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





"Top Scientist" Anthony Fauci does not know what OspA is, but then again, US News and World Report has become another Israeli Rag.  Oh, and by the way, Mort Zuckerman is a sponsor of the Israeli criminal gang.

Meanwhile, according to the famous plan of the NIH to hook up with BigPharma to market half-dead drugs, no one mentions the fact that
Fauci owns a patent for the treatment of immune suppression outcomes of fungal infections or exposure to Osp-A:

  1. "Illustrative of specific disease states in treatment of which the present invention can be applied are HIV infection and other characterized by a decrease of T-cell immunity, for example, mycobacterial infections like tuberculosis and fungal infections such as cryptococcal disease." 

    A method for activating a mammalian immune system entails a series of IL-2 administrations that are effected intermittently over an extended period. Each administration of IL-2 is sufficient to allow spontaneous DNA synthesis in peripheral blood or lymph node cells of the patient to ..


    120516;  Uncle Sam Magoo says: "Nevermind the relationship between
    "1) vaccines-induced 'autism' (activated viruses from fungal contamination or vaccination of immunosuppressed children),
    "2) the chronic Lyme-like disease caused by OspA (triacyl lipopeptide TLR2/1 agonist) vaccination, and
    "3) the fact that TNF-blocking immunosuppression therapy have the same, reactivated-viruses outcomes"

    Immunosuppression therapy and resultant reactivation of herpes/viral infections mimic the Chronic/Fatigue/Chronic Lyme outcomes of LYMErix vaccination:

    Tumor necrosis factor blockade and the risk of viral infection.


    And Uncle Sam Magoo also says, "Nevermind the fact that 20% of the child deaths globally are due to the fact that there can never be a vaccine made out of a fungal antigen (see the 'Famous Harvard Business School/Mormon Religion' article in WaPo, below) like LYMErix or OspA and that we should have been told that 20 years ago, when Allen Steere falsified the testing for Lyme in Europe, alone, in order to falsify the OspA vaccine outcomes."

    "Nevermind the fact that Yale, et al, - the Lyme criminals formally known as (a commercial enterprise) and now known as - are now responsible for all those 20 years of 20% of child-lives lost because they lied about Lyme and LYMErix...."

    On Leadership: If Harvard were a religion
    There are leadership values that deeply underpin the Mormon faith — and they’re the same ones taught at Harvard Business School.

    Maybe we could get someone from HBS to ASK the NIH what OspA (the LYMErix vaccine that was ordered off the market by the FDA) is? Since we know that that is the "right question" (read the article). 

    When we ask, we're thrown in jail or threatened with jail - directly, by NIH Director Francis Collins' office (read more about that below).


    Cc:,, "Allen,Marin (NIH/OD) [E]" <>,,, "Strikas,Raymond A. (Ray) (CDC/OID/NCIRD)" <>,,,,,,,,,,,
    Subject: WaPo "On Leadership" and the NIH's Threats for "Asking the Right Question"

    May 15, 2012 9:06 AM

    Dear Sir,

    Regarding your article on Leadership in WaPo:

    We were wondering if you could "ask the right question" for us to the NIH (Francis Collins and Anthony Fauci would be fine).

    No one at the NIH, CDC, Yale or has been able to answer the question of what exactly the Lyme vaccine (LYMErix or ImmuLyme) was.  Of course we know they were "recombinant lipoproteins of Outer Surface Protein A of the Lyme spirochete," but we wanted to know its ***exact structure,*** since as you know, Structure Equals Function.

    When I called last Friday (a week ago), Francis Collins' little secretary would not allow me to speak - I merely wanted to give her the results of Collins referrals to others at the NIH to ASK what was OspA - She instead blurted out that she would call the police if I kept asking the NIH what was that vaccine that the CDC and NIH
    said was a vaccine:

    "We've had an effective vaccine, but it's the kind of vaccine that you have to essentially vaccinate people each year. And from the standpoint of it's use, it has not been used as efficiently as it could have been used. So scientifically, we had a vaccine and still do have a vaccine, but it's not really well used." -- Anthony Fauci


    That OspA vaccine was ordered removed from the market in 2002 when Karen Forschner of the Lyme Disease Foundation (Hartford, CT) presented the FDA with a patent owned by [Bridgette] Huber at Tufts indicating that OspA "bound the HLA molecule" or was technically a toxin for people who have the (only) genetic background that tests positive for "Lyme Disease" (as redefined in Dearborn, Michigan in 1994, in a "consensus" conference held by the CDC).

    Meanwhile, for the people who do not have the new, Dearborn, 1994 definition of Lyme "hypersensitivity"
    or "binds the HLA molecule" (inferring a binding of the antigen-presenting molecule with greater energy or kinetics, producing a toxin, itself as the complex of HLA-antigen), ***there is another outcome from the chronic exposure to OspA,*** either from vaccination (the regimen for the vaccines experiments was 3 injections of the OspA vaccines) or from the autovaccination of spirochetal blebbing.

    [Blebbing is to a spirochete what shedding is to a dog; by merely having a chronic infection with spirochetes - and all spirochetal infections throughout history are known to be chronic, a Lyme victim is subject to this autovaccination or shedding or blebbing.]

    In other words, the other outcomes of chronic exposure to OspA were the definitions of "Lyme Disease" that were left out of the Dearborn "consensus" conference definition - the outcomes of chronic Lyme previously identified by Yale and the in their journal, "Infectious Disease Reviews," or the New Great Imitator outcomes of MS, Lupus, ALS, and similar neurological outcomes that seem to be associated with B cell mutations
    that look like Epstein-Barr reactivation.

    It turns out that over the years, there is nothing but more and more additive scientific evidence that something about this fungal antigen, OspA, mutes the immune response, produces no antibodies (interferes with antibody production), and seems to act in synergy with viruses like Epstein-Barr (EBV), in that both OspA
    and EBV either donate to or add to anti-apoptosis of
    an infected cell.

