Radolf Explains why Lyme and Syphilis are the Great Imitators (and "stealth pathogens")
Mort Zuckerman
gary_w...@nymc.edu, scientifi...@ostp.gov,
pkru...@princeton.edu, Stanle...@fiu.edu,
emcsw...@niaid.nih.gov, afa...@niaid.nih.gov,
Spin...@yahoogroups.com, kshe...@calea.org, fit...@gmail.com,
patrick.f...@usdoj.gov, model...@sbcglobal.net,
jdr...@nejm.org, let...@courant.com, Jgerb...@cdc.gov,
michae...@po.state.ct.us, con...@po.state.ct.us, executive-
edi...@nytimes.com, managin...@nytimes.com, news-
ti...@nytimes.com, biz...@nytimes.com, for...@nytimes.com,
nati...@nytimes.com, dv...@cdc.gov, brigidc...@optonline.net,
tr...@hotmail.com, illino...@aol.com, jle...@courant.com,
tinaj...@yahoo.com, jhorn...@fff.org, thomas...@usdoj.gov,
thoma...@po.state.ct.us, kur...@washpost.com,
georg...@washpost.com, p...@allegorypress.com,
commissi...@po.state.ct.us, brans...@comcast.net,
vts...@comcast.net, o...@po.state.ct.us, freet...@charter.net,
scott....@po.state.ct.us, govern...@po.state.ct.us,
attorney...@po.state.ct.us, randall...@usdoj.gov,
Robert....@yale.edu, edi...@greenwich-post.com,
harol...@yale.edu, sedm...@nswbc.org, rrmcg...@aol.com,
fr...@nytimes.com, dpr...@stmartin.edu
Cc: fra...@ucia.gov, dr-ahma...@president.ir,
eugener...@washpost.com, afa...@niaid.nih.gov,
bmi...@newstimes.com, tr...@hotmail.com, rast...@aol.com,
billc...@gmail.com, amcg...@rms-law.com, rjmu...@aol.com,
paulcrai...@yahoo.com, sidney_b...@yahoo.com,
criminal...@usdoj.gov, karla.d...@usdoj.gov,
christophe...@usdoj.gov, richar...@yale.edu,
harol...@yale.edu, james.p...@yale.edu, inq...@aldf.com,
ly...@idsociety.org, meganm...@theatlantic.com
Subject: Radolf Explains why Lyme and Syphilis are the Great Imitators
(and "stealth pathogens")
Date: Dec 19, 2009 1:01 AM
Radolf Explains why Lyme and Syphilis are the Great Imitators (and
"stealth pathogens"):
RADOLF:
http://www.ncbi.nlm.nih.gov/pubmed?term=11441098[uid]&cmd=DetailsSearch&log$=details
"Despite the ability of MTB 19-kDa lipoprotein to activate
microbicidal and innate immune functions early in infection, TLR 2-
dependent inhibition of MHC-II expression and Ag processing by MTB 19-
kDa lipoprotein during later phases of macrophage infection ***may
prevent presentation of MTB Ags*** and decrease recognition by T
cells. This mechanism may allow intracellular MTB to evade immune
surveillance and maintain chronic infection."
TRANSLATION: "May prevent the production of
ANTIBODIES" which means, "is stealth."
This is why seronegative Lyme - the
thing that results in all the other
Imitators EXCEPT ARTHRITIS - is so
dangerous:
http://www.actionlyme.org/CHP_9_IDSA_REVIEWS.htm
That is the ^^ Chapter on IDSA's publication
on "How Lyme got to be called the New Great
Imitator" (IDSA did not turn this data
over to Richard Blumenthal because it is
too self-indicting).
OspA, according to, now, UConn's Justin Radolf
(as seen in the above article), is the very
thing that rendered the Tuberculosis
and HIV vaccines NOT VACCINES:
http://www.actionlyme.org/FUNGAL_VACCINES.htm
You can see why this character, Radolf
makes me furious. Yet, he is the only
real scientist the crooks have on their
team.
Odd.
Weird, I know.
Now, most recently, Radolf is talking like the
arthritis outcome is the more serious disease,
when we know from Dattwyler, Wormser and Klempner
(and even Sikand and Steere), that people with
Lyme arthritis are "IMMUNOCOMPETENT" (make enough
antibodies to fight the infection and the down
stream Imitators).
Dattwyler:
"THE SERONEGATIVE LYME VICTIMS ARE
THE SICKEST:"
http://www.actionlyme.org/ARTHURWEINSTEIN.htm
Above (again), we have Radolf, explaining that
these Pam3Cys-OspA type borrelial (and Tuberculosis
and apparently the HIV gp120 and 41, or those vaccines,
too), are responsible for the NON-PRODUCTION
of antibodies, or the seronegative/MS-like
Lyme result...
