Six million dead or displaced in Iraq and Afghanistan and 8 million
Syrians scattered... and the damned cowards running for president have no
clue what happened in the past or even that this is no longer 1945 and
70 years past America. They don't remember the oil
embargoes, America going green before Reagan, the reason we started
importing small light Japanese cars, ...
The GOPtard presidential candidates cling to the model of capitalism that
is only supposed to happen within the confines of a country. They have
no clue what the IMF does (nation rape) or that Europe is in peril and may
have to cling to the side of the true anti-ISIS defenders, Russia.
Americans and the GOPtards don't know what the neocons did. Americans
- especially the retarded GOPsters - don't know about PNAC, 9/11 Thermate
(should be called 9/10 Thermate) or that all this chaos was ORDERED or
prescribed by the neocons: "Securing the (Israeli) Realm," taking
advantage of Yeltsin, the Israeli oligarchs rape of Russia (rape number 2 by
the same gang), etc...
Nothing. They know nothing. They are anencephalic. The
major news agencies let these speak to the public and repeat their moronical
notions. Wolf Blitzer, the Israeli president of America, has a
"Situation Room," on CNN, where he pretends everything is seriously about
Israel's security. It's all ridiculous.
It's all transparent, cowardly materialism. Greed; me, me me, mine!
REPORT IN THIS BOX IS THE OCCAM'S RAZOR report.
Astonishingly, people are asking basic
questions, still, on Facebook, that are answered here, while pretending to
be authorities on Lyme disease, and with no science backgrounds.
People are really, really stupid, man. They'll read nonsense and
repost to Facebook, but they refuse to read the real science and discover on
their own that certain people are not experts on spirochetal diseases in any
way. Yet, nearly all this information is discoverable in PubMed or
just through Google, isn't it?
“Endotoxin tolerance [Lyme,
LYMErix-Disease, CFIDS, etc]
protects the host by limiting excessive 'cytokine storm' during sepsis, but
compromises the ability to counteract infections in septic shock
survivors."- Medvedev, Oct 13, 2015, see below.
We’re taking over
medical science and science reporting.
BACKGROUND OF THE
”Science,” “doctors” and
the “journals” all defaulted. There are 30 million people in the United
States alone with Fibromyalgia, Lyme, chronic fatigue syndrome, Gulf War
Illness, Mitochondrial disorders, Ehlers Danube or whatever it’s called
– we know what they mean –,…and all we get is the various explanations that
involve VooDoo witch magic
with the self-backfiring incantations (“somatoform”), etcetera etcetera
The recently-former Director of the
National Institute of Mental Health, Thomas Insel, said this
about psychiatry (it is not valid, it's just a religion or a belief
"The goal of this new manual, as with all previous editions, is to provide a
common language for describing psychopathology. While DSM has been described as
a “Bible” for the field, it is, at best, a dictionary, creating a set of labels
and defining each. The strength of each of the editions of DSM has been
“reliability” – each edition has ensured that clinicians use the same terms in
the same ways. The weakness is its lack of validity. Unlike our
definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are
based on a consensus about clusters of clinical symptoms, not any objective
laboratory measure. In the rest of medicine, this would be equivalent to
creating diagnostic systems based on the nature of chest pain or the quality of
fever. Indeed, symptom-based diagnosis, once common in other areas of
medicine, has been largely replaced in the past half century as we have
understood that symptoms alone rarely indicate the best choice of treatment.
.. Patients with mental disorders deserve better..."
Richard Horton, editor of Lancet:
“The case against science is straightforward: much of the scientific
literature, perhaps half, may simply be untrue,”
Dr. Horton commented
in The Lancet.
what the editor of the Lancet and Thomas Insel say to be true.
Medical science today is all bullshit and mentally incompetent.
New Great Imitator. That’s a lot
of diseases under one umbrella. Multiple Sclerosis,
Chronic Fatigue Syndrome,
Dementia, Rheumatoid Arthritis,
LYMErix also caused strokes and "vascular events" also),
ALS, … and “after
30 40 years we have nothing,” – Willy Burgdorfer.
Someone assigned Allen Steere to it. No one knows why. Perhaps someone
at the CDC detected he was unhappy with medicine as a profession – after
all, it was one he chose to avoid the
VietNam draft – and that he also had a severe case of myopia. At
the 1998 FDA meeting on LYMErix, Dattwyler said of Steere’s Bad Knees
"I see a lot of patients, and I must say that treatment resistance
lyme arthritis in our center is low, it is very rare. We see maybe
one case a year. And, you know, that is using very strict criteria,
saying that the person had, you know, CDC criteria for seropositivity,
good history, and usually is monoarticulate knee arthritis."
Dattwyler sees about uno cases a year. There aren’t very many
Dearborn, CDC, 2-tiered
positive cases of “Lyme disease.” There never were.
It was never
about arthritis. Neither the disease nor the OspA vaccine trial results
were ever really about arthritis. What “Lyme disease” is really about
(and LYMErix too), is much much worse.
years down the drain. No one is getting better. ‘Too much research
fraud and downright stupidity (definition: willful ignorance). We can’t
believe the science. We can’t believe how science is reported.
We can’t believe the FDA never looked at the Dearborn case
definition. They told us so. This is the reason Senator Richard
Blumenthal and company had to have the Office of Budget and Management
ORDER the FDA to assure the Lyme testing is valid according to the FDA’s
rules on the validation of an analytical method.
The first criterion in a validation is ACCURACY, or, “does your
method detect 100% of the samples where the analyte in question is known
to be present? (and then give the range of what % of the known
analyte your method found, but the first premise is that is should
detect SOME of the analyte if it is known to be there).” If it can’t be
100% for anti-flagellar antibody cases (it is about 95% present in
known, erythema migrans sampled, DNA for Borrelia, cases), it should be
close. And for this reason, to increase SENSITIVITY (or how low in
concentration of the analyte in question can your method detect), this
problem was addressed in 1992 by the late Lou Magnarelli and the people
who own the patent for the only FDA-valid test for Lyme – and who are
also the owners of the LYMErix patent, Yale’s Fikrig and Flavell:
Comparison of whole-cell antibodies and an antigenic flagellar epitope
of Borrelia burgdorferi
in serologic tests for diagnosis of Lyme borreliosis.
recombinant protein (p41-G) of an antigenic region of flagellin was
used in a standard and amplified enzyme-linked immunosorbent assay
(ELISA) to detect antibodies to Borrelia burgdorferi,
the causative agent of Lyme borreliosis. Comparable sensitivities (88 to
94%) were noted when sera from 17 persons who had erythema migrans and
antibodies to whole-cell B. burgdorferi were tested against the p41-G
antigen. In tests of a second study group of 36 persons who had erythema
migrans but no detectable antibodies to whole-cell B. burgdorferi, 3
(8%) were positive when the p41-G antigen was used. Assay specificity
likewise increased when the p41-G fragment was included in an ELISA with
human sera containing treponemal antibodies. Recombinant flagellar
proteins of B. burgdorferi, such as the p41-G antigen, can be used in an
ELISA and may help confirm Lyme borreliosis during early stages of
infection and improve specificity.”
Fikrig, Magnarelli and Flavell basically said, “Here we have made the
common anti-flagellar antibody (found in most Lyme patients – and
the ONLY specific biomarker for Borrelia burgdorferi, thus
meeting 2 FDA validations requirements, accuracy and specificity) not
only SPECIFIC (FDA validation criterion – does not detect anything
else besides Borrelia burgdorferi flagellin) but even more useful by
adding in or spiking it into an ELISA made of borrelia sonicate,
BECAUSE … some people don’t even make a lot of anti-flagellar
antibodies, the one most people make if they make any at all. And if
one wanted to go nano tech, the thing to do is put these sorts of
fragments of Borrelias-specific flagellins on nanotubes and look for
these specific antibodies in human blood, since antigen itself is less
likely to be there. Borreliae like to live in the brain.”
The NIH’s Lyme-And-MS Division of NINDS found in 2006, however, that
exposure to the shed fungal antigens like OspA, found on spirochetal
blebs (more about that below) can also turn off the function of the TLR5
receptor that handles flagellin. This could be the reason some Lyme
victims are totally seronegative (no antibodies against Lyme at all).