    Now, meanwhile I remind you that there is no Tuberculosis
    vaccine or HIV vaccine, because these vaccines that
    were similar to LYMErix produced the same outcomes
    as the LYMErix trials: increased susceptibility to
    infection and no antibodies.

    You can go ahead and look that up or ask someone at
    Harvard.  I assume there will be someone at Harvard
    who can show you how to use the PubMed database.

    But, as you know, there is today another outcry apparently
    by vaccine manufacturers supported by the CDC [since
    the CDC does nothing more than support vaccine
    manufacturers, even going so far as to co-own 5
    patents with SmithKline in Europe from 1992
    , wherein
    they identify the 2 distinct outcomes of Lyme: 1) the
    hypersensitivity or allergy or "bad knees" response
    and 2) the non-"bad-knees" response or the cases of
    Lyme that do not test positive according to the CDC's
    1994, falsified (even if we just judged the outcome
    of the conference on the basis of consensus, since
    there was no consensus, not even close) Dearborn criteria]
    about the high rate of death in children because
    there is no Pneumonia vaccine.

    Daily Disruption – Study: Pneumonia Leading Cause of Death Among Children Under The Age of 5 -..

    Pneumonia is MYCOBACTERIA pneumonia.

    Get it?

    No fungal vaccines?

    Not whether they were apparently the HIV-LYMErix
    or the TB-LYMErix or the MRSA-LYMErix.  They all

    Now, don't you think it is odd that the NIH and CDC
    refuse to answer our question as to what OspA was?

    Maybe you could show us some of that Mormon-Harvard
    Leadership and ask the right question on our behalf: 
    "What Is OspA?

    Since it failed so many times and is associated
    with so many medical failures, not the least of
    which are all the myco-contaminated childhood
    vaccines that give the result we like to call

    1) "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."

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


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

    An ^^^ immunosuppressed pregnant cow was given a Brucella (LYMErix-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 (LYMErix-like) contaminated vaccines.


    4) 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."


    WaPo and the Harvard Business School and
    the Mormons call this Leadership.  When
    American Government's Crime Victims
    ask the right question, we're thrown and
    jail and threatened with jail.

    This is the opposite of leadership, but

    I hope you can put your money where your
    Mormon/HBS mouth is and ask Francis Collins
    what OspA is and get back to us.

    Thank you.

    Kathleen M. Dickson
    former Pfizer Analytical Methods
    and Validations chemist


    120514; Monday Criminal REtard Uncle Sam Magoo Update: 

    The primary, dominant global science says that LYMErix (OspA) could never have been a vaccine.  And if so, what are we to make of's and the CDC's position on "Lyme" or anything else ?

    The current "Lyme Program Officer" at the NIAID (under Anthony Fauci) agreed with me that flagellin from all the Relapsing Fever borrelia is the only sane (valid) antibody test for "Lyme." 

    Given that fact, there are no "guidelines."


    New old-news on immunosuppression (including no-antibodies) caused by Lyme and LYMErix:

    Macrophage p38 MAP Kinase Activity Regulates iNK Cell Responses During Infection with Borrelia burgdorferi...

    Previously, we learned from Ray Dattwyler in 1988, regarding this same NK cell activity inhibition:

    Ray Dattwyler (1988):


    Other Lyme Immunosuppression News:

    Delays and Diversions Mark the Development of B Cell Responses to Borrelia burgdorferi Infection.

    ("Uh, what?  Lyme is not 'an autoimmune T cell disease?'  It's a B-cells-are-effed-disease?  What's that you say?")


    Other, related news

    ("Oh, Ya mean fungal (pneumonia) antigens like OspA or LYMErix can't be made into a vaccine?  Oh."):
    Pneumonia is the leading cause of death among children under 5, according to a new study led by researchers at the Johns Hopkins Bloomberg School of Public Health. They examined the distribution of child deaths globally by cause in 2010 and found that 64 percent were attributable to infectious caus...
    More Old News on How LYMErix Could Never Have Been a Vaccine, from the UK:


    J Infect Dis. 2010 Jun 1;201(11):1753-63.

    Bacterial lipoproteins differentially regulate human primary and memory CD4+ T and B cell responses to pneumococcal protein antigens through Toll-like receptor 2.


    Department of Cellular and Molecular Medicine, University of Bristol, Bristol, UK.



    Bacterial lipoproteins (BLPs) [like LYMErix] are expressed across a range of bacteria and are able to activate Toll-like receptor 2 (TLR-2). BLPs enhance immune responses in naive individuals and have therefore been tested as candidate vaccine adjuvants. It is not known whether BLPs affect any preexisting immunity (eg, memory cell response in primed individuals). Colonization with pneumococcus (PNC), which primes for memory cell response, is common in young children.


    We studied effects of BLPs on memory and primary B and CD4+ T cell responses to pneumococcal proteins using adenoidal cells from children.


    Although BLPs enhanced the primary antibody responses seen in some children with no detectable nasal PNC, BLPs unexpectedly reduced the memory antibody responses in children with positive nasal culture results. Likewise, BLPs augmented the naive but inhibited the memory antigen-driven CD4+ T cell response. The downregulation of the memory responses was associated with increases in interleukin 10 and inducible costimulatory molecule expression, as well as a decrease in CD28 expression in memory CD4+ T cells; all were blocked by anti-TLR2 and anti-B7h antibodies. Augmentation of naive CD4+ T cell proliferation was blocked by anti-B7.2.