The B cell mutations:
http://www.actionlyme.org/Duray.htm
And the cancer outcomes (see Joe Tully).
The ALS (tolerance to mycoplasma).
The Fatigue (tolerance to mycoplasma,
which hijack erythrocyte metabolism).
A time bomb.
A Trojan Horse.
An immunological time bomb deployed
by the autovaccination with shed Osps
though a process called blebbing:
http://www.actionlyme.org/BARBOURS_STEALTH_BOMBERS.htm
Or just plain old regular LYMErix:
http://www.actionlyme.org/SCHOEN_INSTRUCTING_DOCS_TO_BLOW_OFF_LYMERIX_INJUREES.htm
But Radolf is *now* executing a 180
to protect the Lyme crooks from criminal
charges, while admitting, if you notice,
the mechanism of TOLERANCE to OspA:
http://www.ncbi.nlm.nih.gov/pubmed?term=20011115
"compromising the induction of tolerance in macrophages and
engendering more severe and persistent inflammatory responses to B.
burgdorferi"
Nobody cares about ^^^ that.
Those people are "fine except for
aching knees:"
Wormser and Klempner:
http://www.journals.uchicago.edu/doi/pdf/10.1086/432733
"Patients generally feel well aside from their arthritis symptoms."
Duray:
http://www.actionlyme.org/Duray.htm
http://www.actionlyme.org/080924.htm
◄"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.
http://www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770/ref=sr_1_2?ie=UTF8&s=books&qid=1214848669&sr=1-2
John Dunn, et al, at Brookhaven National
Laboratory (probably Dattwyler and Luft)
say:
http://www.actionlyme.org/JohnDunn_Brookhaven.htm
"It's the perfect stealth bacteria," says one frustrated physician.
He's talking about Borrelia burgdorferi, the bacterium that causes
Lyme disease. This illness, which is often mistaken for diseases
ranging from multiple sclerosis to Lupus, can inflict excruciating
headaches and muscle pain, affect the brain and nervous system, attack
major organs, and inflame joints."
- - - - -
Justin Radolf, on the Stealth Pathogen:
Mol Microbiol. 2009 Jun;72(5):1081-6. Epub 2009 May 4.
Treponema pallidum, the stealth pathogen, changes, but how?
Radolf JD, Desrosiers DC.
Department of Medicine, University of Connecticut Health Centre,
Farmington, CT 06030-3715, USA. JRa...@up.uchc.edu
Treponema pallidum rapidly disseminates from a genital site of
inoculation to diverse organs where it establishes persistent
infection. T. pallidum has long been regarded as a stealth pathogen
because of its poorly antigenic and non-inflammatory surface. There is
now increasing evidence that antigenic variation also contributes to
the ability of the spirochaete to evade host defences. Among the small
number of proteins encoded by the T. pallidum genome with sequence
similarity to well-characterized transcription factors is TP0262, an
orthologue for cAMP regulatory protein (CRP) of Escherichia coli.
Giacani and co-workers identified sequences matching the CRP consensus-
binding motif upstream of the promoters of tprE, tprG and tprJ, three
members of the T. pallidum repeat (tpr) gene family (subfamily II).
Using electrophoretic mobility shift assay, DNaseI footprinting and an
E. coli-based reporter system, they demonstrated that TP0262
specifically recognizes the putative binding sequences and that DNA
binding is cAMP-dependent. Their report, a major methodological
advance for syphilis research, suggests that T. pallidum has
appropriated a paradigmatic global regulator of metabolic processes in
heterotrophic bacteria to further its capacity for immune evasion in
its obligate human host.
"to further its capacity for immune
evasion in its obligate human host."
Immune Evasion is the *Game* of
Spirochetes. That's what they
do, because they're intracellular
and extracellular *parasites.*
Like Mark Klempner says:
http://www.ncbi.nlm.nih.gov/pubmed?term=1634816[uid]&cmd=DetailsSearch&log$=details
They're intracellular parasites that
evade antibiotic demise due to
intracellularity, spheroplast formation
and, by embedding or cloaking
in host cell membranes.
They turn off the immune system and
gum up the normal mechanisms of
INFLAMMATION, due to inhibition
of antibody production, inhibition
of the *inflammatory* cytokines, the
production of un-inflammatory cytokines
(IL-10):
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC108257/?tool=pubmed
and the autokill kinases:
http://www.actionlyme.org/Pam3Cys_Version15.htm
Kathleen M. Dickson
http://www.actionlyme.org
http://www.relapsingfever.org
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci