bogus “long term retreatment” trial wherein 2/3 of his victims never had had intravenous meds before, and which was dependent upon the false belief that the Dearborn standard was real.  The “IDSA Guidelines” reinforce the notion that Dearborn was real and the notion that the Lyme crooks all still believe it is real.  We know this is not true.  Wormser was there.  Even he admitted that the Steere proposal was way off base, too. 


JJ Halperin knows the Dearborn standard does not detect his ALS cases of Lyme.  You can look at the Western Blots in that,
Halperin’s report:

You can look at the above Western Blots and see that these sick patients would not test positive to the criminal “two-tiered” criteria.  This is a murder charge and explains JJ Halperin’s hysterical behavior – trying to get some neurology group to come up with similar “guidelines” - when Senator Richard Blumenthal subpoenaed all the crooks records in the Antitrust lawsuit against IDSA:

Said Blumenthal in that decision:
”The IDSA portrayed another medical association's Lyme disease guidelines as corroborating its own when it knew that the two panels shared several authors, including the chairmen of both groups, and were working on guidelines at the same time. In allowing its panelists to serve on both groups at the same time, IDSA violated its own conflicts of interest policy.”

This crazy hysterical BS that has been going in since 1990 when the American Lyme Disease Foundation ( was founded by the DNA patenteers and Kaiser-Permanente at New York Medical College, is all about Gary Wormser, Robert Schoen, Allen Steere, Barbara Johnson, Alan Barbour, Eugene Shapiro, Lenny Sigal, Henry Feder, JJ Halperin, J Nowakowski, Peter Krause, Mark Klempner, Edward McSweegan, Phil Baker, Durland Fish, et al, not going to jail for negligent homicide over the Dearborn stunt.  And here, these patents owned by CDC officer Barbara Johnson, make clear the reason Steere went to Europe to leave out the non-HLA linked cases.  You can’t sell a vaccine for a disease that is known to make no antibodies.  So, they said “only people with certain HLAs are allowed to have a ‘disease.’”


anti-EBV/herpes drugs (mabs), anti-virals


Wall Street Journal, 2011:  Unlocking Chronic Fatigue Syndrome

- "Other scientists are trying to understand why other infections, such as mononucleosis, appear to prompt chronic fatigue
syndrome in some patients. And in a program at New York's Columbia University, researchers are seeking to identify pathogens that may appear prominently in patients with the disorder. Researchers will be testing "for all those agents that we know affect vertebrates on this globe," says Mady Hornig, who heads the Columbia program….

- ”Dr. Montoya's team enrolled 30 patients with elevated levels of antibodies against Epstein-Barr virus and HHV-6, a herpes
virus, in a trial and treated them with valganciclovir, an anti-viral medicine. Dr. Montoya says patients on the drug showed
improvement in cognition and fatigue.”

Norway, et al:
“Clinical impact of B-cell depletion with the anti-CD20 antibody rituximab in chronic fatigue syndrome: a preliminary case series.”


But why do these and the Brian Fallon/Columbia U. Chronic Lyme patients who received 14 weeks of antibiotics relapse?


No drug for TLR2 tolerance.  The mycoplasma come back.  The fatigue comes back. 

No drug for TLR2 tolerance. The mycoplasma come back.   And Duray’s bad B-cells? What to do about them? The spirochetes are un-eradicable but the ILLNESS - the fatigue - comes back.



SECTION 11: Epstein-Barr’s Famous and well-known Chronic-, Autoimmune Disease- and Cancer- Associations

A friend advises me that it is not common knowledge that EBV causes cancer, MS, Lupus, arthritis, et al. That means I will briefly deploy the following science-artillery upon your little pin head and hope you forward it to all the other journals, against the possibility that such Alzheimery type “editors” are also at their helms.

As for the so-called autoimmune diseases: 
PubMed is loaded with data.

As for the Cancer outcomes of EBV:
Over 9000 articles.


As for Joe Tully of “Tully and Shope, Rockefeller Institute and Yale Bioweaponeers at Large” from the last century?

Tully Volume 3, Number 1—March 1997
Mycoplasmas: Sophisticated, Reemerging, and Burdened by Their Notoriety Diseases and Cancer

“Malignant Transformation
“As early as the mid-1960s, mycoplasma-infected cell lines were associated with chromosomal aberrations, altered morphologies, and cell transformation (77,78). These abnormal oncogenic cell traits continued even after the apparent elimination of mycoplasmas, and evidence implied increased tumorigenicity of these transformed cells in animals. This issue has been revisited in studies demonstrating that longterm, persistent mycoplasmal infection of mouse embryo cells initiated a multistage cellular process that resulted in irreversible cell transformation, karyotypic alterations, and tumorigenicity in nude mice (6). Do these oncogenic events associated with mycoplasma-mammalian cell coincubation relate to the ontogeny of human cancers?”