    Differential regulation of primary and memory responses by BLPs through TLR2 may have important implications for therapeutic and vaccination strategies against bacterial infection. [Like the definition of "Lyme Disease, which was falsified in order to falsify LYMErix as a BLP "vaccine" - the intention of which is to produce antibodies]

    But in the fact that Lyme is not an inflammatory disease and LYMErix therefore could never have been a vaccine, Yale is not interested.  It has zero to do with penises, which are Yale's and the State of Connecticut's only topic.  I am sorry to say that Yale has no topics.  But Yale itself, with its no-topics is an anthropological topic:


      120514, KMDickson



      Uncle Sam Magoo's School of Driving and
      Health dot gov

      Funny!  Nobody employed by Uncle Sam knows anything, so with what would we be indoctrinated?  LMAO!!

      An American military document just uncovered appears to detail an US Army plan that calls for detaining political activists at re-education camps staffed by military-hired PSYOP officers in both America and abroad.

      Alleged US Army doc: re-education camps and psy-op missions aimed at activists

      We're gonna hear all about how the moon is made of green cheese, LYMErix was a vaccine,...


      120504: Frankie (Collins)  & Tony (Fauci) in the Hot Seat:  Medical News: FDA, NIH Respond to Charges of Lax Oversight - in Washington-Watch, Washington Watch f

      I called Francis Collins' (NIH Director) office this AM to leave a message that "No one in the NIH and CDC will answer the question as to what OspA is," and then leave it at that for Collins to follow up.  Collins' office previously referred me to NIAID, who could not answer the question.  His secretary then said this to me:

      "We're asking that you no longer contact this office and we will be forwarding you to the police after this call," and then the secretary hung up.

      There ya go.  Cowardice drives all US "government" operations.  They're obviously pretty damned scared of being put on the spot over OspA and "Lyme."  Excellent.

      What OspA does, is the disease. And it's not inflammation, but a form of AIDS.
      The NIH refuses to answer because then you would see 200,000 instantaneous lawsuits against Yale, Tufts, NYMC, New Joisey Medical and Dental ....
      That would be the end of Yale's Endowment fund. Their Endowment fund funded L2 Diagnostics - Schoen's RICO operation with Corixa and Imugen. All of that was based on the lie of LYMErix.
      They're terrified of everyone discovering that ***they're all up for murder charges.***

      Especially Allen Steere and Robert Schoen over the Dearborn standard and falsifying the LYMErix outcomes.

      Gary Wormser and Mark Klempner, too, over the "guidelines."

      Wormser is an easy one to charge with murder because
      he so clearly said Dearborn only detected 15% of the cases in IgG:  (read carefully, he specifically states that he is assessing Steere's IN EUROPE proposal, where he leaves OspA and B out of the standard and uses high-passage strains)

      That's definitely a homicide charge and not a negligent homicide charge because of all the subsequent slander, libel and perjury against Lyme victims.  The lies told, and the aggression towards us fits the USDOJ's criteria of RICO.

      They act exactly like the mafia.

      And now you see that Francis Collins is part of that mob.

      • The LYMErix Story:

        Ian Malcolm: I'll tell you the problem with the scientific power you're using here: it didn't require any discipline to attain it. You read what others had done, and you took the next step. You didn't earn the knowledge for yourselves, so you don't take any responsibility for it. You stood on the shoulders of geniuses to accomplish something as fast as you could, and before you... even knew what you had, you, you've patented it, and packaged it, you've slapped it on a plastic lunchbox, and now
        [pounds table with fists]
        Dr. Ian Malcolm: you're selling it.
        [pounds table again]
        Dr. Ian Malcolm: You want to sell it, well...
        John Hammond: I don't think you're giving us our due credit. Our scientists have done things which nobody's ever done before...
        Dr. Ian Malcolm:
        Yeah, but your scientists were so preoccupied with whether they could that they didn't stop to think if they should.

      Lipopolysaccharide Binding Protein Binds to Triacylated and Diacylated Lipopeptides and Mediates Innate Immune Responses

      "The strong proinflammatory capacities of lipoproteins were first described for outer surface proteins A and B of Borrelia burgdorferi, which are also highly immunogenic (17) and have lately been the basis for a Lyme disease vaccine development (18). These compounds exhibit an triacylated lipid anchor structure comprising an N-palmitoyl-S-[2,3-bis(palmitoyloxy)-(2RS)-propyl]-(R)-cysteinyl (Pam3Cys) moiety at the N terminus (19), a feature that was previously described for the Braun lipoprotein from Escherichia coli (20). Because the N-terminal Pam3Cys modification is essential for immunoactivation caused by lipoproteins of B. burgdorferi as well as of another spirochete, Treponema pallidum (21), subsequent studies investigating immune responses to spirochetes used synthetic lipopeptides (22). The Pam3Cys moiety was also reported to be present in cytokine-inducing lipoproteins of Mycobacterium and Mycoplasma spp. (23, 24); thus, it can be regarded as a highly conserved molecular motif among different classes of bacteria."

      and, here we see Pam3Cys HIV, SIV:

      "We are currently using several mass spectral techniques to characterize the amino acid sequences of the Pam3Cys peptide found in the envelop glycoproteins of HIV-1 and the Simian Immunodeficiency Virus (SIV) 17.  Conventional fast-atom bombardment-mass-spec analysis using standard matrices, such as glycerol and nitrobenzyl alcohol, is nor particularly effective for these molecules, largely due to their tendency to aggregate."

      full text at:


      The people who wrote the following report cited bioweaponeer Joe Tully from 1963, talking about mycoplasma, fatigue and erythrocytes. 'Totally on the money with Lyme and HIV bearing the same types of immunosuppressing molecules:

      Immunological response of rodents to murine myc... [Infect Immun. 1970] - PubMed - NCBI

      "A positive correlation was demonstrated between ability of the mycoplasma to induce disease and lack of MI antibody formation by its natural host. It is suggested that the apparent inability of the various animals to produce MI antibodies against their natural mycoplasmal parasites may enable the mycoplasmas to become established in their hosts."



      And soon thereafter, a seronegative, Mycoplasmal-antigen bearing, chronic fatigue-causing modified Borrelia showed up 10 miles from Plum Island.


