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09 Feb 2012
HOME
Pharma/CDC on Brain
damage from vaccines, Fauci, Phages, Bioweapons manufacture
HHS.gov is
Incompetent; BMJ calls fraud "crime.")
Official: CFIDS and MS-Lyme are the
same disease; Epstein-Barr
CDC Greed
(won't answer the FOIA)
ELISA = arbitrary cutoff.
Disclaimer
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.
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"It was considered whether p13 was identical to one of the other low
molecular weight B. burgdorferi proteins to which antibodies have been
developed. Like antibody to p13, antibody to a 10 kDa protein, as reported
(Katona et al., 1992), bound to only a small proportion of Osp-bearing cells
in immunofluorescence assays. However, the molecular size of 10 kDa protein
did not vary between strains and uniform fluorescein labeling was seen in
fixed cell preparation when probed with mAb to 10 kDa protein (Katona et al.,
1992). Furthermore, 15G6 does not bind to the 10 kDa in Western blots
(Habicht, 1993). The presence of a 14 kDa protein of B. burgdorferi was
reported (Sambri et al., 1991). This was identified with a mAb and by
immunofluorescence of live borrelias. In contrast with what was observed with
mAbs to p13 and with antibody to the 10 kDa protein (Habicht, 1993), antibody
to the 14 kDa protein of Sambri et al. bound to the majority of cells
(Sadziene et al., 1993A). These differences suggest that p13 is neither the
10-kDa nor 14-kDa proteins of B. burgdorferi."
..
Barbour's Patents for Borrelia Alone
What's to know about Alan Barbour?
Barbour-Land See his grants, below. The Vmps are OspC-like
proteins, OspC is associated with Neurovirulence.
OspC is upregulated when the tick begins a
bloodmeal, and is thought to be a ligand for something on red blood cells.
By the time an erythema migrans
rash appears, 2/3 of victims will already have the spirochete in their
brain/central nervous system. Too late to ever get rid of them.
--Barbour's mouse antibiotic
treatment studies demonstrated the permanent brain infection of the
borrelioses.
http://aac.asm.org/cgi/reprint/40/11/2632.pdf
--Barbour studies the neurotropism of
Borreliae, and has more patents than anyone, including the patent for the
Connaught
vaccine. And rights to royalties from Yale's vaccine, LymeRIX.
--Barbour published "Lyme Disease; the Cause, The Cure, the Controversy", an
unreferenced book. There really is no controversy, but the reader will note the
the history of "Lyme disease".
"Lyme disease" was spun, to suit the false positive vaccines outcomes.
Some people suspect Barbour did not actually write this book,. but that it was
written by some marketing firm. Why would a man like Barbour write an
unreferenced book? It makes no sense.
--Barbour holds more patents for Borrelia-related programming and product (DNA) than anyone on the entire planet.
(So, everywhere is really "Barbour-Land".)
--Barbour associated borrelial
genomics with trypanosomes (antigenic variation), and this is the key, really,
to any Lyme ""Controversy". The
borrelia switch antigens. There could not have been a vaccine trial,
unless the serodiagnosis was falsely "frozen" in time, and within the
expression only, of 72% people who have a
genetic predisposition to hyperactive immune response (Lyme arthritis),
which was the
Dressler/Steere standard. The strength of that data was 39/54.
39 out of 54 people with the genetic predisposition to a reactive arthritis,
may at some point have Dressler/Steere's version of "Lyme disease" or LymeRIX
disease. Only 30-35% of the USA population are so prediposed.
Do the math: ~32.5 % X .72 = 0.234
100 - 23.4 = 76.6.
What was the safety and efficacy of LymeRIX?
76%
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9673298&dopt=Abstract
This false standard, the Dressler/Steere
standard, assured that 76 % of the data would be thrown out of the vaccine
trial results, because it can only detect LymeRIX disease, 23 % of the time.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8308100&dopt=Abstract
That report was interesting because it was
published the same month that Dressler/Steere was published:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8380611&dopt=Abstract
See the Charts of the results, here:
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
That data says, as soon as Asymptomatically
infected individuals got the vaccine, they moved into the "Unconfirmed Lyme"
group. The vaccine did not "Prevent Asymptomatic Infection" as
SmithKline claimed. It just made people sick.
rOspA. What's
bad about it?
--The correct serodiagnosis, therefore, was
the original serodiagnosis. The one associated with the genome;
Antigenic variation.
Permanent brain
infection
| J Infect Dis 1993
Jul;168(1):143-51 |
|
Experimental infection of the
mouse brain by a relapsing fever Borrelia species: a molecular analysis.
Cadavid D, Bundoc V, Barbour AG.
Department of Microbiology, University of Texas Health Science Center, San
Antonio 78284-7758.
The spirochetal disease relapsing fever is notable not only for multiphasic
antigenic variation but also for central neurologic manifestations. To further
characterize involvement of the brain in this disorder, immunocompetent and
-deficient mice were infected with Borrelia hermsii. Immunodeficient mice were
treated while spirochetemic with neutralizing IgM monoclonal antibodies to the
infecting serotype. Blood, cerebrospinal fluid, and brain tissue were examined
by culture and polymerase chain reaction. In immunocompetent mice, antigenic
variation occurred in the brain as well as in the blood. In immunodeficient
mice, the infecting serotype was still present in the brain after it had been
eliminated from the blood by the administered antibodies. These latter results
cannot be accounted for by contamination of brain tissue and cerebrospinal
fluid by blood and, hence, establish the direct involvement of the central
nervous system in this experimental infection. PMID: 8515101 [PubMed -
indexed for MEDLINE]
| Antimicrob Agents Chemother 1996
Nov;40(11):2632-6 |
|
In vivo activities of ceftriaxone
and vancomycin against Borrelia spp. in the mouse brain and other sites.
Kazragis RJ, Dever LL, Jorgensen JH, Barbour AG.
Department of Medicine (Infectious Diseases), University of Texas Health
Science Center at San Antonio 78284, USA.
Borrelia burgdorferi, the agent of Lyme disease, and B. turicatae, a
neurotropic agent of relapsing fever, are susceptible to vancomycin in vitro,
with an MIC of 0.5 microgram/ml. To determine the activity of vancomycin in
vivo, particularly in the brain, we infected adult immunocompetent BALB/c and
immunodeficient CB-17 scid mice with B. burgdorferi or B. turicatae. The mice
were then treated with vancomycin, ceftriaxone as a positive control, or
normal saline as a negative control. The effectiveness of treatment was
assessed by cultures of blood and brain and other tissues. Ceftriaxone at a
dose of 25 mg/kg of body weight administered every 12 h for 7 to 10 days
eliminated cultivable B. burgdorferi or B. turicatae from all BALB/c or scid
mice in the study. Vancomycin at 30 mg/kg administered every 12 h was
effective in eliminating infection from immunodeficient mice if treatment was
started within 3 days of the onset of infection. If treatment with vancomycin
was delayed for 7 days or more, vancomycin failed to eradicate infection with
B. burgdorferi or B. turicatae from immunodeficient mice. The failure of
vancomycin in eradicating established infections in immunodeficient mice was
associated with the persistence of viable spirochetes in the brain during
antibiotic treatment.
PMID: 8913478 [PubMed - indexed for MEDLINE]
Antigenic variation
Antigenic variation in Borrelia.
Saint Girons I, Barbour AG.
Unite des Leptospires, Institut Pasteur, Paris.
Antigenic variation was demonstrated for the agent of relapsing fever,
Borrelia hermsii. The phenomenon is correlated with changes in major surface
proteins called Vmp. The genes encoding these antigens are located on linear
plasmids. Expression occurs by transposition of genes encoding Vmp to a
telomeric expression site located on another linear plasmid. Activation of a
vmp gene occurs by placing it downstream from a promoter.
Resemblance to the antigenic variation of trypanosomes is
discussed.
Antigenic variation in vector-borne pathogens.
Barbour AG, Restrepo BI.
University of California Irvine, Irvine, California 92697-4025, USA.
abarbour@uci.edu
Several pathogens of humans and domestic animals depend on hematophagous
arthropods to transmit them from one vertebrate reservoir host to another and
maintain them in an environment. These pathogens use antigenic variation to
prolong their circulation in the blood and thus increase the likelihood of
transmission. By convergent evolution, bacterial and protozoal vector-borne
pathogens have acquired similar genetic mechanisms for successful antigenic
variation. Borrelia spp. and Anaplasma marginale (among bacteria) and African
trypanosomes, Plasmodium falciparum, and Babesia bovis (among parasites) are
examples of pathogens using these mechanisms.
