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Overview
 


TUSKEGEE - By Jerry Leonard


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

Bush/Gore  Oil/War-(Oct,2000)  

Bush's own explainer (Oct 2000): Iraq Oil

Iraq was an oil-theft war.




 

 

Besides the obvious:   PubMed ID 9394822    "None of the mice previously immunized with OspA peptides were protected against experimental infection, in spite of the appearance of protective antibodies."

 

rOSPA WAS NOT A VACCINE

1)  Yale did not demonstrate that there were not spirochetes in the ticks:

 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1608951&dopt=Abstract

Elimination of Borrelia burgdorferi from vector ticks feeding on OspA-immunized mice. 
Fikrig E, Telford SR 3rd, Barthold SW, Kantor FS, Spielman A, Flavell RA.
Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5418-21.

 

2) To assess outcomes, use chromosomally and not plasmid-coded DNA:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8234271&dopt=Abstract

Borrelia burgdorferi is clonal: implications for taxonomy and vaccine development.
Dykhuizen DE, Polin DS, Dunn JJ, Wilske B, Preac-Mursic V, Dattwyler RJ, Luft BJ.
Proc Natl Acad Sci U S A. 1993 Nov 1;90(21):10163-7.

 

3)  rOspA vaccination results in escape mutants or variants spirochetes which INCREASE at a greater rate than normal.

Selection of variant Borrelia burgdorferi isolates from mice immunized with outer surface protein A or B.
Fikrig E, Tao H, Barthold SW, Flavell RA.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7729870&dopt=Abstract

 

4)   Experiments in vitro in which complement is added demonstrate the antibodies to rOspA alone do not kill the spirochetes:

Borrelia burgdorferi escape mutants that survive in the presence of antiserum to the OspA vaccine are killed when complement is also present.
Sole M, Bantar C, Indest K, Gu Y, Ramamoorthy R, Coughlin R, Philipp MT.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9596714&dopt=Abstract

 

5) OspA vaccination was not demonstrated to protect monkeys from infection:

The outer surface protein A (OspA) vaccine against Lyme disease: efficacy in the rhesus monkey.
Philipp MT, Lobet Y, Bohm RP Jr, Roberts ED, Dennis VA, Gu Y, Lowrie RC Jr, Desmons P, Duray PH, England JD, Hauser P, Piesman J, Xu K.
Vaccine. 1997 Dec;15(17-18):1872-87.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9413097&dopt=Abstract

 

6) rOspA vaccination did not protect rabbits:

Comparison of protection in rabbits against host-adapted and cultivated Borrelia burgdorferi following infection-derived immunity or immunization with outer membrane vesicles or outer surface protein A.

Shang ES, Champion CI, Wu XY, Skare JT, Blanco DR, Miller JN, Lovett MA.

Department of Microbiology and Immunology, Department of Medicine, School of Medicine, University of California, Los Angeles, California 90095, USA.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10858236&dopt=Abstract

"Analysis of the antibody responses to outer membrane proteins, including DbpA, OspA, and OspC, suggests that the remarkable protection exhibited by the infection-immune rabbits is due to antibodies directed at antigens unique to or markedly up-regulated in host-adapted B. burgdorferi." 

Natural infection was better in infection-immune rabbits, because of adaptation to antigenic variation.

 

7) OspA was not shown to protect mice, and why, by Russell Johnson:

Resistance to tick-borne spirochete challenge induced by Borrelia burgdorferi strains that differ in expression of outer surface proteins.

Kurtti TJ, Munderloh UG, Hughes CA, Engstrom SM, Johnson RC.
Infect Immun. 1996 Oct;64(10):4148-53

There was no reduction of strain 297 spirochetes in ticks that fed on four hamsters immunized with M297, but the hamsters were protected.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8926082&dopt=Abstract

The journal publications of Russell Johnson-->  MEDLINE:  "Johnson RC [au] and spirochete"

 

8) Other lipoprotein vaccine failures and activation of latent infection:

The 19-kD antigen and protective immunity in a murine model of tuberculosis. 
Yeremeev VV, Lyadova IV, Nikonenko BV, Apt AS, Abou-Zeid C, Inwald J, Young DB.

"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."

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10792376&dopt=Abstract


Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits Mycobacterium smegmatis-induced cytokine production by human macrophages in vitro.