      Other reports that cited 1963 Joe Tully - a well-known bioweaponeer - on seronegative, fatigue-causing mycoplasma in the blood:

      Mycoplasmal, OspA-like, HIV-like antigens cause seronegative disease.  Get it?  1963.

      Later, of course,
      Ray Dattwyler in 1988 found the same thing re fungal infections and... Lyme Borreliosis.


      Pope:  Evil people are not going to be too good at science:

      "the decline of thought and the weakening of the capacity of intelligence for what is real."


      We knew that.

      More on Stupid Science at BUBBA_HEARTS_ALLEN_STEERE.htm

      IDSA's Explanation:  "Lyme causes nothing," "no disease outcomes happen from Lyme,"  "nothing causes anything," "Lyme victims are looney," "Lyme victims have paranoid delusional wannabee diseases," and "Lyme victims are TERRORISTS!!!, But get the mysterious, unknown OspA vaccine."

      Confronting "government" "employees" over their scientific incompetence

      I sent 2 letters May Day, 2012 to the NIH, CDC, Yale, Francis Collins, Anthony Fauci, Paul Auwaerter, the editors of the Lancet, and so on as you can see below.  The whole world can stand by and see if they reply.   And by "reply," I mean, answer the "What is OspA" question and answer what they think of the proposed RULE on fungal antigens/vaccines and resultant activated viruses causing the brain damage we call autism:

      Subject: No one at the NIH, CDC, Yale, or IDSA knows what OspA is.

      Date: May 1, 2012 4:54 AM


      I see that there is a job opening for what looks like
      Sally Rockey's job:

      I am wondering if Ms. Rockey is leaving becuase no one
      at the NIH knows what OspA is?

      As most of you know, I have been asking around for over a month.

      WHAT IS OSP-A (the structure)?

      No one at Yale knows.

      IDSociety doesn't know.

      NIAID doesn't know.

      Francis Collins can't/won't answer the question.

      Paul Auwaerter's office tells me he does not know.

      Lawrence Tabak hasn't answered me.

      No one at the CDC knows (despite CDC officers
      owning several patents for recombinant antigens
      of Borrelia burgdorferi).

      Nobody knows what OspA is.

      I find this odd, since this vaccine designed the "disease." 
      Allen Steere left OspA and B out of the diagnostic
      for Lyme disease using illegal (according to the
      NIH Rocky Mountains Lab) "high-passage" strains of Bb
      and recombinant antigens of the protein ends of OspA and B
      without the lipid attached to leave OspA and B out of the current
      CDC diagnostic standard, only to find the Western Blots of OspA-vaccinated
      people were unreadable anyway:
      (presumably ^^ because OspA sticks to itself as CDC officer
      Alan Barbour once claimed).

      The first order of business is the clarification of falsified antibody testing for “Lyme Disease.”
      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 [per the DNA/RNA Shell Game - never used to detect spirochetes in humans after treatment]  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)."  

      Without the lipids attached, the outer surface proteins are
      less likely to produce antibodies.

      Now, at one time (1991), Allen Steere wrote that
      there were 2 outcomes to Lyme: RA and MS.

      Currently, only the RA outcome is recognized
      (see the CDC's Dearborn definition where only
      the HLA-linked hypersensitivity response without
      OspA-B is recognized) as a "case."

      The basis of the 4.7 million dollar grant that
      went to Mark Klempner was to study the 30 day
      intravenous ceftriaxone treatment of people
      among whom 2/3rds never had had intravenous
      ceftriaxone before:
      "A total of 42 (33 percent) of the patients had previously received intravenous antibiotic treatment for a mean (±SD) of 30±12 days. All other previous treatment consisted of oral antibiotics." 

      Klempner ^^^ found that 30 days of IV ceftriaxone was
      not enough ceftriaxone for people who had never
      had ceftriaxone before.

      Perhaps no one was looking too closely at
      the grant they approved.  Klempner found
      that the "standard of care" - arbitrarily defined
      in the first place - was not enough intravenous
      antibiotics for these people.

      But that's a tough call, isn't it?  You don't
      need INTRAVENOUS antibiotics for knee diseases -
      the "case definition."

      Maybe if we knew what OspA was.  After all, it
      defined the disease.  Both in the classical
      commercial sense (the Dearborn definition) and in
      Allen Steere's HLA-linked hypersensitivity sense.

      A man named Roland Martin left his job at
      the NIH once he found out OspA actually caused
      the disease he was studying - the MS outcome:
      "Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression."
      "These results show that signaling through ***TLR1/2*** [note- remember the structure/function relationship-added by KMD] 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."

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

      "Toll-like receptors (TLRs) trigger innate immune responses via the recognition of conserved pathogen-associated molecular patterns. Lipoproteins from Borrelia burgdorferi, the agent of Lyme disease, activate inflammatory cells through TLR2 and TLR1. We show that stimulation of human monocytes with B. burgdorferi lysate, ***lipidated outer surface protein A, and triacylated lipopeptide Pam3CysSerLys4 results in the up-regulation of both TLR2 and TLR1 but the down-regulation of TLR5, the receptor for bacterial flagellin, and that this effect is mediated via TLR2.*** TLR4 stimulation had no effect on TLR2, TLR1, and TLR5 expression. Human monocytes stimulated with TLR5 ligands (including p37 or flaA, the minor protein from B. burgdorferi flagella) up-regulated TLR5. ***In addition, TLR2 stimulation rendered cells hyporesponsive to a TLR5 agonist.*** These results indicate that diverse stimuli can cause differential TLR expression, and we hypothesize that these changes may be useful for either the pathogen and/or the host."

      I hypothesize that TLR2/1 agonists suppress
      the immune response and that everything Mark
      Klempner and IDSA, Yale, and the CDC say is

      What do you say?


      Anyone know what OspA is?

      The CDC to this day maintains that it is
      a vaccine.  NIH never retracted their statement
      that it was.