Antigenic variation poses a challenge in the development of vaccines against
vector-borne pathogens.
Trypanosomes:
http://tryps.rockefeller.edu/crosslab_intro.html
| J Clin Invest 1986
Oct;78(4):934-9 |
|
Antigens of Borrelia burgdorferi
recognized during Lyme disease. Appearance of a new immunoglobulin M response
and expansion of the immunoglobulin G response late in the illness.
Craft JE, Fischer DK, Shimamoto GT, Steere AC.
Using immunoblots, we identified proteins of Borrelia burgdorferi bound by IgM
and IgG antibodies during Lyme disease. In 12 patients with early disease
alone, both the IgM and IgG responses were restricted primarily to a 41-kD
antigen. This limited response disappeared within several months. In contrast,
among six patients with prolonged illness, the IgM response to the 41-kD
protein sometimes persisted for months to years, and late in the illness
during arthritis, a new IgM response sometimes developed to a 34-kD component
of the organism. The IgG response in these patients appeared in a
characteristic sequential pattern over months to years to as many as 11
spirochetal antigens. The appearance of a new IgM response and the expansion
of the IgG response late in the illness, and the lack of such responses in
patients with early disease alone, suggest that B. burgdorferi remains alive
throughout the illness.
PMID: 3531237 [PubMed - indexed for MEDLINE]
Persisting and expanding IgM and IgG.
Therefore, serodiagnosis of burgdorferi borreliosis would be acceptably the
presence of IgM or/and IgG specific
bands.
Grants:
| Grant Number: |
5R01AI024424-12 |
| PI Name: |
BARBOUR, ALAN G. |
| PI Email: |
abarbour@uci.edu
|
| PI Title: |
PROFESSOR |
| Project Title: |
MOLECULAR BASIS OF BORRELIA PATHOGENESIS |
Abstract: DESCRIPTION (Adapted from the applicant's abstract): The
long-term goal of this project is to understand the pathogenesis of relapsing
fever and Lyme disease; the primary focus for the next project period is
relapsing fever. The current model of relapsing fever is that changes of the
polymorphic Vmp lipoproteins are the determinants of antigenic variation
during infection, that changes in Vmp proteins are the result of
intermolecular or intramolecular recombinations at the vmp expression site,
and that some genetic switches are followed by a period during which further
diversity is generated through templated partial gene conversions. The
project's specific hypotheses are these: (i) Some if not all Vmp proteins
differ in structure to the extent that not only are they distinctive with
respect to the host's immune system but also with respect to their in situ
associations with and effects on host tissues. (ii) The sequence of the
transcriptionally active vmp gene at the expression site determines in part
which of several possible vmp genes follows it during an infection. (iii)
Post-switch mutations of newly- arranged vmp genes are the consequence of
either epigenetic differences between otherwise identical vmp genes at
different loci or transient differences between expression sites after
intramolecular deletions and those after gene conversions. The specific aims
to address these hypotheses are the following: (1) Further characterize the
function and structure of Vmp proteins by (a) identifying the mechanism(s)
for entry by one serotype of B. turicatae into the central nervous system
under conditions in which another serotype of the same strain is excluded, (b)
quantitatively assessing the pathologic and functional effects of CNS invasion
by borrelias, and (c) initiating investigations of the conformation of Vmp
proteins. (2) Further define the relationship between the vmp repertoire's
diversity and requirements for establishing an infection and avoiding the
immune response by (a) continuing the identification of expressed and silent
vmp genes and pseudogenes, (b) analyzing sequences of vmp genes and Vmp
proteins with respect to their evolution, and (c) comparing by DNA sequence
relapse serotypes resulting from infections with clonal populations of
serotypes representing different vmp sub-families. (3) Further define the
genetic mechanisms for changes at the expression site by (a) assessing whether
more than one Vmp protein is expressed at a time by individual cells, (b)
determining whether there are epigenetic differences between vmp genes and/or
whether otherwise identical expression sites transiently differ consequent to
the type of recombination that produced them, and (c) developing a genetic
system whereby mutations or reporter genes are introduced into borrelias.
