Jonathan Freedland: Socialism's one-time interest in eugenics is dismissed as an accident of history. But the truth is far more unpalatableYale would have had to learn about the kind of autism Einstein had - it is associated with Neurofibromatosis. I can tell you with certainty Yale rejected this information when I gave to them.
It has to do with a reversed duplication of a BCL-2 class gene and has similarities with the mechanisms of dysimmunity associated with "Lyme Disease" (OspA) in that both OspA and the Epstein-Barr it activates promote or contain BCL-2 genes or anti-apoptotic behavior.
A reversed duplication of a BCL-2 like gene results in the inhibition of normal synaptic pruning (large brains), I gave this information to Yale and the State of Connecticut in 2003. (It was already published in the journals.)
How could anyone at Yale even attempt to or pretend to create a race of very smart people, when they themselves have no idea what smart is? It's like watching a bird try to train an elephant. It's very funny. Yale does not want the information they would need to create the New Aryans.
They still don't.
Yale staff have no creative talent or ability. By their fruits shall you know them.
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 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:
To: sr393d@nih.gov, francis.collins@nih.gov, AllenM1@mail.nih.gov, zach_dann@blumenthal.senate.gov, francis.collins@nih.gov, ras8@cdc.gov, olib@od.nih.gov, afauci@niaid.nih.gov, joseph.breen@nih.gov, michael.greenwood@yale.edu, richard.horton@lancet.com, astrid.james@lancet.com, m.zecevic@lancet.com, ideditorial@lancet.com, Lawrence.Tabak@nih.gov, pgauwaerter@gmail.com
Subject: No one at the NIH, CDC, Yale, or IDSA knows what OspA is.
Date: May 1, 2012 4:54 AM
Greetings,
I see that there is a job opening for what looks like
Sally Rockey's job:
http://www.fins.com/Finance/Jobs/212548/Director-Office-of-Policy-for-Extramural-Research-Administration
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
standard 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:
http://cid.oxfordjournals.org/content/31/1/42.long
(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."
http://www.nejm.org/doi/full/10.1056/NEJM200107123450202#t=articleMethods
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."
http://www.ncbi.nlm.nih.gov/pubmed/16783164
"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."
and
"Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes."
http://www.ncbi.nlm.nih.gov/pubmed/16479520
"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
garbage.
What do you say?
Anyone?
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.
Hmmm.
It would be nice to know what OspA is.
We might be able to end the OspA-linked
"controversy."
Kathleen M. Dickson
former Pfizer Analytical
Methods Development and Validation
chemist.
To: sr393d@nih.gov, francis.collins@nih.gov, AllenM1@mail.nih.gov, zach_dann@blumenthal.senate.gov, francis.collins@nih.gov, ras8@cdc.gov, olib@od.nih.gov, afauci@niaid.nih.gov, joseph.breen@nih.gov, michael.greenwood@yale.edu, richard.horton@lancet.com, astrid.james@lancet.com, m.zecevic@lancet.com, ideditorial@lancet.com, Lawrence.Tabak@nih.gov, pgauwaerter@gmail.com
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
Greetings,
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."
http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%
2Fsrchnum.htm&r=1&f=G&l=50&s1=7%2C632%2C510.PN.&OS=PN%2F7%2C632%2C510&RS=PN%2F7%2C632%2C510
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)
http://www.cdc.gov/mmwr/preview/mmwrhtml/00053391.htm
"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
http://www.cdc.gov/mmwr/preview/mmwrhtml/00051495.htm
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."
http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%
2Fsrchnum.htm&r=1&f=G&l=50&s1=7,771,728.PN.&OS=PN/7,771,728&RS=PN/7,771,728
5) The effect of exogenous corticosterone on West Nile virus infection in Northern Cardinals (Cardinalis cardinalis) http://7thspace.com/headlines/410671/the_effect_of_exogenous_corticosterone_on_west_nile_virus_...
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:
http://www.ncbi.nlm.nih.gov/pubmed/20466055
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
pandemic."
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 !!!":
http://www.ncbi.nlm.nih.gov/pubmed/21867956
"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 IDSociety.org, 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:
The following is a letter sent to them regarding Paul Auwaerter, the current blowhard/mouthpiece of IDSA:
(UPDATE ON PAUL AUWAERTER - HE DOES NOT KNOW What OspA IS):
To: KMDickson <janmusinski@earthlink.net>, "Strikas,Raymond A. (Ray) (CDC/OID/NCIRD)" <ras8@cdc.gov>, olib@od.nih.gov, afauci@niaid.nih.gov, joseph.breen@nih.gov, michael.greenwood@yale.edu
Subject: Paul Auwaerter Does Not Know What OspA Is Either
Date: Apr 20, 2012 4:35 AM
Greetings,
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
either.
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."
http://www.ncbi.nlm.nih.gov/pubmed/16783164
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."
http://www.ncbi.nlm.nih.gov/pubmed/16479520
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).
http://www.hopkinsmedicine.org/awomansjourney/baltimore/2009_speaker_profiles/2009%20_paul_auwaerter_profile.html
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:
http://www.ncbi.nlm.nih.gov/pubmed?term=huber+bt
Fourthly, Adrianna Marques lists on *HER*
website, that her areas of expertise are
Lyme and Epstein-Barr (and some other herpes
viruses).
http://www.niaid.nih.gov/labsandresources/labs/aboutlabs/lcid/clinicalstudiesunit/Pages/marques.aspx
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) reported
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?
Anyone?
Ticks are a great place for transkingdom
plasmid-sharing according to Barbour and
Burgdorfer.
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??
Anyone?
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."
http://www.ncbi.nlm.nih.gov/pubmed/22547698
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.
http://www.ncbi.nlm.nih.gov/pubmed/10865170
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."
http://www.ncbi.nlm.nih.gov/pubmed/20375899
120430.htm
previous homepage selections:
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:
"18For (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." http://www.nytimes.com/2008/07/01/science/01tier.html
Update:
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 (PDF
)].
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.
http://www.sciencedirect.com/science/article/pii/S0006349511054075
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."
http://projectreporter.nih.gov/project_info_description.cfm?aid=8228508&icde=12284856&ddparam&ddvalue&ddsub&cr=1&csb=FY&cs=DESC
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."
http://projectreporter.nih.gov/project_info_description.cfm?aid=8300386&icde=12284856
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!"
Background:
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." http://www.ncbi.nlm.nih.gov/pubmed/2814170
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 psych.org 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 |
|
Psych.org 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 |
15950179
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.] |
|
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|
|
|
|
| EBV & LMP1 |
|
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|
Oncogene BCL2-like in EBV |
|
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|
EBV & mycoplasma |
|
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|
EBV inhibits p53
auto-kill kinase |
|
|
|
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|
NF-Kappa B and Herpes (PubMed,
General search) |
|
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|
|
| Herpes Simplex Immunosuppression (NF-kappa) |
|
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Epstein-Barr and anti-CD20 (Rituximab)
(PubMed,
500+)(and CFIDS) |
|
|
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|
|
|
|
|
|
|
|
IL10>>CD4- = EBV |
|
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EBV & IL-10 |
|
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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?
http://www.ncbi.nlm.nih.gov/pubmed/12768017
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)." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC58807/?tool=pubmed
CDC, Jan 2012: In 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." http://www.ncbi.nlm.nih.gov/pubmed?term=22056389
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."***
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC125880/?tool=pubmed
See
More At:
KISSINGER_NAZI_PAPERCLIP.htm
"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."
120430.htm
"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."