      My personal observation is that, like Roland
      Martin is revealing, OspA caused the seronegative
      neurological disease outcome sometimes called
      Multiple Sclerosis - the job he was hired to study
      at the NIH.

      OspA does something to the immune system that
      is not like what Allen Steere and the CDC claim
      with their "case definition."

      And MS is largely recognized to be caused
      by Epstein-Barr/Similar herpes viruses.


      It would be nice to know what OspA is.

      We might be able to end the OspA-linked

      Kathleen M. Dickson
      former Pfizer Analytical
      Methods Development and Validation



Subject: A 5-points rule on fungal vaccines and brain-damaged children (failed TB and Lyme fungal vaccines notwithstanding)
Date: May 1, 2012 6:00 AM


I would like to propose a rule on fungal antigens and vaccines
which is related to the OspA outcomes:

1) "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."

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


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

An ^^^ immunosuppressed pregnant cow was given a Brucella (LYMErix-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 (LYMErix-like) contaminated vaccines.


4) 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."


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

Do not ^^ cause immunosuppression/stress as
it causes increased mortality from existing
infections and especially do not cause stress to
humans by treating them to *ABUSE* instead
of medicine when they don't the special "controversial"
disease that fits the commercial (unknown) vaccine model:

Because ^^ that - the abuse - activates Epstein-Barr.


RULE:  Don't give immunosuppressed mammals live attenuated vaccines, and especially
don't give them vaccines that contain fungal or mycoplasmal antigens like LYMErix or OspA.

What do you say?   Do you like that rule?
Especially if we added the OspA/MS/Roland Martin
"Immunosuppression>> MS Outcome of Lyme" data
to that data set?

What about if we added the 1918 Spanish
Flu data to the rule:  "People with strong
(Steere-HLA-like, Dearborn definition-like)
immune responses are likelier to choke to death
on the pneumonia (fungal) that follows the influenza,
whereas immunosuppressed people won't produce a
hyperinflammatory response and thereby survive the

We haven't had any new Rules in a while.

All we ever hear is that "Lyme causes nothing"
and "no disease outcomes happen from Lyme"
and "nothing causes anything" and "Lyme victims
are looney" and "Lyme victims have paranoid
delusional wannabee diseases" and the latest:
"Lyme victims are terrorists !!!":

"But get the mysterious unknown OspA vaccine."

- - - - - - -


What do you think?

How about that for a rule?

You might have to find out what OspA is, first.

No hurry.  It was ordered removed by the FDA
in Feb, 2002 for producing "chronic Lyme-like"
illness (clue).

And that was the last time Uncle Sam said
anything *TRUE* about "Lyme Disease."

10 years....

Kathleen M. Dickson
former Pfizer Analytical Methods Development
and VALIDATION chemist


120420; "Lyme Disease" Update from the CDC, NIH, NIAID, Yale and, none of whom, in a month's time, has been able to tell me what OspA (the Lyme vaccines) is - they all say they do not know:

Dr. Paul Auwaerter PhotoThe following is a letter sent to them regarding Paul Auwaerter, the current blowhard/mouthpiece of IDSA:


To: KMDickson <>, "Strikas,Raymond A. (Ray) (CDC/OID/NCIRD)" <>,,,,

Subject: Paul Auwaerter Does Not Know What OspA Is Either

Date: Apr 20, 2012 4:35 AM


I called Auwaerter's office (Johns Hopkins)
and left a message asking if he knows what
OspA is. The answer was no, he did not.

I guess he is not an expert in Lyme Disease

Now, all of this is amusing given the fact
that Roland Martin quit the NIH's MS-Lyme
group once he found out OspA was causing
the immune suppression (and seronegative,
non-Dearborn Lyme) resulting in the MS
form of Lyme (known to be associated with
reactivation of Epstein-Barr):
"Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression."

as does Adrianna Marques, who publishes these
articles with him:

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

That^^ all means Chronic Lyme is seronegative
and the chronic exposure to OspA/Borreliosis
results in NO ANTIBODIES. We now know for
sure that Klempner's "study" can be thrown out
since the study design was based on the
fraudulent Dearborn diagnostic standard.

[Dearborn was fraudulent because there was
no consensus (I have the booklet) and because
Steere formulated the antibody panel via
classic research fraud, using high passage
strains and recombinant OspA and B without
the antibody-producing lipids attached, setting
up his own little racketeering enterprise with
Dave Persing (Corixa) and Yale's Robert
Schoen (L2 Diagnostics) for the intended
post-LYMErix monopoly on blood, patentable
goodies in the blood, and grants.]

Secondarily, Paul Auwaerter lists as his
expertise, Lyme and Epstein-Barr (known to
be activated by Lyme and probably LYMErix
as shown by Marques and Martin, above).

Thirdly, Bridgette Huber at Tufts, who
published with Allen Steere ("Lyme causes
only the HLA-linked hypersensitivity response")
but her area of expertise also includes
Lyme and Epstein-Barr (EBV activating a
human HERV, the favorite of Harold Varmus
former director of the NIH:

Fourthly, Adrianna Marques lists on *HER*
website, that her areas of expertise are
Lyme and Epstein-Barr (and some other herpes

So, it looks to me that "Post Lyme Syndrome" is,
in Marques' words, "Chronic Active Epstein-Barr."

Especially since Paul Duray (US Army and
the National Cancer Institute)
twice in IDSA's journals that the lymphocytes of
chronic Lyme victims "look like Epstein-Barr
transformed cells
" in 1989 and 1992.

How this happens, how these fungal antigens
seem to reactive Epstein-Barr, I do now know
exactly, other than the association to
exposure to OspA and subsequent production
of the immunosuppressive cytokine, IL-10.
(I won't produce the references for that
because they're well known and accessible.)

Now, the problem with Adrianna Marques is that
she is recruiting chronic Lyme victims to see
if she can get clean ticks to become infected
with Borrelia from biting post-treated Lyme
victims - from the blood.