Here are the 2 reports by this MS-Lyme group that say OspA is
responsible for causing nearly complete immunosuppression, in the end:
That was 1991 and 1992. Fikrig and Flavell own (patented) that test (US
# 5,618,533). They own the LYMErix patent,… and they own this method,
the only FDA-valid test to assess it. But they very clearly did not use
a valid test to assess LYMErix. We know why.
At the time, lots of researchers were looking for ways to use the anti-flagellar
antibody as the primary means of diagnosis. You can look this up. Use
the National Lilbrary of Medicine. That was you know back in the day
when there was less research fraud, that is, the late 1980s, early
1990s. A common thing. A common idea. Valid, because most people with
Lyme are known to at least have the flagellar antibody. Here is the
report from 1991 that goes with the Yale flagellin method patent:
Recall that the bogus Klempner long term
non-retreatment study where 2/3rds of his victims had never had IV ceftriaxione before - the standard of care at the time -, and which was
assessed with the non-scientifically valid FIQ or Fibromyalgia Impact
Questionaire ("questionaires" or "check lists" mean psychiatry is the
dominant assessment criteria for a real medical illness), when the IDSA/CDC
Lyme crooks were the authors of all the scientifcally valid physiological
biomarkers of brain and CNS destruction, was
based on the
inclusion/exclusion criteria of the fraudulent Dearborn case definition,
rendering the entire study invalid. Yet, this Klempner report is the
basis of the IDSA 2001 and 2006 "guidelines" on the non-diagnosis and
non-treatment of Lyme disease. Therefore once the fraud of the
Dearborn event is prosecuted, out go all of IDSA's "guidelines" :
Go ahead and read that for all the ridiculousness and
false statements they make and in which they repeatedly quote their own
previous research fraud. Mark
Klempner himself found ceftriaxone did not kill all the spirochetes even
when there weren't human cells to hide inside:
the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in
vitro. [FULL TEXT]
"The Lyme disease spirochete, Borrelia burgdorferi, can be recovered long
after initial infection, even from antibiotic-treated patients, indicating
that it resists eradication by host defense mechanisms and antibiotics.
Since B. burgdorferi first infects skin, the possible protective effect of
an antibiotic commonly used to treat Lyme disease, ceftriaxone, was
examined. Human foreskin fibroblasts protected
B. burgdorferi from the lethal action of a 2-day exposure to ceftriaxone at
1 microgram/mL, 10-20 x MBC. In the absence of fibroblasts,
organisms did not survive. Spirochetes were not protected from ceftriaxone
by glutaraldehyde-fixed fibroblasts or
fibroblast lysate, suggesting that a living cell was required. The ability
of the organism to survive in the presence of fibroblasts was
not related to its infectivity. Fibroblasts protected
B. burgdorferi for at least 14 days of exposure to ceftriaxone. Mouse
keratinocytes, HEp-2 cells, and Vero cells but not Caco-2 cells showed the
same protective effect. Thus, several eukaryotic cell types provide the Lyme
disease spirochete with a protective environment contributing to its
As you will see later in this report (G.,
below) Mark Klempner and Gary Wormser re-state that there are 2 kinds of
Lyme: the HLA-linked hypersensitivity "one case a year" bad-knee only, and
everyone else, the 85% left out of the Dearborn case definition - the
definition that includes the Triad of Fatigue, Musculoskeletal signs, and
Neurocognitive deficits -, all well known long term outcomes of Sepsis.
Since the Dearborn "case definition" only describes and refers to the HLA-linked,
arthritis associated "monoarticular arthritis and no other illness signs,"
the "guidelines" only apply to people with that genetic background.
This is the current, 1994, CDC
falsified, Dearborn case definition:
“It was recommended that an IgM
immunoblot be considered positive if two
of the following three bands are
present: 24 kDa (OspC)*, 39 kDa (BmpA),
and 41 kDa (Fla) (1).
“It was further recommended that an IgG
immunoblot be considered positive if
five of the following 10 bands are
present: 18 kDa, 21 kDa (OspC)*, 28 kDa,
30 kDa, 39 kDa (BmpA), 41 kDa (Fla), 45
kDa, 58 kDa (not GroEL), 66 kDa, and 93
This is research fraud - How Steere falsified
the testing in Europe, excluding all but late Lyme arthritis:
And there is more to it that this:
Steere used high passage strains
(which drop plasmids, and which is why spirochetes become less virulent over
time, if they are not pharmed back into multiple-pathogen-infected ticks
periodically) with recombinant OspA and B without the lipids attached.
If the lipids are not attached, this is barely an
antigen and not likely to produce antibodies. Hence, OspA and B,
bands 31 and 34 were excluded from the Dearborn case definition. This
was what KMDickson told the FDA when she blew the whistle: Although
you may have 5 bands, if one or more of them are OspA and B, you don't have
a "case" of Lyme, even though supposedly OspA and B are so specific they
made vaccines out of them.
OspA is specific enough to prevent Lyme, they say,
but not specific enough to diagnose?
So, while Mark Klempner said at one time that Lyme was incurable due to
intracellular spirochetes, now, in the "guidelines" he says there is no such
thing as neurologic Lyme. The reason these criminals do not want
anyone diagnosed with Lyme disease, in whatever form, is because antibiotics
don't cure it. It is an AIDS-like disease, with reactivated viral
infections, and most accurately called Post Sepsis syndrome or Endotoxin
Tolerance,... with the multiple herpes virus reactivation, fungal antigen
tolerance and B cell changes that are like mutations or pre-cancerous.
The FIRST MAIN REASON, for this Lyme-fraud-in-perpetuity, is that the
LYMErix or OspA vaccines caused the same
Post-Sepsis Syndrome, or
Endoxin Tolerance or AIDS-like disease - with the
Chronic Fatigue Syndrome (Yale and Steere)
Fibromyalgia (Steere) being predominant
features -, being a worse fungal toxin for humans than
lipopolysaccharide or LPS (TLR4 agonist) and they lied about this to the FDA
and to the public and in the journals. The second reason is
that the mechanisms of illness in Lyme and CFIDS betray the mechanisms of
the Autism pandemic.
There are other examples of research fraud in this report perpetrated by CDC
officers, particularly Suzanne Vernon, as you will see. A "stealth
disabler" would have the same definition: no antibodies, or makers of
classic "inflammation," or allergy or hypersensitivity or "autommunity"
(they all basically mean the same thing). If you wanted to create a
biowewapon against a certain racial population, you would look to see if
there low- to no- genetic HLA link to a hypersensitivity response in that
population. That scam is GAME OVER at this point; all that remains are
You will see many times in this report, that OspA
never could have been a vaccine. It was the complete opposite.
It was a fungal toxin that caused generalized immunosuppression.
You will see that spirochetes and Epstein Barr hang out together in the
lymph nodes. You will see that OspA, spirochetes shedding OspA,
and Epstein-Barr inhibit apoptosis. That seems to be the first
step in all dysimmunity outcomes. Inhibition of Apoptosis of an
infected cell. The IDSA, UConn, Yale, ALDF.com, and CDC Lyme
criminals have done nothing besides attack their victims since the early
1990s in order to maintain the PRETENSE - a false
position (that being that Deabrorn was real, Stere in Europe falsifying
the testing was not research fraud, that OspA vaccines were not research
fraud) - that the Dearborn case definition of "Lyme is just a bad knee
with no other illness signs," was real because they do not want to go to
jail. Falsifying the case definition at
Dearborn is a homicide charge.
It is also RICO.
CDC patent-owning staff are the ones behind the whole scam.
Barbara Johnson, Alan Barbour, et al. They did this
FOR THEMSELVES, for the vaccine and test kit patent
royalties. But most vector borne diseases of this type bear fungal
antigens, and you can't make vaccines out of them. These guys are
STUPID and this was a major screw up, scientifically, affecting all
disease research for the last 25 years.
Occam’s Razor, yup, Lyme is a razor. That is how you “get it.”
(If the treatment fits the model the science presents, Rituximab, with
its 2/3rds' cure rate, it must be a pretty close model...)
hear of Occam’s Razor? It’s the principle that the simplest explanation
is usually the correct one. If you hear hoofbeats, think ‘horses,’ not
‘zebras.’ If it quacks like a duck…etc. Don’t overthink this stuff. It’s
all there. You just have to look at the big picture.