Post FA, Manca C, Neyrolles O, Ryffel B, Young DB, Kaplan G.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11179309&dopt=Abstract

The 19-kDa lipoprotein of M. tuberculosis, expressed in M. vaccae or M. smegmatis (M. smeg19kDa), abrogates this protective immunity....Thus, the immunosuppressive effect is dependent on glycosylated and acylated 19-kDa lipoprotein present in the phagosome containing the mycobacterium. 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.
 

RELATED: 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=pubmed_pubmed&from_uid=11179309

 

rOspA-4_Yale_Schoen_Cancers

Benach and Radolf →  Extremely high titers of OspA- antibody are necessary to be protective

 

POST LYMErix SYNDROME

Vaccination with lipoprotein vaccines exacerbate infection and make the disease undetectable.

FDA_1998_Vaccine_Minutes 

 

The evidence from the vaccine trial and adverse events reported afterwards, suggests rOspA activates latent infections. 

OspA is biologically active in the free form (1). 

OspA binds Plasminogen, an enzyme which degrades membranes

OspA induces the expression of the anti-inflammatory cytokine IL-10 (2) (causes immune suppression)

Borreliosis, itself, is associated with activation of Epstein-Barr virus (3). 

Epstein-Barr virus is associated with B cell changes. Borreliosis is associated with B cell changes. (Dorward, Spleens )

Giving asymptomatically infected Borreliosis patients the vaccine therefore appears to have created a disaster, not the least of which is new neoplasms, not reported in this abstract, and likely not reported to the World Health Organization, because Yale wrote that they scewed the results to fit into WHO's adverse events listing.

Mycoplasmal lipoprotein vaccine have failed to protect, in Tuberculosis.   The lipoproteins seem to be related to fungi (that is, they are identical).  Indeed, the mycobacterial lipoproteins of 19 and 35 kD tried as vaccine in tuberculosis seem to have the same negative effects as OspA

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=pubmed_pubmed&from_uid=11179309

"Thus, the immunosuppressive effect is dependent on glycosylated and acylated 19-kDa lipoprotein present in the phagosome containing the mycobacterium. 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."

 =========

OspA and IL-10: MEDLINE

 

ActionLyme History   

ActionLyme, 2001, Vaccine Presentation of Empirical Results, and that OspA was not a vaccine.  It was not qualified with a valid standard   http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf 

Pam Weintraub:  http://www.whale.to/m/lymerix8.html

LYME FOUNDATION     Re LymeRIX

LYME ASSOCIATION    Re: LymeRIX

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

1) Binds a human degradive enzyme plasminogen and is active in the free form:

OspA and plasminogen


Infection 1996 Mar-Apr;24(2):190-4

The outer surface protein A (OspA) of Borrelia burgdorferi: a vaccine candidate and bioactive mediator.

Kramer MD, Wallich R, Simon MM.

Institut fur Immunologie, Universitat Heidelberg, Germany.

In the search for a suitable vaccine candidate for Lyme borreliosis the principles of protective immunity were studied in a murine model of Borrelia burgdorferi infection. It was found that the spirochetal outer surface protein A (lipOspA) in its native and recombinant lipidated form induces monospecific immune sera, which in passive transfer experiments protect SCID mice against experimental and tick-borne infection and disease. These and similar findings of independent groups led to the development of a vaccine formulation containing lipOspA. When tested in clinical phase I/II safety trials the recombinant lipOspA vaccine was shown to be safe, immunogenic and able to elicit borreliacidal antibodies. At present, clinical phase III efficacy trials are being conducted. B. burgdorferi infection involves the dissemination of the spirochetes from the site of the tick bite, infection of distant organs, and induction of a chronic inflammatory process. Recent studies indicate that the spirochetes may utilize host-derived enzyme systems to increase their virulence/pathogenicity. It was found that lipOspA serves as a surface receptor for the host-derived proteolytic enzyme plasmin(ogen), the central component of the so-called plasminogen activator system. Moreover, it was found that spirochetes are able to activate endothelial cells and blood-derived leukocytes, such as monocytes/macrophages, B cells and T cells, to express functions and/or secrete molecules, which are known to promote inflammatory responses. Part of these activities were exerted by the isolated lipOspA. The studies indicate an important role of lipOspA, both for the induction of a protective immune response by the host, as well as for the pathogenic processes elicited during B. burgdorferi infection.  PMID: 8740121 [PubMed - indexed for MEDLINE]

Which means, who knows what's happening to people who receive this as vaccination if this mechanism is at work.

 

2)  Induces the antiiflammatory cytokine IL-10 (suppresses the immune response).