But that's not really what's going on, is it?

It's going to be mycoplasma to which we have
become tolerant via exposure to OspA (blebbing
is the same as autovaccination), and some kind
of herpes, et al, correct?


Ticks are a great place for transkingdom
plasmid-sharing according to Barbour and

You're thinking of *that* ^ when Marques tries to
pharm Borrelia not known to be in the peripheral
blood of human victims due to the tissue penetrating,
plasminogen-hijacking OspA??


Kathleen M. Dickson

120430.htm previous homepage

NEW (120430, Barthold):   

Delays and Diversions Mark the Development of B Ce... [J Immunol. 2012] - PubMed - NCBI

"Finally, there is a slow accumulation of long-lived Ab-secreting plasma cells in bone marrow, reflected by a strong but ultimately ineffective serum Ab response. Overall, the study indicates that B. burgdorferi might evade B cell immunity by interfering with its response kinetics and quality."  

OLD (2000, Gary Wormser):

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

"The modulation of human lymphocyte proliferative responses was demonstrated with a recombinant outer surface protein A (OspA) vaccine preparation for the prevention of Borrelia burgdorferi infection. After exposure to either the unaltered vaccine preparation or OspA prepared in saline, normal lymphocyte responses to the mitogens concanavalin A, phytohemagglutinin-M or pokeweed mitogen, or the antigen BCG were consistently reduced. Whole cell extracts of B. burgdorferi also modulated immune responses but required a much greater quantity of protein than needed for the OspA preparation. The magnitude of modulation was directly dependent on the quantity of OspA. OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression. Future studies designed to delete the particular region or component of the OspA molecule responsible for this effect may lead to improved vaccine preparations.


‎INTERMEDIATE (Bridgette Huber, Steere's partner at Tufts):

"The spirochete also modulates its surface protein profile upon infection
[meaning the Dearborn diagnostic standard is moot in IDSA's late, persistent Lyme because Lyme is merely a relapsing fever organism and does not deserve its own "disease" name- the nature of the relapse is antigenic variation] and induces anti-inflammatory cytokines, favoring survival of the pathogen. The host defense involves toll-like receptors (TLRs), such as TLR2 [OspA is an immunosuppressive TLR2-agonist, structure equaling function] and others, in B. burgdorferi recognition."


120430.htm previous homepage selections:

Update 120429; LYMErix Disease® /Chronic Fatigue Syndrome is in the Cancer class, not Autoimmune:

"In fact, the more we understand about autoimmune disease, the better we will understand cancer because they're opposite ends of the same problem, he says. Cells are too quick to attack healthy tissue in autoimmune disorders and too slow to fight in cancer, allowing harmful tissue to grow out of control."

This A) confirms the mycoplasma-contamination theory of Childhood Vaccinations resulting in active viral infection of the brain (see more data by the CDC, below), and B) is why you so often see Leukemia as an outcome of Lyme and LYMErix, especially in children.

Yes, you can now wonder if the vaccines cause Leukemia in children.

Update 120427-30; - No Action Yet on the "What Is OspA?" question from the NIH, CDC, Yale, IDSA, The Lancet, or the Dean of Johns Hopkins Medical School to whom I complained about the still-unprosecuted "Lyme Disease" blackmailing criminals' scientific fraud and racketeering, and Paul Auwaerter's scientific incompetence.  The best we have is a grant given to Tufts where they recognize that Lyme and LYMErix may cause immunosuppression, and an image of OspA (Pam3Cys) by a Japanese group published in February, 2012.  See more below.

Don't Miss This by Ray Dattwyler (1988):


If Lyme and LYMErix cause immunosuppression, then Lyme is not "an inflammatory disease," as is falsely claimed.  The current ELISA-Western Blot protocol enforced by the CDC and their partners in crime, insurance companies like Kaiser-Permanente, is not only a murder charge, but inhibited discovery in every disease and is a biowarfare-ignorance threat. 

"Lyme Disease" is the worst case of cowardly victim-blaming ever witnessed in US Medical history, performed by people who have astonishingly little understanding of basic science (structure equaling function).  But it had one good outcome:  it revealed that psychiatry is neither a science nor anything medical.  The Lyme criminals' subjective descriptions of Lyme, while having performed all the scientifically valid biomarker analyses themselves, allows the subjects of "subjective" and "psychiatry" to coalesce into the motif of the confusing fugue of Western Society: the human will attempting to trump any truths.  Ours is the New Dark Age, where any superstition or hypothetical mystery is literally passed off as law.  But Lyme Cryme "blew the top off the illusion," as they say. 

Note:  Science Proves The Word to be True and Valid:

For (AJ)the wrath of God is revealed from heaven against all ungodliness and unrighteousness of men who (AK)suppress the truth in unrighteousness,  19because (AL)that which is known about God is evident within them; for God made it evident to them.

"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."


But the (secret) information regarding what OspA is also has bioweapons applications.  

There is a class of bioweapons called "stealth disablers." The intention of them is to disable the immune system and produce no antibodies.  Oddly, Lyme and HIV showed up at the same time, and they both apparently bear OspA-like, TLR2-agonist-like, fungal-like-antigens.  There is some evidence that HIV's gp120 is OspA in triplicate [1) antibodies, 2) the failed STOP HIV vaccine trial results were identical to the failed Lyme and failed TB trial results, and 3) the Korean MassSpec results

See for yourself that it nearly impossible to find an image (structure) of the HIV gp120 or OspA (with the lipid attached).

"Cause Known" Updates 120427: 
Japanese also identify the structure of OspA; It appears to be Pam3Cys:
A delicate interplay of structure, dynamics, and thermodynamics for function: a high pressure NMR study of outer surface protein A.

But the CDC says they do not recognize foreign research.  The CDC only apparently only recognizes their own foreign research, such as sending Allen Steere to Germany to falsify the diagnostic standard for Lyme

An Admission that Lyme and LYMErix cause immunosuppression (Tufts):
"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."