I. Start with the
most compelling data; Yale/CDC Lyme perps did a 180 on everything.
1) The CDC, IDSA and Yale claim that only the HLA linked arthritis cases
were allowed to be called “Lyme disease.” This is the Dearborn, 1994
but current “case definition.” The 2005 Klempner and Wormser HLA report
re-stated that the case definition was HLA-linked and the victims had no
other illness signs but arthritis. So, that’s the only “case” of Lyme
one is allowed to have. It means you may have arthritis, only; an HLA-linked
hypersensitivity response with lots of antibodies, and no fatigue or
meningitis or anything else. The other symptom set people, the non-HLA
linked people, well, that’s a mystery, right? Must be psychiatric.
2) But this definition came after the same people claimed Lyme caused
everything (MS, Lupus, ALS, dementia, stroke, Chronic Fatigue Syndrome,
Fibromyalgia, etc.), and particularly that chronic neurologic Lyme was
incurable in half the cases (Dattwyler, Luft, Sigal, Steere, in 1989
IDSA Review special supplement on Lyme and Spirochetal diseases) and
that spirochetal diseases were incurable, even with ceftriaxone, even
when there were no human cells for the spirochetes to hide in (Klempner,
3) At that time, in the 1989 IDSA Reviews, a one Paul Duray,
pathologist for Yale, the US Army, the National Cancer Institute, etc,
found that the immune cells in the spinal fluid of chronic neurologic
looked like immature-, and mutated, or neoplastic or EBV-transformed.
Look those words up, “EBV-transformed” or “EBV-immortalized” cells is a
known thing and very relevant to the OspA crime.
CAUTION: If the reader is not familiar with what “EBV transformed”
means, please study the topic and do not make assumptions based on no
the OspA vaccine victims were acquiring the same “multi-system,” (Dave
Persing), “protean” (Ben Luft) disease manifestations that the ALDF.com,
CDC, Yale and later IDSA threw out of the case definition at Dearborn.
The Chronic Fatigue Syndrome, the Fibromyalgia, the chronic systemic
disease with dementia signs and neurological signs, etc,. – thrown out
of the vaccine trial results and described as “Unconfirmed Lyme.” Those
cases were not counted as vaccine failures.
Never lose track of this statement by U.S. Department of Energy and
likely a physician at SUNY-StonyBrook:
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..."--
Energy Science News, pnl.gov
Lupus are not “solely a monoarticular arthritis with a high antibody
concentration against Borrelia with no other symptoms” – the current CDC,
Dearborn “case definition.” Says them.
II. So what exactly is
OspA? “I did not get the vaccine so this does not concern me.”
yes, you got the vaccine. Everyone with Lyme got LYMErix. Here is what
LYMErix is, and how this vaccine-was-the-disease works:
It’s Pam3Cys or a triacylated lipoprotein, the degree of acylation is
equated with its toxicity. So what is acylation? It’s the zig-zaggy
lines that mean Carbon-Carbon-Carbon, yes, hydrocarbons, like margarine
or octane. Exactly, the name just refers to the number of carbons in
each carboxyl or acyl group. Palmitic (the Pam in Pam3Cys) has X number
of carbons, gasoline, 8, linoleic acids, like 14. Look up what are
alkanes then add a COOH group and you have one of these fatty acids.
Something highly acylated like this (3 or more fatty acids hanging off)
are managed by Toll-like Receptor (TLR) 2 and TLR1, together.
Therefore a “TLR2/1-agonist” is another term that generally refers to
lipoproteins like those from Borrelia, mycoplasma, mycobacteria, and
others like Brucella. (But they can manage other compounds.)
This thing, Pam3Cys and fungal lipid molecules like it, is shed with the
blebs. In other words, like this:
likes of OspA is on these blebs. They go to the brain, inflame it, get
eaten up by immune cells - which renders them incompetent-, they go to
the kidneys (LUAT), etc. You will find this to be so in an NIH-owned
patent (5,217,872) and elsewhere.
So, the fungal antigens are on the shed blebs and they go everywhere and
they render the immune cells incompetent, resulting in an AIDS like
disease. Everyone who has Lyme disease also has LYMErix disease.
The NIH patent
explaining how Lyme causes LYMErix-disease (“stealth bomber”):
invention relates to novel antigens associated with Borrelia burgdorferi
which are exported
(or shed) in vivo and
whose detection is a means of diagnosing Lyme disease. The antigens are
and other bioproducts including the major extracellular protein antigen.
Another object of the invention is to provide antibodies, monoclonal
and/or polyclonal, labeled and/or unlabeled, that are raised against the
antigens. A further object of the invention is to provide a method of
diagnosing Lyme disease by detecting the antigens in a biological sample
taken from a host using the antibodies in conventional immunoassay
formats. Another object of the invention is to provide kits, for the
diagnosis of Lyme disease, comprising the antibodies and ancillary
reagents. The advantage of the antibodies used in the invention is that
they react with the antigens from geographically diverse strains of
Borrelia burgdorferi, but do not react with antigens from related
The shed blebs (or exosomes
or vesicles) have LYMErix on them (delayed fuse or “time bomb”):
multiprotein complexes of the Borrelia burgdorferi outer membrane
"Although we uncovered the existence of at least 10 distinct OM
complexes harboring several unique subunits, the complexome is dominated
by the frequent occurrence of a limited diversity of membrane proteins,
most notably P13, outer surface protein (Osp) A, -B, -C, and -D
The thing you should
be doing, now that establishment medicine and all the universities have
basically defaulted on the BigPicture (20-30 million people disabled
from the incompetent witch phenomenon), is follow up on these reports in
PubMed, and “See Related” articles, and “See Cited by” articles and do
your own research. Don’t be afraid to take your time to develop the
vocabulary; use multiple sources for basic biology and chemistry facts.
By using multiple sources, you’ll capture some sources that use a
language set you already have. Then you can cross over and back to
other sources until the picture is clearer for you. And VERIFY, VERIFY,
VERIFY. Don’t be afraid. There are no experts.
III. And now some of the
Alphabet, A-L, which all point to, well, LYMErix was never a vaccine and
caused the same immunosuppression disease as Chronic Lyme. What are
the common opportunistics we see emerge in immunosuppression cases?
next we see Brucella and its TLR2/1 agonist antigens do the same thing:
turning off the immune response and causing immunosuppression or
producing no antibodies. MHC II or HLA molecules deliver antigens to
the surface of the immune cell against which antibodies will be made.
If, along comes a TLR2/1 agonist, in time, this function stops. No more
antigen is presented, no more antibodies will be made.
There are multiple
explanations for this mechanism but we have a “THE LIST” at the end of
this report with researchers who present information on mechanisms of
TLR2-agonist related immunosuppression.
Use your search feature to look for “MHC” elsewhere in this report.
Vesicles from Brucella
Bacterial Internalization by
Human Monocytes and Modulate Their Innate Immune Response
studies have shown that smooth and rough strains of Brucella spontaneously
release OMVs that contain outer membrane proteins, LPS and other
bacterial components , .
While these OMVs were initially characterized by chemical and
immunochemical methods, a proteomic analysis performed more recently  revealed
that such vesicles contain several factors known or presumed to be
related to the virulence of the bacterium, including the outer membrane
proteins Omp16, Omp19, Omp25 and Omp31. It has been shown that Omp16 and
Omp19 are lipoproteins that modulate MHC II expression in
On the other hand, Omp25 has been linked to the ability of Brucella to
modulate TNF-α secretion in human macrophages .
Therefore, it can be speculated that OMVs from Brucella may
mediate the transfer of virulence factors to the host cell to generate
immunomodulation or other effects that may favor the survival
of the pathogen within cells. To our knowledge, the
interaction of Brucella OMVs
with mammalian cells and the potential immunological consequences of
such interaction have not been studied. The evaluation of these
phenomena was the goal of the present study.”
let us for once and for all, pay attention to the fungal antigen
specialist, Clifford Harding; “several studies have shown fungal
antigens like LYMErix (TLR2-agonists) decrease antibody production or
Regulation of antigen
presentation by Mycobacterium
a role for Toll-like receptors
”Several studies have demonstrated that M.
tuberculosis-infected macrophages have decreased MHC class
II molecule expression and decreased antigen presentation, reducing CD4+ T
cell recognition of infected macrophages20,22–24,30,32–38.