OspA and IL-10

 

3) Borrelia and Epstein-Barr

People with Lyme borreliosis often test positive to Epstein-Barr.  That is, IgM to Epstein-Barr apparently "cross-reacts" with Borrelia burgdorferi OspC.  That is, people who are infected with Borrelia, and who are "treated" to the CDC's Dearborn serodiagnostic criteria, and therefore told they have Chronic Fatigue Syndrome (Chronic Epstein-Barr), may have also activation of latent Epstein-Barr, as described here:

 
 
Borreliosis induced activation of latent Epstein-Barr virus and downstream pathology...
 
 
Folia Biol (Praha) 2003;49(1):40-8

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

Hulinska D, Roubalova K, Schramlova J.

National Reference Laboratory on Borreliosis, Electron Microscopy, National Institute of Public Health, Prague, Czech Republic.

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.

PMID: 12630667 [PubMed - in process]

 

3)  "Blot-smudging"   The question that arises is, if OspA is "sticky" (according to an Alan Barbour patent), how can we be sure free OspA molecules are the actual immunogen a person is injected with, if the outcome, in antibodies, is as below?  It appears that clumps of OspA of various sizes are being injected into people.  And if OspA is the reactive molecule it is claimed to be, how do we know it is not causing Immune complex vasculitis?, as part of the Post-LYMErix Syndrome?

This same thing occurred in the Monkey trials of rOspA.  It was not reported that this problem was addressed.

http://www.journals.uchicago.edu/CID/journal/issues/v31n1/991200/991200.html



Go to high resolution image (254kb)

 

Figure 1.     Results of Western blotting (MarBlot for detection of IgG antibody to Borrelia burgdorferi; MarDx, Carlsbad, CA) of serum specimens from 14 recipients of the recombinant outer surface protein A Lyme disease vaccine. Representative molecular weights (in kDa) are identified in the far left column. P, a positive control subject with PCR analysis–positive Lyme arthritis; N, a negative control subject. Study subjects 1–10: A, baseline; B, 30 days after dose 3. Study subjects 11–14: A, baseline; C, 30 days after dose 2; D, 8 months after dose 3; E, 24 months after dose 3.

Discussion in text | Next figure

Clinical Infectious Diseases    2000;31:42-47
© 2000 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2000/3101-0010$03.00


Detection of Multiple Reactive Protein Species by Immunoblotting after Recombinant Outer Surface Protein A Lyme Disease Vaccination

Philip J. Molloy,1,2 Victor P. Berardi,2 David H. Persing,2,3,a and Leonard H. Sigall4

1Rheumatology Associates of Southeastern Massachusetts, Plymouth, and 2IMUGEN, Norwood, Massachusetts; 3Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota; and 4Division of Rheumatology, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick

 

Received 31 August 1999; revised 3 December 1999; electronically published 17 July 2000.

Laboratory confirmation of the diagnosis of Lyme disease is based on the detection of an immune response to Borrelia burgdorferi. The serodiagnosis of B. burgdorferi infection is complex and may be further confounded by the immune response to the recombinant outer surface protein A (OspA) Lyme disease vaccine. To describe how the serological response to the recombinant OspA Lyme disease vaccine affects testing for antibody to B. burgdorferi, 240 specimens from 80 study subjects were obtained at defined intervals after recombinant OspA Lyme disease vaccination. Samples were tested by indirect enzyme-linked immunosorbent assay (ELISA), antibody capture enzyme immunoassay (EIA), and Western blotting (WB). After recombinant OspA Lyme disease vaccination, ELISA for 98% of the study subjects revealed reactivity. WB with use of OspA-containing B. burgdorferi strains as sources of antigens demonstrated multiple bands. Results of testing with a US Food and Drug Administration–approved WB kit showed homogeneous reactivity in the molecular weight region >30 kDa. Testing with OspA-free strains completely eliminated all vaccine-associated reactivity by both antibody capture EIA and WB.

 


     For collection of serum samples, there was separate institutional review board approval, and informed consent was obtained from the study subjects.
     Guidelines for human experimentation of the US Department of Health and Human Services and/or those of the authors' institutions were followed in the conduct of the clinical research.
     a Current affiliation: Corixa Corporation Infectious Disease Research Institute, Seattle Life Sciences Center, Seattle, WA.
     Reprints or correspondence: Victor Berardi, IMUGEN, 220 Norwood Park South, Norwood, MA 02062 (vberardi@imugen.com).