Intracellular Lyme Grant intended to further the Intracellularity discovered by Mark Klempner in 1992:  "Specifically, we propose to: (1) Characterize the invasion of borrelia burgdorferi into primary fibroblasts. The working hypothesis here is that B. burgdorferi exploits invasion as an additional mechanism to avoid host clearance. Our preliminary studies demonstrate that B. burgdorferi invasion is not dependent on host fibronectin, but does involve ?1 integrins other than... ?5?1. In this Aim we will identify the ??subunit that pairs with ?1 to promote invasion and will also evaluate how B. burgdorferi traffics within these cells; and (2) Determine if invasion is required for B. burgdorferi persistence in vivo. Our working hypothesis is that invasion contributes to persistence by providing an immunoprotected niche for B. burgdorferi. Since Src kinases are required for borrelial internalization in vitro, we will determine whether Src kinase inhibitors aler the infectivity potential of B. burgdorferi in vivo. In addition to standard cultivation and molecuar approaches, novel in vivo imaging will be employed to assess how the inhibitor affects colonization. The overall goal of these studies is to determine the extent in which an intracellula locale contributes to borrelial persistence."


111221-120503; Table Summarizing what we know so far about mechanisms and markers in EBV-Borrelia co-activation

Nearly every disease is represented here, from the mechanisms by which childhood vaccines contaminated with mycoplasma might be giving children the very diseases the vaccines were meant to prevent, to antibiotic resistance genes being transferred to the likes of Staph aureus via bacteriophage-vectored transfer of "virulence determinants" under the cover of a SLYMErix (TLR2-agonist/TLR2, stealth, tolerance) biofilm.  From cancer to the failure of the MRSA-LYMErix, Tb-LYMErix, and HIV-LYMErix "vaccines"- which happened years after the falsified failure of LYMErix.

And to think Yale and SmithKline owned all that proprietary data all these years.
[Yale and SmithKline (a UK company) own the proprietary antibiotic-resistance data because resistance (TLR2 tolerance) is caused by Lyme and LYMErix; they admitted they knew this at the 1998 FDA meeting!)]   Yale staff are quite notorious for not understanding the meaning of the word "system."  That is, Yale staff believe that one should not speak about markers of illness or illness induction by fungal antigens and that to do so means the speaker is a "terrorist like Ted Kascynski."  Which, you know, how does one deal with that kind of insanity?  It's like George Bush claiming, "We have interests in the Middle East."   ("Wait, what?")

That kind of stupidity we know for sure is due to the "diabolical delusion" predicted to envelope Western society in the end times.  
"Postmodernists believe that truth is myth, and myth, truth. This equation has its roots in pop psychology. The same people also believe that emotions are a form of reality. There used to be another name for this state of mind. It used to be called psychosis." -- Brad Holland

You can't educate psychiatrists because they're True Believers in people operating solely in their own self-interest.  But psychiatrists deserve to suffer a life of such cynicism, because in the end, and after all, you know it when you do something wrong.  Read Hostage to the Devil and the other case histories of exorcisms.  These demons admit they're crazy.
Meanwhile, persons who believe we have an obligation to facts and scientific realities, Yale says are insane.  No one sane can figure this out, "The same people also believe that emotions are a form of reality," but it's true that Yale psychiatrists believe this crazy shit.  You can study it and ponder it forever, but it will never make sense to a real scientist or someone grounded at least in the 4 dimensional reality.

"Injustice and Cruelty follow Pride and Self-Worship."  Yep.  That's the Western Culture, where tards like prison guards, cops and the whores of the "Child Protective Services" ruin lives for money.  Thence, the prison-industrial complex.  Thence, the genocides of Iraq and Afghanistan.  The Bankster Bailout.  Warmongering by GOP for Israeli Dollars.  ...  "It's All About Meeee!"


1989, Paul Duray (in IDSA's journal), Clinical pathologic correlations of Lyme disease.

“Frank signs of meningeal irritation herald stage II illness, reflected by an increase of CSF lymphocytes and plasma cells and moderate increases in total protein in CSF [9,16,17].  Immature B cells can also be seen in the spinal fluid.  These cells can appear quite atypical- not unlike transformed or neoplastic lymphocytes."
IDSA_CLINIPATH_DURAY.htm ("Epstein-Barr-like transformed B cells")

1992 Duray:
"On occasion, these atypical-appearing large lymphocytes have been misinterpreted in biopsy by several laboratories as cells of a malignant lymphoma or leukemia.  Bb antigens, then, may stimulate growth of immature lymphocytic 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

This table is working.  We see the hijacking of the Life of a Cell ...  Or as Gary Wormser declared in 2000 (while OspA was still on the market), "OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression."   It's like immunological paralysis.  To go with the NIH's intellectual paralysis.  Additionally, it seems flagellin and other bacterial antigens (besides TLR2 agonists) activate mouse EBV.

Herpes Mouse Herpes/ XMRV Fungal/Viral Spirochetes Myco/OspA EBV/HERVs Flagellin MRSA/Chlamydia Tuberculosis Cysts Q Fever
Interleuken-10 (caused by Lyme &  LYMErix) inhibits the management of EBV (1991)
This article was cited over 100 times.
Flagellin activates Mouse Gammaherpes TLR2 Signaling Depletes IRAK1 and Inhibits Induction of Type 1 by TLR7/9  (viruses)--

-Clifford Harding, 2012 "Bacterial/Viral Coinfections"

  NIH: says "OspA suppresses & reprograms immunity" (wins Nobel; means Dearborn is a lie as are "Lyme" "guidelines" EBV transformed cells help present fungal antigens       Chp 19, Cryme Disease - the History of Relapsing Fever  
Stevil Straus: Characterization & treatment of chronic active EBV disease: 28yrs, USA (CFIDS is Chronic EBV)