Comparison of the T cell responses to model antigens presented by M.
tuberculosis-infected macrophages and to antigens presented
by uninfected macrophages showed that M.
antigen presentation by macrophages 12–18 hours or more after infection32,35.
have provided insights into the molecular mechanisms involved in the
inhibition of MHC class II antigen presentation by M.
tuberculosis. Viable M.
not required for inhibition of macrophage MHC class II expression and
antigen presentation, which can be achieved by exposure of macrophages
Biochemical fractionation was used to identify M.
that inhibited MHC class II molecule expression, and several M.
tuberculosislipoproteins, including LpqH32, LprG40 and LprA41,
were found to be key inhibitors. These lipoproteins, as well as PhoS1 (also
known as PstS1), are agonists of TLR2 (REFS 23,32,40–43)
1), and their inhibition of MHC class II molecule expression
and antigen presentation is dependent on TLR2 and its adaptor, myeloid
differentiation primary-response protein 88 (MYD88)19,23,32,40.
Furthermore, MHC class II inhibition that is mediated by viable M.
itself also largely dependent on TLR2 (REFS23,32)
and, to an even greater degree, on MYD88 (REF. 23),
although some MHC class II inhibition might be due to non-lipoprotein
components of M.
could be MYD88 independent18,19,21.
"Thus, prolonged TLR2 signalling induced by M.
(and, potentially, by other TLR2 agonists expressed by M.
results in inhibition of MHC class II molecule expression and antigen
presentation by M.
Fungal antigens cause immunosuppression and no antibodies against
Borrelia, particularly not OspA. Not TLR2/1 agonists. Not Pam3Cys.
No. It does not result in antibodies. Period. You have this outcome
if you have “chronic Lyme.” OspA never could have been a vaccine.
Clearly Yale falsified their LYMErix vaccine results. And Dearborn,
with the requirement for high antibody production, is research fraud.
Lyme Osps, Brucella Omps, and Mycobacteria Lprs…. and several
studies say so.
Whoever does not know what LYMErix disease is does not know what Lyme
disease is. This includes ILADS.org and all of the Lyme non-profits.
One has to know what the antigen is, in order to know what it does.
This is basic science.
on how OspA vaccination caused the same disease as chronic Lyme:
Neuropathy and cognitive impairment following vaccination with the OspA protein
of Borrelia burgdorferi.
“Neurological syndromes that follow vaccination or infection are often
attributed to autoimmune mechanisms. We report six patients who
developed neuropathy or cognitive impairment, within several days to 2
months, following vaccination with the OspA antigen of Borrelia
burgdorferi. Two of the patients developed cognitive impairment, one
chronic inflammatory demyelinating polyneuropathy (CIDP), one multifocal
motor neuropathy, one both cognitive impairment and CIDP, and one
cognitive impairment and sensory axonal neuropathy. The patients with
cognitive impairment had T2 hyperintense white matter lesions on
magnetic resonance imaging. The similarity between the neurological
sequelae observed in the OspA-vaccinated patients and those with chronic
Lyme disease suggests a possible role for immune mechanisms in some of
the manifestations of chronic Lyme disease that are resistant to
antibiotic treatment.” http://www.ncbi.nlm.nih.gov/pubmed/15363064
Donald H. Marks
on how LYMErix caused the same disease as chronic Lyme:
Neurological complications of vaccination with outer surface protein A (OspA).
wide range of neurological complications have been reported via the
medical literature and the VAERS system after vaccination with
recombinant outer surface protein A (OspA)
of Borrelia. To explore this issue, 24 patients reporting neurological
adverse events (AE) after vaccination with Lymerix, out of a group of 94
patients reporting adverse events after Lymerix vaccination, were
examined for causation. Five reports of cerebral ischemia, two transient
Ischemic attacks, five demyelinating events, two optic neuritis, two
reports of transverse myelitis, and one non-specific demyelinating
condition are evaluated in this paper. Caution is raised on not actively
looking for neurologic AE, and for not considering causation when the
incidence rate is too low to raise a calculable difference to natural
could be that a person has an HLA-linked outcome to one of the secondary
infections like Epstein-Barr or HHV-6, reactivated by the AIDS-like Lyme
and LYMErix. Those people would for instance have the official,
hypersensitivity outcomes of MS or Lupus or whatever. But they are not
also called Incompetent Incantation-ators and they are not mistreated by
the entire universe (family, friends, Social Security, “doctors,”
everyone, including ILADS and the non profits).
It’s not “Autoimmune.” It’s Subimmune. This Subimmunity represents the
entire class of the DSM VooDoo Somatoformia – as well as cancer. Cancer
is in the Subimmune class, at the other end of the immunity spectrum
from Autoimminity. This fact or condition completely flips the entire
medical paradigm where you have to have a biomarker that is above-, or
more-than- the normal range. Lyme is not an inflammatory disease.
There are always negative correlations to biomarkers of autoimmunity or
illness or infection except when using sophisticated DNA techniques
using spinal fluid, in particular. Henceforth, Autoimmunity will be an
obsolete word that connotes the previous Medical Establishment where
BigPharma is going to “block” something with their drugs. They are
dinosaurs. You can’t block a mechanism that is already permanently
blocked and you can’t unblock it.
Luft at the 1998 FDA Vaccine Meeting on LYMErix:
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. 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 seropositive, you can start to
have a different take on when someone has an adverse event or 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. ..." http://www.fda.gov/ohrms/dockets/ac/98/transcpt/3422t1.rtf
Dave Persing who together with Yale’s Robert Schoen
developed this test in 1994 or 1995 says this about the similarities
between Lyme and LYMErix disease:
"Additional uncertainty may arise if the vaccines are not completely
protective; vaccinated patients with multisystem complaints
characteristic of later presentations of Lyme disease may be difficult
to distinguish from patients with vaccine failure....”
Oh, you mean LYMErix causes the same disease as Lyme?
Latov, Marks, Luft, Persing and Schoen all say LYMErix
produced a disease we know of as Chronic Lyme. We have seen that Lyme
arthritis barely exists (Dattwyler), and we actually DO know how
to detect Lyme disease with 95% accuracy. We have seen what OspA is,
how it gets around, and that it is a fungal toxin. Later we will see
who else says LYMErix never could have been a vaccine and acts as the
complete opposite. We will see who jumped ship from Lyme to only MS,
and who only specializes, oddly, in Lyme and Epstein-Barr (and
very disease definition left out of the Dearborn case definition, the
chronic neurologic, MS, Lupus, etc, was caused by the vaccine in at
least 11% of the LYMErix victims. You can look up those trial results.
It turns out CDC officer Alan Barbour and one of the original
founders of the ALDF.com (which later hijacked IDSociety.org),
Durland Fish had written a paper
together in 1993 trashing the non-arthritis people and incidentally
stating that the Phase I and II trials of OspA were underway. You can
conclude Dearborn happened so that the most serious cases of Lyme -
caused by the vaccine, too – could be excluded. The kind of Lyme
detected by the Dearborn case definition? Barely exists. Good way to
have a vaccine trial.
Design a fake disease serology that no one has, then have a fake vaccine
trial. No one has the disease. Viola, your vaccine is amazing.
Still no one has that disease. Oh, and deploy the DSM because no one is
really looking at the DSM and psychiatry’s inconsistent perceptions and
attitudes towards the paranormal, not to mention their kaleidoscopic
cornucopia of interchangeable “disorders” and drugs. The evanescent
Chronic Fatigue Syndrome and Fibromyalgia. They’re a totally handy
thing. Twelve million of us have and not a nickel towards research on
the cause. Because it is actually known, and no one cares, since nearly
everyone already has most of the herpesviruses, and especially
CDC themselves held the Dearborn conference, being owners of several
useless vaccine candidates, including Alan Barbour who owned one of the
OspA vaccine patents (ImmuLyme), which threw out the most serious
adverse events to LYMErix and which were identical to the case
definition thrown out at Dearborn. In other words, Dearborn was
constructed to falsify the OspA vaccines outcomes and they clearly knew
these adverse events/neurologic, chronic cases were being caused by the
vaccine. Dearborn excludes 85% of all cases (the non-HLA-linked
arthritis, lots of antibodies, hypersensitivity cases), and 100% of all
the neurologic Great Imitator outcomes. You now may only have a disease
if you have no disease. Just a bad knee. We are not making this up.
