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





This asshole Sepkowitz is busted.  See the other one, Joseph Alpert.



Complaint re Kent Sepkowitz - not knowing about biofilms and TLR2-agonism (Daily Beast article)
Date: Apr 14, 2014 11:09 AM


Greetings, Dr. Cottington,
(BIO: )

- - - - -

My complaint about your employee Sepkowitz is in regards to this bogus article in the Daily Beast:

The Lyme vaccine was OspA or Pam3Cys or a tripalmitoyl cysteine-based recombinant lipoprotein, basically, and a TLR2/1 agonist,... which means it is a fungal antigen..
Would you like to see what its structure is?

It was the same stuff apparently as Fauci's Failed HIV vaccine, a trial he stopped in 2008 :)  This HIV-LYMErix vaccine gave the same results as the failed LYMErix vaccine.  You can give Fauci a call if you like and ask him about the NO ANTIBODIES and the INCREASED SUSCEPTIBILITY to disease resulting from this LYMErix-Do-Over as a Failed HIV vaccine: 

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


Now, one would think someone like Sepkowitz would know a little about TLR2-agonists since he claims to be in charge of infection control at Sloan Kettering. Biofilms and MRSA are basically covered in SLYMErix, and that is the reason for all the trouble with these antigens.  The chronic agonism of TLR2 by fungal antigens turns off the immune response in humans.

Do I need to provide you the references or you can look this up on your own?

"Collectively, these findings demonstrate that S. aureus biofilms are capable of attenuating traditional host proinflammatory responses, which may explain why biofilm infections persist in an immunocompetent host."

That is just ^^^ one and specific to MRSA, which, I assume would be one of Sepkowitz's "specialties."

- - -

The Lyme vaccine, OspA, failed not because it caused arthritis, but because it caused the same systemic disease as "Chronic Lyme."  That is, Lyme, as the New Great Imitator - known to cause Lupus and MS - was really the Great Detonator, after all, since it appears to activate Epstein-Barr (or similar herpesviruses) the real culprit in "Chronic Lyme," MS and Lupus, (and cancer).

It was not just me and the vaccine recipients themselves reporting that LYMErix caused systemic disease, Ben Luft (SUNY-SB) also reported the same at the 1998 FDA meeting on LYMErix:

BEN LUFT:    "The point that I wanted to make in regard to the study is that there is very heavy dependence on serologic confirmation. And when we start thinking about the adverse events, *** it was stated originally when we got the overview of the disease that the disease is really quite protean [means not limited to "bad knees- KMD]. And actually the adverse events are very similar to what the disease manifestations are.**** And if you start to, as I think Dr. Hall was eluding to -- if you start to kind of say well how often do you actually become sero positive, you can start to have a different take on when someone has an adverse event of whether it is disease specific or infection specific versus vaccine specific. And I think that that is an important issue that we have to deal with. I can only say from my own ..."

Dave Persing reported the same thing in his ***RICO-Within-The-RICO patent (US Patent # 6,045,804),*** which showed the reason the testing for Lyme was falsified at the 1994 Dearborn Consensus Farce: 
[Steere falsified the ^^^ testing in Europe to set up this little RICO with Imugen, Corixa and Yale's L2 Diagnostics; they filed a statement with the SEC that they would be the 3 "partners" licensed to use this testing post-LYMErix approval - the ONLY ones in the USA and Canada,
so it's nice if you can *get* such a national monopoly on national-bloodwork-and-all the-DNA-patentable-goodies-in-human-blood-scam :)
They say:
"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.*** "]

Would ^^^ have been a nice little enterprise, founded upon LYMErix succeeding, but these clowns really went just too far by trashing Lyme and LYMErix victims, routinely.  Red Flag City :)))

- -

The chronic agonism of TLR2 (such as by spirochetal blebbing or giving people 2 or more injections of LYMErix) in humans produces the well known result of Endotoxin Tolerance and Cross Tolerance, and conversely, Classic TLR4-agonism causes cross TLR2-agonism [tolerance].

The reason we put Thimerosal in vaccines is to prevent fungal/mycoplasmal contamination, right?  And why is that a problem, this fungal-viral synergy?

How does OspA activate EBV/Similars?

Well we have of course the initial evidence by the late US Army and NCI pathologist Paul Duray who in IDSA's own journal published that the lymphocytes in the spinal fluid of Lyme victims looked like immature and EBV-like transformed cells.
You can find his name here, if you like:
to see for youself what Duray actually published:

"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 H. Duray, NCI, NIH, Ft. Detrick, at the 1992 Cold Spring Harbor Crooks' Conference, published in Steve Schutzer's  Lyme Disease: Molecular and Immunologic Approaches.


"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." --

 -- Paul H. Duray, 1989, IDSA's Journal

What other evidence do we have?

Well, IL-10 plays a role (produced by exposure to TLR2-agonists like OspA or spirochetal blebbing), and so does, apparently the first step - the "GAME CHANGER" first step, the inhibition of apoptosis of infected cells caused by both EBV [with it's own version of a human BCL2- gene (I am sure you know this since I am talking to Sloan Kettering)]...  *** AND OspA or LYMErix. ***

Would like the specifics on that or you believe people like Gary Wormser when they publish that fact?
Again, look for his name here: 

Wormser says:
"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.

^^^^  So that's a "vaccine?" 




Now in addition to the role IL-10 plays in the activation of EBV/Similars from Lyme, what else besides the first step, the Game Changer, inhibition of apoptosis of infected cells?*+and+EBV 

Well, it could be that both spirochetes and EBV love B cells.

Maybe someone at Sloan would like to investigate that.  I know Varmus was interested in this at one time.


And what say we ask Sepkowitz what his real agenda was here, if he is in fact competent to the science that says fungal antigens are immunosuppressive?

Kathleen M. Dickson