CFIDS = EBV Seronegative (4 reports)

Down-regulation of MHC class II expression through... [J Immunol. 2009] - PubMed - NCBI


Mouse Herpes 68 hijacks MAVS and IKKbeta TLR2 agonists synergistically increase the proliferation of EBV


Duray at Ft. Detrick in 1992 and reporting to IDSA about EBV- transformed lymphocytes in 1989 Chronic Lyme is seronegative because Lyme is chronic
(downregulation of MHC-II; Justin Radolf) due to (blebbing)
Harold Varmus, Denise Huber
Huber says there is 2 kinds of Lyme: the EBV evoking kind and Steere's "knees"
Formation of cysts within cells results in the release of flagellin (See H. pylori&EBV Lipoteichoic acid (LTA) of Streptococcus pneumoniae and Staphylococcus aureus activates immune cells via Toll-like receptor (TLR)-2, lipopolysaccharide-binding protein (LBP), and CD14, whereas TLR-4 and MD-2 are not involved. 101016.htm 111106.htm
US Army: Spirochetal cysts are in dried animal urine.
Q-Fever/Chronic Lyme (activation of viruses) TLR agonism becomes seronegative.
Update, Mayo Clinic on RA and Cytomegalovirus (120202)

A profile of immune response to herpesvirus... [Arthritis Res Ther. 2012] - PubMed - NCBI

NCI/XMRV  and NF-kB prostate cancer from the imaginary XMRV ?? Interleukin-10 [produced by exposure to OspA] inhibits apoptotic cell death in infectious mononucleosis T cells.(1994) "Pam3Cys keeps the precursors in a more immature stage"  (IL-17)

Borrelia & IL-17


Tolerance induced  Pam3Cys (Yale's LYMErix "vaccine") is due to ablation of IL-1R-associated kinase-1. 15294992   Flagellin (and other antigens) activates Mouse Gammaherpes PubMed: Chlamydia and TLR2 EBV transformed cells help present fungal antigens Steere's lab workers inhaled Borrelial cysts. Coxiella agonizes TLR2 (would be seronegative)

"Conclusions: EBV DNA was often found together with other microbial findings in CSF of immunocompromised [LYMErix- or Lyme-Disease]  patients." 


  "Conclusions: EBV DNA was often found together with other microbial findings in CSF of immunocompromised [LYMErix- or Lyme-Disease]  patients."   

101016.htm Epstein-Borreliosis datapage; Note: Harding explains Steere's Knees (HLA-antigen complex is shed)

OspA induces IL-10

IL10>>CD4- = EBV

EBV & IL-10  

OspA delays apoptosis through inhibition f caspase-3 activity:  CD14&TLR-2.  (Ireland,  BLP (OspA) inhibits neutrophil mitochondrial membrane depolarization"

"It has been demonstrated that LPS inhibits PMN apoptosis preferentially through stabilization of the mitochondrial membrane and subsequent inhibition of caspase-3 (33)."

    PubMed: Chlamydia and Epstein-Barr  


Mario Philipp's monkey study = transfer of cysts.  Called the MIT. Gulf War Illness Q Fever

No one can be diagnosed with anything that's  a bioweapon.

Stress steroid hormones literally activates EBV Which means is trashed, once again   Interaction of Borrelia burgdorferi sensu lato with Epstein-Barr virus in lymphoblastoid cells Structure of Leptospira TLR2 agonists  They say not to use mice TLR2. TLR2 and nf-kappa         Q Fever &  inhibition of apoptosis Could be missed.  Crooks  playing RNA/DNA ShellGame is trashed (NYT)   "Internal"  Lyme spirochetes increase EBV  replication. Lyme causes CLL Leukemia

(Look up the symptoms of that)

IL-10 (induced by OspA)

IL10>>CD4- = EBV


          RML:  Sustained of Akt and Erk1/2 is required for Q Fever anti-apoptotic activity
EBV alters mitochondrial membrane

CDC: EBV wrecks mitochondria.

      TLR2 activation inhibits embryonic neural progenitor cell proliferation     H. pylori works with EBV     C. burnetii inhibits activation  apoptosis through a mechanism that involves preventing cytochrome c release from mitochondria
EBV transformed cells help present fungal antigens       Systemic stimulation of TLR2 (such as in vaccination with OspA) impairs neonatal mouse brain development     H. Pylori/EBV affect NF-kappa-B    


EBV LMP1 reduces p53 protein levels independent of the PI3K-Akt pathway. Dec 21, 2011

111222: HSV-1 Infection Activates the Epstein-Barr Virus Replicative Cycle via a CREB-Dependent Mechanism

  H. pylori works with EBV

H. Pylori/EBV affect NF-kappa-B



Treatment of Throat Cancer Caused by Epstein-Barr is to Reverse Dattwyler's NK-Cell Suppression:              
Despite the NIH anti-CD20 datapage      


Seronegative EBV (downregulation of MHC-II)

BCL-2 Homolog BHRF1


PubMed: "Endotoxin Tolerance and TLR2" [means LYMErix (OspA) was not a vaccine, Dearborn is a lie, and Borrelial antigens are immunosuppressive as TLR2 agonists.]

EBV & LMP1          
Oncogene BCL2-like in EBV          


EBV &  mycoplasma                    
EBV inhibits p53 auto-kill kinase                    
NF-Kappa B and Herpes (PubMed, General search)      


Herpes Simplex Immunosuppression (NF-kappa)                    
Epstein-Barr and anti-CD20 (Rituximab)
(PubMed, 500+)(and CFIDS)
IL10>>CD4- = EBV                    
EBV & IL-10                    


Here is what we know about what is the requirement for a pandemic flu human strain to take off:

Chinese: Characterization of H9 subtype influenza viruses from the ducks of southern China: a candidate for the next influenza pandemic in humans? 

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

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

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

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

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

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


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