Here is exactly what Klempner and Wormser said about the HLA-link to the
Dearborn case definition, 11 years later:
Study to Examine HLA Haplotype Associations in Patients with
Posttreatment Chronic Lyme Disease (Wormser and Klempner)
disease is caused by infection with the tickborne bacterium Borrelia
Antibiotic treatment is highly effective for the acute symptoms of Lyme
disease and is also effective for
late septic manifestations
There appear to be at least 2 distinct syndromes in patients with
persistent symptoms after antibiotic treatment. One syndrome has
localized symptoms that are similar to pretreatment symptoms. Patients
with this syndrome often have recurrent episodes of arthritis/synovitis.
Results of synovial fluid cultures and polymerase chain reaction (PCR)
for B. burgdorferi are
Patients generally feel well aside from their arthritis symptoms.
Specific HLA haplogroups (i.e., HLA-DR4 and HLA-DR2) have been
associated with the failure to respond to antibiotics in this group of
patients, and their arthritis may be due to molecular mimicry between a
dominant epitope of outer surface protein A (OspA) of B. burgdorferi and
lymphocyte function–associated antigen–1 (LFA-1) .
A much more common syndrome of persistent symptoms is a systemic illness
that is characterized by profound fatigue, myalgias, polyarthralgias
without arthritis, paresthesias, and mood and memory disturbances.
This syndrome has been variously referred to as “chronic Lyme disease,”
“post–Lyme disease syndrome,” and “posttreatment chronic Lyme disease” (PTCLD).
The cause of the persistent systemic symptoms in these patients is
unknown. However, we have reported elsewhere that the impact that PTCLD
has on health-related quality of life was highly significant and that
treatment with placebo or 90 days of additional antibiotics did not
differentially affect patients’ health-related quality of life .
We also did not find evidence of persistent infection with B. burgdorferi or
exposure to other tickborne infectious agents that could explain the
persistent systemic symptoms.”
So, there are
2 distinct diseases: Arthritis (“one case a year” - Dattwyler), and the
other thing – the chronic neurologic. The first thing, where people do
not feel sick, is a Dearborn “case” of Lyme. But, these criminals
claim, those chronic neurologic cases are not sick from B.
No, it’s much much
worse. The OspA, Pam3Cys, LYMErix and ImmuLyme vaccines caused it,
too. And then there’s those irksome “Epstein-Barr like mutated B cells
in the spinal fluid of chronic neurologic Lyme victims…”
And there’s the venom, the slander, the libel, the trashing, the Salem
Witch Trials dealt chronic neurologic Lyme victims all these years,
started by the ALDF.com [Durland Fish, Gary Wormser, Barbara Johnson (CDC),
Alan Barbour (CDC), Dave Persing, Robert Schoen, John Nowakowski, Mark
Klempner, Edward McSweegan, Allen Steere, Stanley Plotkin, a guy named
Sood, Vijay Sikand, Eugene Shapiro, Henry Feder, Larry Zemel, Lenny
Sigal, Dave Dennis, Phil Baker, etc.]. … Suttins up.
ILADS was there.
ILADS.org did not exist in its present form at the time of the
vaccines scandals, in the late 1990s and early 2000s. They were
mere an e-list called MMI. But they did exist in the middle of
2001. (Kathleen Dickson wrote their original Klempner rebuttal in
June 2001; it was a simple list of proofs that the whole report was
invalid, starting with Dearborn being invalid, since Dickson had
already shown that to the FDA in Jan 2001. Analytical Methods
development and validations is what she did for a living at Pfizer.)
They, ILADS.org knew what went down with that vaccine and how
Dearborn was falsified, as Dickson was on their list and also
testified at the FDA hearing on LYMErix in January, 2001. Yet,
they, ILADS.org say nothing about it, because they’re treating “Lyme
Meanwhile the OspA vaccines alone caused the same disease ILADS
alleges to be treating. It’s no wonder people get second and third
mortgages and end up with no house in addition to not being any
better from their chronic Lyme. ILADS and the Lyme non-profits
clearly do not care. It is obvious no one is getting better. Look
at all the celebrities who have all kinds of money. We all know if
Lyme is not caught early, it is incurable. But is it incurable?
Perhaps not if the Cause is Known.
You’ve Heard this
We will get to this in more detail in this report, but basically the
disease is this: when your immune system is turned off by constantly
shed “vesicles” or “exosomes” or “blebs,” or blobs of protoplasm,
some of which contain DNA, are in the end causing the
reactivation of disease those latently ubiquitous herpes viruses can
be reactivated. HSV, CMV, HHV-6, Zoster, and especially EBV. It
very much appears – and we are not the only ones saying so - , these
viruses are the true culprits behind what we know as chronic Lyme
disease. Little else explains the variety show of MS, Lupus,
Chronic Fatigue, or an AIDS like outcome. That this happens is
claimed by many: Washington University in St Louis, MO, and even the
NIH. They refer to it as post-sepsis and you have heard us remark
about this phenomenon before (all roads pointing to OspA-induced or
fungal antigen-induced AIDS-like disease):
This phenomenon of blebbing or shedding vesicles or microbial
sharing of DNA goes for nearly all organisms, not just spirochetes.
In particular the Borrelia blebs have OspA-ish or fungal antigens on
them. And these shed blebs go all around the body, into the brain
and into the kidneys as we have shown, and so says the NIH in one of
their patents from 1995. Igenex tried to capture them in the old
days with their urine antigen capture method called the LUAT. SUNY
Stony Brook also had an antigen-antibody de-complexing method for
spinal fluid analyses. But blebs, and OspA antigen on them is what
they were looking for to show active infection regardless of a
patient’s antibiotic history. There are many more of them than
there are spirochetes. Immune cells pick them up, and then,...
they’re stuck. Literally.
Back Up, “beep beep beep…” Has anyone ever tried to make fungal antigens
into vaccines before?
Let’s look at some
other fungal-type, lipoprotein (managed by TLR2/1 as a pair, together,
meaning it is such and such type of antigen, in this case, highly
lipidated, tri-acyl or higher) vaccine attempts to see if the
same outcome LYMErix gave happened in parallel? That should be a good
researcher’s first thought. Apparently neither ILADS nor IDSA nor even
the entire U.S. Department of Health and Human Services (under which are
all the National Institutes, OMG) had any such first thoughts:
antigen and protective immunity in a murine model of tuberculosis.
"The 19-kD antigen
is a cell wall-associated lipoprotein present in Mycobacterium
tuberculosis and in bacille Calmette-Guérin (BCG) vaccine strains.