Thesaurus Terms:
Borrelia, bacterial protein, borreliosis, gene expression,
protein structure /function, virulence bacterial antigen, bacterial genetics,
central nervous system disorder, conformation, evolution, gene conversion,
genetic recombination, genetic strain, microorganism immunology, nervous
system infection, pseudogene
X ray crystallography, crystallization, epitope mapping, immunocytochemistry,
laboratory mouse, nucleic acid sequence, polymerase chain reaction
| Institution: |
UNIVERSITY OF CALIFORNIA IRVINE |
| |
CAMPUS DR |
| |
IRVINE, CA 92697 |
| Fiscal Year: |
1997 |
| Department: |
MICROBIOL & MOLECULAR GENETICS |
| Project Start: |
01-DEC-1986 |
| Project End: |
30-APR-2001 |
| ICD: |
NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES |
| IRG: |
BM |
CRISP results (Barbour's current grants)
| Rank |
Score |
Grant Number |
PI Name |
Project Title |
| 1 |
76 |
2R37AI024424-16 |
BARBOUR, ALAN |
MOLECULAR BASIS OF BORRELIA PATHOGENESIS |
| 2 |
76 |
5R37AI024424-17 |
BARBOUR, ALAN |
MOLECULAR BASIS OF BORRELIA PATHOGENESIS |
| 3 |
76 |
5R37AI024424-18 |
BARBOUR, ALAN |
MOLECULAR BASIS OF BORRELIA PATHOGENESIS |
| 4 |
63 |
5R01AI024424-09 |
BARBOUR, ALAN |
MOLECULAR BASIS OF BORRELIA PATHOGENESIS |
| 5 |
51 |
2R01AI024424-10 |
BARBOUR, ALAN |
MOLECULAR BASIS OF BORRELIA PATHOGENESIS |
| 6 |
38 |
5R01AI037248-02 |
BARBOUR, ALAN |
INTERFACE OF BORRELIA SURFACE PROTEINS AND ANTIBODIES |
| 7 |
38 |
5R01AI037248-04 |
BARBOUR, ALAN |
INTERFACE OF BORRELIA SURFACE PROTEINS AND ANTIBODIES |
| 8 |
38 |
5R01AI037248-05 |
BARBOUR, ALAN |
INTERFACE OF BORRELIA SURFACE PROTEINS AND ANTIBODIES |
| 9 |
38 |
2R01AI037248-06A1 |
BARBOUR, ALAN |
BIOLOGY AND CONTROL OF LYME DISEASE BORRELIA |
| 10 |
38 |
5R01AI037248-07 |
BARBOUR, ALAN |
BIOLOGY AND CONTROL OF LYME DISEASE BORRELIA |
| 11 |
38 |
5R01AI037248-08 |
BARBOUR, ALAN |
BIOLOGY AND CONTROL OF LYME DISEASE BORRELIA |
| 12 |
38 |
5R01AI037248-09 |
BARBOUR, ALAN |
BIOLOGY AND CONTROL OF LYME DISEASE BORRELIA |
| 13 |
25 |
5R01AI024424-12 |
BARBOUR, ALAN |
MOLECULAR BASIS OF BORRELIA PATHOGENESIS |
| 14 |
25 |
5R01AI024424-13 |
BARBOUR, ALAN |
MOLECULAR BASIS OF BORRELIA PATHOGENESIS |
| 15 |
25 |
5R01AI024424-14 |
BARBOUR, ALAN |
MOLECULAR BASIS OF BORRELIA PATHOGENESIS |
| 16 |
25 |
5R01AI024424-15 |
BARBOUR, ALAN |
MOLECULAR BASIS OF BORRELIA PATHOGENESIS |
| 17 |
13 |
7R01AI024424-11 |
BARBOUR, ALAN |
MOLECULAR BASIS OF BORRELIA PATHOGENESIS |
| 18 |
13 |
7R01AI037248-03 |
BARBOUR, ALAN |
INTERFACE OF BORRELIA SURFACE PROTEINS AND ANTIBODIES |
Barbour's patents:
US Patent Office, assigned patents, only.
European Patent database (all):
http://ep.espacenet.com/
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