Tully’s reference, 18:
Murphy WH, Gullis C, Dabich L, Heyn R, Zarafonetis CJD. Isolation of Mycoplasma from leukemic and nonleukemia patients.
J Natl Cancer Inst. 1970;45:243–51.PubMed

Why would Joe Tully say such a thing in the CDC’s own publication, no less?

Why would the National Cancer Institute’s, the US Army’s and Fort Detrick’s own Paul Duray publish such a thing as “these look like Epstein-Barr transformed cells” in IDSA’s own journal.

Imagine the boldness.

Joe Tully, the bioweaponeer and mycoplasma and tick, on MedLine:[Author]%20AND%20%28%22mycoplasma%22[MeSH%20Terms]%20OR%20%22mycoplasma%22[All%20Fields]%29%20AND%20%28%22ticks%22[MeSH%20Terms]%20OR%20%22ticks%22[All%20Fields]%20OR%20%22tick%22[All%20Fields]%29&cmd=DetailsSe


Says Harold Varmus (have you ever heard of Varmus, Mr. Alpert?)

“Unseen Enemies

“At a session in Orlando on the future of cancer research, Dr. Harold Varmus, the director of the National Cancer Institute, described the Provocative Questions initiative, a new effort to seek out mysteries and paradoxes that may be vulnerable to solution.

“In our rush to do the things that are really obvious to do, we’re forgetting to pay attention to many unexplained phenomena,” he said. “Why, for example, does the Epstein-Barr virus cause different cancers in different populations? Why do patients with certain neurological diseases like Parkinson’s, Huntington’s, Alzheimer’s and Fragile X seem to be at a lower risk for most cancers? Why are some tissues more prone than others to developing tumors? Why do some mutations evoke cancerous effects in one type of cell but not in others?

“With so many phenomena in search of a biological explanation, “Hallmarks of Cancer: The Next Generation” may conceivably be followed by a second sequel — with twists as unexpected as those in the old “Star Trek” shows. The enemy inside us is every bit as formidable as imagined invaders from beyond. Learning to outwit it is leading science deep into the universe of the living cell.”


- - - - - - -

And last, but not least, let us consider the possibility referred to by Paul Duray, 1992 – (mouse gammaherpesviruses and/or mouse
cytomegalovirus in ticks): 

"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."

”Molecular detection of murine herpesvirus 68 in ticks feeding on free-living reptiles.

“Block of death-receptor apoptosis protects mouse cytomegalovirus from macrophages and is a determinant of virulence in
immunodeficient hosts.”


There is always the possibility that this criminal IDSA gang is doing to the tick borne viruses what they’re doing with “Lyme disease” – falsely claiming each new Borrelia is distinct, narrowing disease definitions, limiting our knowledge of what is in ticks to what they have already patented (such as Barbour’s 1996 patent for cow Relapsing Fever, now known as Masters’ Disease – but again, no one has it ??), and not allowing anyone to have a disease until the commercial product is ready. And I am not talking about the known co-infections, which have been discussed openly at NIH “Rare Diseases” hearings since the mid-1990, but nothing has been done about them, of course.

Thirty-eight years and we’re still wondering what the hell happens after a tick attachment. Twenty-three years since the ALDF was founded by Kaiser-Permanente and the greedy DNA patent mongers… and we know nothing about chronic “Lyme disease” except for IDSA’s statement, “There is no disease for which there were two vaccine trials.”

And now, today, Jan 2013, we are subjected to you, Mr. Alpert, and your corrected video announcements. Yikes.

Spare us, please, in the future, from having to publicly point out that you need to retire due to something like Alzheimer’s.  That is, if your actions are not just plain criminal.



Kathleen M. Dickson

PS: I probably left some important junk out, but ultimately, the Dearborn booklet is scanned into my website, so the whole world can see how we got this ludicrous testing standard despite the non-recommendation of the labs invited to “participate" in the Dearborn proceedings, all the way back in 1994. It wasn’t really a consensus conference, so even excluding its technical non-merits, it needs to be investigated, which was what I told the USDOJ when I filed the RICO complaint in 2003.