Expression of the 19-kD antigen as a recombinant protein in two
saprophytic mycobacteria-M. vaccae and M. smegmatis-resulted in
abrogation of their ability to confer protection against M. tuberculosis
in a murine challenge model, and in their ability to prime a DTH
response to cross-reactive mycobacterial antigens. Induction of an
immune response to the 19-kD antigen by an alternative approach of DNA
vaccination had no effect on subsequent M. tuberculosis challenge. 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. Targeted inactivation of genes encoding selected
antigens represents a potential route towards development of improved
Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits
Mycobacterium smegmatis-induced cytokine production by human macrophages
“Vaccination of mice
with Mycobacterium vaccae or M. smegmatis induces some protection
against M. tuberculosis challenge. The 19-kDa lipoprotein of M.
tuberculosis, expressed in M. vaccae or M. smegmatis (M. smeg19kDa),
abrogates this protective immunity. To investigate the mechanism of this
suppression of immunity, human monocyte-derived macrophages (MDM) were
infected with M. smeg19kDa. Infection resulted in reduced production of
tumor necrosis factor alpha (TNF-alpha) (P < 0.01), interleukin-12
(IL-12) (P < 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared to
infection with M. smegmatis vector (M. smegV). Infection with M.
smeg19kDa and with M. smegV had no differential effect on expression of
costimulatory molecules on MDM, nor did it affect the proliferation of
presensitized T cells cocultured with infected MDM. When MDM were
infected with M. smegmatis expressing mutated forms of the 19-kDa
lipoprotein, including non-O-glycosylated (M. smeg19NOG), nonsecreted
(M. smeg19NS), and nonacylated (M. smeg19NA) variants, the reduced
production of TNF-alpha or IL-12 was not observed. When the purified
19-kDa lipoprotein was added directly to cultures of infected monocytes,
there was little effect on either induction of cytokine production or
its inhibition. 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
Mycobacterium tuberculosis recombinant 27-kilodalton lipoprotein induces
a strong Th1-type immune response deleterious to protection.
immune response is essential in the protection against mycobacterial
intracellular pathogens. Lipoproteins trigger both humoral and cellular
immune responses and may be candidate protective antigens. We studied in
BALB/c mice the immunogenicity and the protection offered by the
recombinant 27-kDa Mycobacterium tuberculosis lipoprotein and the
corresponding DNA vaccine. Immunization with the 27-kDa antigen resulted
in high titers of immunoglobulin G1 (IgG1) and IgG2a with a typical Th1
profile and a strong delayed hypersensitivity response. A strong
proliferation response was observed in splenocytes, and significant
nitric oxide production and gamma interferon secretion but not
interleukin 10 secretion were measured. Based on these criteria, the
27-kDa antigen induced a typical Th1-type immune response thought to be
necessary for protection. Surprisingly, in 27-kDa-vaccinated mice
(protein or DNA vaccines) challenged by M. tuberculosis H37Rv or BCG
strains, there was a significant increase in the numbers of CFU in the
spleen compared to that for control groups. Furthermore, the protection
provided by BCG or other mycobacterial antigens was completely abolished
once the 27-kDa antigen was added to the vaccine preparations. This
study indicates that the 27-kDa antigen has an adverse effect on the
protection afforded by recognized vaccines. We are currently
studying how the 27-kDa antigen modulates the mouse immune response.”
“A deleterious effect on immunity,” “an
adverse effect on the protection,” “the immunosuppressive effect,”
“diminished protection,” “reduced T cell activation,…”
THEY DON’T WORK; lipoproteins are the opposite
Raymond Dattwyler, 1988
Not surprisingly, that data on the failed Tuberculosis (Tb) fungal
vaccines is all quite reminiscent of what Ray Dattwyler said about
Borrelial supernatant - the stuff that floats on the top, the oil of
the oil and vinegar, yeah, the oil, the lipids, the lipoproteins, the
From: 1988, Modulation of natural killer cell activity by Borrelia
Golightly M, Thomas
"Effect of B burgdorferi Culture on Normal PBL
"..when lymphocytes are cultured in the presence of growing Bb there is
a marked inhibition ( p < .0005 ) of NK activity on days 3, 5,
and 7 when compared to lymphocytes cultured in BSKII media in the
absence of spirochetes. This effect is not due to a selective depletion
or or toxicity to endogenous NK since viability studies and monoclonal
antibodies demonstrate no significant changes after culture with the
inhibition is directly attributable to the organism or its supernatants
(data not shown)."
Lipoproteins BLUNT immunity. Here is what Gary Wormser said
about OspA vaccines for dogs in July, 2000, while LYMErix was still on
Modulation of lymphocyte proliferative responses by a canine Lyme
disease vaccine of recombinant outer surface protein A (OspA).
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 theOspA 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 theOspA molecule
responsible for this effect may lead to improved vaccine preparations.”
Once more (you’ve just seen 5 examples), lipoproteins and lipoprotein
vaccines suppress immunity, even in animals, which are known to have
more broad natural immunity than humans (making animals diseases very
good sources of human disease bioweapons). Three Tb vaccines based on
lipoproteins, Dattwyler, et al, claiming Borrelia oily lipoproteins
blunt immunity, and Gary Wormser himself said lipoproteins do that
mysterious thing… “blocking of cell cycle phase progression.” Later we
will learn OspA inhibits apoptosis, which is the same thing EBV does.
That is what “EBV-immortalized” means. The infected cell does not
kill itself, or undergo apoptosis as a way of keeping the pathogens from
BCL2 Class molecules and OspA inhibit
apoptosis; No “biofilms” in vivo
BCL2 class molecules
do the same thing, they inhibit apoptosis or they block the auto-kill or
apoptosis kinases (enzymes). BCL means B Cell Lymphoma (clue). If you
have too many copies of a BCL2 class gene, as is the case with “nerve
overgrowth syndromes” such as Neurofibromatosis or/and Autism (the
Einstein, Telsa, Newton, Grandin kind), their over expression leads to
inhibition of apoptosis. This is thought to be the case with the
genetic, large-brain kind of Autism; a “lack of normal synaptic
pruning.” A BCL2 class gene happens to co-confer with other copies in
the case of reversed duplication, as shown here:
Organisation of the pericentromeric region of chromosome 15: at least
four partial gene copies are amplified in patients with a proximal
duplication of 15q.
"We identified a fourth pseudogene, BCL8, which maps to the
pericentromeric region and is coamplified along with the NF1 sequences.
Interphase FISH ordering experiments show that IgH D lies closest to the
centromere, while BCL8A is the most distal locus in this pseudogene
lipoproteins act like extra BCL2 molecules, inhibiting apoptosis. This
is shown in numerous examples of the literature with mycoplasmal and
mycobacterial lipoproteins, as well as Brucella lipoproteins. One can
use PubMed or the National Library of Medicine Anyone can find out
OspA is the basic Pam3Cys molecule. It occurs naturally and is
synthetic (Braun lipoprotein). Epstein-Barr has its own human homolog
(similar gene copy), of BCL2. The first step in dysimmunity, one
could claim, is the inhibition of apoptosis. Fungal lipoproteins,
of the TLR2/1 type, highly lipidated, with 3 or more acyl (fatty acid,
like palmitic acid or linoleic acid, etc) groups, gum up immunity. They
inhibit apoptosis. In particular, OspA is sticky and even sticks to
itself. This may be the reason spirochetes appear to cluster in
vitro. However they don’t cluster or grow in colonies in humans;
biofilms are not the reason antibiotic treatment fails. This data
summary and explanation of the science abundantly shows spirochetes and
“biofilms” are not what makes Chronic Lyme chronic. Especially not if
the vaccine caused the same chronic neurologic disease.
Paul Duray :
Morphology of Borrelia burgdorferi:
structural patterns of cultured borreliae in relation to staining methods.
"The microscopic recognition of Borrelia burgdorferi
in biologic fluids and tissues is difficult and challenging because of
low numbers of organisms occurring as single isolated spirochetes, the
apparent lack of colony formation in tissues, and differing lengths
and structural morphologies."
Anyone who has a
science background, which includes anyone with an ‘MD” after their names
has for 15 years been able to discover what exactly OspA was and why it
caused systemic disease and why it failed.
the Alphabet of data points that point to Lyme being like AIDS with
reactivated viral infections due to immunosuppression. These next 9
we’ll call the “L” group because we are going to run out of letters.
formerly of NINDS' MS-Lyme group and who now works for NIAID, and
specializes only in Lyme and the MS and herpesviruses (clue):
“When Lyme Disease Lasts and Lasts,” by Jane Brody in the New York
“'Complicating the picture is the fact that some people with PTLDS
symptoms apparently never had Lyme disease in the first place,’ Dr.
Marques said in an interview. ‘There are other infectious organisms—Epstein-Barr
virus, for example—that can produce similar symptoms and may be the
Says another NIH employee of post sepsis-herpes-AIDS:
"Surviving Sepsis: Detection and Treatment Advances” by Carolyn Beans
for the National Institutes of Health, August 18, 2014
“…Some people who survive sepsis can develop secondary infections days
or even months later. A research team that included Richard Hotchkiss,
Jonathan Green and Gregory Storch of Washington University School of
Medicine in St. Louis suspected that this is because sepsis might cause
lasting damage to the immune system…The researchers looked for
viruses like Epstein-Barr and herpes simplex that are often dormant in
healthy people but can reactivate in those with suppressed immune
The NIH supports the Hotchkiss, Washington
University report on Sepsis and Post-Sepsis outcomes, see "P.," below.
The CDC/IDSA/Yale OspA-criminals claim what happens after early Lyme is
called "Post-Lyme Syndrome," and that that is psychiatric. But
actually you saw Klempner call it a Septic event
("G.," above), particularly as regards for the Central Nervous
System (CNS). People should be aware that these criminals are the
authors of all the scientifically valid signs or
BIOMARKERS of CNS degradation.
That is why the psychiatric slander, libel and downright genetic
discrimination ("No arthritis HLA's? You must be crazy") is a criminal
charge. The biomarkers will not be found in the blood. Being
the authors of all those BIOMARKERS while
libeling their victims is a separate criminal
charge. It is a "Color of Law" abuse, Discrimination, and
shows "Intent to Cause Harm" - necessary for a
specializes in only Lyme and herpesviruses:
of Tufts, former partner with Allen Steere in “Lyme is Only a Bad Knee
Theatre,” who now specializes in ONLY herpesviruses (actually, claiming
EBV could be reactivating a human endogenous retrovirus or a HERV):
pathologist Colonel Paul H. Duray (NCI, Yale, US Army Ft. Detrick)
were still alive, you could ask him why he said, “these look like
Epstein-Barr transformed cells" in the spinal fluid of chronic
neurologic Lyme victims in 1989, in IDSA's journal.
Clinical pathologic correlations of Lyme disease.
"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."
Or why Duray said it again, in 1992: "In Chronic Lyme victims'
cerebrospinal fluid, I see what look like Epstein-Barr transformed
"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." -
Duray, NCI, NIH, Ft. Detrick, at the
Spring Harbor ALDF.com Conference,
published in Steve Schutzer's Lyme
Disease: Molecular and Immunologic Approaches.
Patricia K. Coyle,
SUNY-SB. Coyle once was the author of several reports and even methods
to detect borrelia antigens in the central nervous system because of the
absence of antibodies…. now only specializes in Multiple Sclerosis???
Roland Martin and Adrianna Marques at the NINDS MS and Lyme
Division. Martin quit and went home to Germany once he found out
LYMErix was responsible for the immunosuppression-come-New Great
Imitator (in other words, that LYMErix or OspAish antigens were
responsible for the MS outcome of Lyme:
burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral
blood monocytes but differentially regulates HLA-class II expression
“…These results show that signaling through TLR1/2 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.”
Anthony FAUCI on immunosuppression and common opportunistics:
Anthony Fauci says this in his patent for IL-2 as an immune booster. He
lists fungi and stuff like common opportunistics, you know like…
"FIELD OF THE INVENTION
"The present invention pertains to a
method for activating the immune system of a patient by intermittently
administering interleukin-2 (IL-2) to that patient. Such administration
of IL-2 can optionally be combined with other therapies, such as
anti-retroviral, anti-bacterial or anti-fungal therapies, suitable for
treatment of the patient's condition. This invention also relates to an
approach to gene therapy that entails administering IL-2 to a patient so
as to facilitate in situ lymphocyte transduction by a retroviral vector
also administered to the patient.
"BACKGROUND OF THE
specific disease states in treatment of which the present invention can
be applied are HIV infection and other diseases characterized by a
decrease of T-cell immunity, for example, mycobacterial
infections like tuberculosis and fungal infections such as cryptococcal
disease. This method also can be used in the treatment of secondary
infections that occur in patients with suppressed immune systems, such
as the opportunistic infections that occur in AIDS patients. ..."
infections may also be treated using the present invention. For example,
AIDS related opportunistic infections are described in Mills et. al.
(1990) Scientific American 263:51-57, which is hereby incorporated by
reference in its entirety. Mills show that common
opportunistic infections are
caused by, for example, Cytomegalovirus,
Pneumocystis carnii, Candida
albicans, Varicella-Zoster virus, Epstein-Barr virus,
Toxoplasma gondii, Mycobacterium avium,
Cryptococcus neoformans. It is envisioned that IL-2 may be administered
along with other compounds used to treat infectious diseases or other
diseases. Examples of other agents include antifungal, antiviral, or
antibacterial drugs. Additionally, IL-2 may be administered in
combination with other efficacious cytokines. For example, combination
therapy may include IL-2 with GM-CSF, G-CSF, M-CSF, IL-3, IL-12, IL-15,
a-, b-, or g-interferons."
“Diseases of immunosuppression like fungal diseases.” “Opportunistic
infections like the herpesviruses and other fungal infections which now
have a free ride due to TLR2-agonist tolerance and cross tolerance.”
Yes. I think so. Common opportunistics, yeah, probably especially
since Epstein-Barr and the other herpesviruses, since those can be
chronic and cause a chronic fatiguing disease – says the CDC -, not to
mention is associated with MS and Lupus. Great Imitators…
CDC’s Suzanne Vernon explaining how Epstein-Barr contributes to
fatigue, How she committed research fraud to try to say fungal antigens
are not involved in fatigue, How we know fungal antigens adhere to
erythrocyte membranes causes hypoxic fatigue, stick to internal cell
components, depolarizing membranes, etc.
Preliminary evidence of mitochondrial dysfunction
associated with post-infective fatigue after acute infection with
Epstein Barr virus.
who developed post-infective fatigue had gene expression profiles
indicative of an altered host response during acute mononucleosis
compared to those who recovered uneventfully. Several genes including
ISG20 (interferon stimulated gene), DNAJB2 (DnaJ [Hsp40] homolog and
CD99), CDK8 (cyclin-dependent kinase 8), E2F2 (E2F transcription factor
2), CDK8 (cyclin-dependent kinase 8), and ACTN2 (actinin, alpha 2),
known to be regulated during EBV infection, were differentially
expressed in post-infective fatigue cases. Several of the differentially
expressed genes affect mitochondrial functions including fatty acid
metabolism and the cell cycle."
"CONCLUSION: These preliminary data provide insights into alterations
in gene transcripts associated with the varied clinical outcomes from
acute infectious mononucleosis." http://www.ncbi.nlm.nih.gov/pubmed/16448567
Vernon commits research fraud by throwing out the mycoplasma before she
even starts to allegedly look for mycoplasmal DNA:
2003; Absence of
Mycoplasma species DNA in chronic fatigue syndrome
“Blood was collected in sodium citrate Vacutainer tubes (Beckton
Dickinson) and shipped by overnight courier to the Centers for Disease
Control (CDC), where plasma was collected by separation on lymphocyte
separation medium (LSM; ICN Biomedicals). Plasma (1 ml) was concentrated
to approximately 250 μl in a Centricon centrifugal filter unit YM-100
(Millipore). Cell-free plasma DNA was extracted by using a QIAamp DNA
Mini kit (Qiagen) according to the manufacturer's instructions and
quantified by using a DyNA Quant 200 fluorometer (Amersham
committed research fraud by centrifuging out the very cells to which
mycoplasma adhere and then said, “How Amazing, there is no mycoplasma
c) Mycoplasma adhere to erythrocytes interfering with membrane
potential and therefore the potential for oxygen to cross the
erythrocyte membrane (causing fatigue):
[The effect of Eperythrozoon suis infection on the osmotic fragility of
“Osmotic fragility of erythrocytes was tested in weaned pigs
experimentally infected with Eperythrozoon (E.) suis. Acute
eperythrozoonosis of splenectomized pigs led to an increase of osmotic
fragility. It is supposed that E. suis infection causes a structural
change in erythrocyte membrane. Possible mechanisms of this cell
membrane injury are discussed.”
Mycoplasma – remember now, thrown out by the CDC, fraudulently and
deliberately, as a contributor to FATIGUE – mess with mitochondrial
membrane potential – as a way of inhibiting apoptosis (consider the
possible synergy here with Epstein-Barr which does the same thing):
inhibits tumor necrosis factor alpha-induced apoptosis in the human
myelomonocytic U937 cell line.
of mitochondrial inner transmembrane potential induced by TNFa is
reduced in U937 cells infected with M.
”In many apoptosis scenarios, including TNF-mediated apoptosis, the
mitochondrial inner transmembrane potential (m) collapses.19, 20 To
investigate whether the antiapoptotic effect of M.
fermentans in TNF-induced
apoptosis is upstream or downstream of the mitochondria, we measured the
loss in Delta-Sigmam,
induced by TNF (20 ng/ml), in
infected and noninfected cells. At 24 h post infection, the cultures
were stimulated with TNF (20 ng/ml)
for 2 h, and each culture was stained with 3,3'-dihexyloxacarbocyanine
iodide (DiOC6 (3))
and analyzed by FACS (a typical experiment is shown in Figure
IF, Epstein-Barr alone were responsible for Chronic Fatigue Syndrome,
then one can see their idiot point of view that “stress” causes
the reactivation of Epstein-Barr (“somatiformical” =
reactivating EBV) and that de-stressing solves the problem.
Maybe that is the case with the somatoformical medical students
and astronauts and the like, who are so well known to have
stress-reactivated Epstein-barr or mono. But here we see
something much more sinister at work. The CDC does not want
anyone to know how fungal antigens cause fatigue and how
tolerance to fungi causes irreversible fatigue and how that
spreads to other infections (“common, now, opportunistics”). We
think the reason has to do with childhood vaccines being
contaminated with fungal antigens, which is the reason for
Thimerosal in the first place. We think the reason for this
fraud on the part of the CDC is that they do not want us to be
aware of the common mechanisms at work in
vaccines-virus-acquired Autism (brain damage is the more correct
term). We think the 20-30 million witches and warlocks in the
country are the price the CDC pays to continue to brain damage
around 1:60 children for life. It’s a great bargain for the CDC.
They even say “it is a calculated risk,” this vaccines
enforcement and the brain damaged for life outcome. CDC does
the calculating. You know who all the real monsters are.
should follow up on these reports; here is one from 2008:
alive: bacterial inhibition of apoptosis during infection.
ability of bacterial pathogens to inhibit apoptosis in eukaryotic cells
during infection is an emerging theme in the study of bacterial
pathogenesis. Prevention of apoptosis provides a survival advantage
because it enables the bacteria to replicate inside host cells.
Bacterial pathogens have evolved several ways to prevent apoptosis by
protecting the mitochondria and preventing cytochrome c release, by
activating cell survival pathways, or by preventing caspase activation.
This review summarizes the most recent work on bacterial anti-apoptotic
strategies and suggests new research that is necessary to advance the
TOLERANCE and CROSS TOLERANCE
One of the most important mechanisms of
synergy between fungal antigens and viruses – and we have mentioned this
many times in our reports and criminal charge sheets against IDSA and
the CDC (see
et al), has to do with tolerance and cross tolerance and we have
explained what this means in the past. Tolerance means your body no
longer sees the invading pathogen’s components are a threat and stops
responding to them immunologically. Cross-tolerance is when an
infection with one pathogen or antigen type, renders the immune system
incompetent to other types. “Endotoxin Tolerance” is a known thing,
known for decades. Endotoxin is considered mainly to be LPS or
lipopolysaccharide (feel free to google the structure or the image)
which are TLR4 agonists. TLR4 agonists are not as toxic as the fungal
TLR2/1 agonists of say spirochetes, mycoplasma, Brucella, or
mycobacteria. You have seen some of this with Clifford Harding (in “P.”
below), and others have proposed other observed the mechanics or
function of other intracellular compounds (“in the mileux”) being
One of the best sources (also in “THE LIST” below):
New, October 13, 2015
Endotoxin Tolerance Inhibits
Lyn and c-Src Phosphorylation and Association with Toll-Like Receptor 4
but Increases Expression and Activity of Protein Phosphatases.
“Endotoxin tolerance protects
the host by limiting excessive 'cytokine storm' during sepsis, but
compromises the ability to counteract infections in septic shock
It reprograms Toll-like receptor (TLR) 4 responses by attenuating the
expression of proinflammatory cytokines without suppressing
anti-inflammatory and antimicrobial mediators, but the mechanisms of
reprogramming remain unclear. In this study, we demonstrate that the
induction of endotoxin tolerance in
human monocytes, THP-1 and MonoMac-6 cells inhibited lipopolysaccharide
(LPS)-mediated phosphorylation of Lyn, c-Src and their recruitment to
TLR4, but increased total protein phosphatase (PP) activity and the
expression of protein tyrosine phosphatase (PTP) 1B, PP2A, PTP
nonreceptor type (PTPN) 22 and mitogen-activated protein kinase
phosphatase (MKP)-1. Chemical PP inhibitors, okadaic acid, dephostatin
and cantharidic acid markedly decreased or completely abolished LPS tolerance,
indicating the importance of phosphatases in endotoxin tolerization.
Overexpression of PTPN22 decreased LPS-mediated nuclear factor
(NF)-x03BA;B activation, p38 phosphorylation and CXCL8 gene expression,
while PTPN22 ablation upregulated LPS-induced p65 NF-x03BA;B and p38
phosphorylation and the expression of TNF-α and pro-IL-1β mRNA,
indicating PTPN22 as an inhibitor of TLR4 signaling. Thus, LPS tolerance interferes
with TLR4 signaling by inhibiting Lyn and c-Src phosphorylation and
their recruitment to TLR4, while increasing the phosphatase activity and
expression of PP2A, PTPN22, PTP1B and MKP1.
person who knows how to use the National Library of Medicine can follow
up on all this. The NIH endorses it, as you have seen. And
it's pretty ridiculous that IDSA thinks they can maintain the ruse that
OspA was a vaccine and Lyme is only about a bad knee with these hundreds
of reports that say the complete opposite is true.
Multiple Sclerosis and EBV? Let’s look:
Some say yes, some say no, some say Cytomegalovirus, some say HHV-6,
some say an EBV reactivated HERV, some say it’s more than one herpes,
and some say Viola! what do you know, immunosuppression from malaria
seems to be associated with EBV-associated Burkitt’s Lymphoma.
Synergy. Another kind of another in-parallelism to our model. One
infection invites the other, such as when in the old days it was known a
cold virus could result in a dual bacterial infection and they gave
children antibiotics to prevent a secondary ear infection. Or when in
1918 we had Spanish Flumonia, wheren one infection invited the other.
Regardless, it seems to be unsettled as to which common virus or which
two or which three, but it does seem to be a consensus that the
herpesviruses are associated with MS.
Where do spirochetes and the herpesviruses live, by the way? (Oh, and
the famous B cell depleter)
Lyme and EBV hang out in the lymph nodes and both live in B cells.
Varicella zoster, the nerve root ganglia. And spirochetes also travel
along nerves, as was proposed long ago and recently when we heard from a
dental group about the frequency of oral spirochetes found in
Alzheimer’s brains (1999)
What is Bell’s Palsy caused by?
Some say EBV, some say Varicella, some say Simplex… Maybe it’s not
spirochetes, maybe it is spirochetes, maybe it is a herpesvirus, maybe
it is a combination of herpesviruses, maybe it is herpesviruses and
spirochetes. But given that more than one kind of spirochete is
associated with Alzheimer’s, and given that immunosuppression diseases
are reactivation of COMMON VIRUSES, well, maybe that is the reason ILADS
can’t cure anyone. They don’t know what they’re doing and willfully do
not look at the big picture.
Lyme spirochetes and
EBV live in B cells(use PubMed). And it just so happens, Rituximab, a
bad B cell depleter works for Chronic Fatigue Syndrome (67% and 64% cure
rate); adds much credibility to the idea that this disease is about post
sepsis immunosuppression and reactivated herpesviruses:
Benefit from B-lymphocyte depletion using the anti-CD20 antibody
rituximab in chronic fatigue syndrome. A double-blind and
B-Lymphocyte Depletion in Myalgic Encephalopathy/ Chronic Fatigue
Syndrome. An Open-Label Phase II Study with Rituximab Maintenance
be about bad B cells, since the treatment fits the model. Ya think?
Remember now, Lyme causes Chronic Fatigue Syndrome and Fibromyalgia, say
the ALDF.com and Yale Lyme cabal. And 12 million people in the United
States alone have those… things. So it can’t be anything too mysterious
if it also causes Lupus and MS.
The Yale "Lupus and Lyme Clinic"
The NIH used to have an MS-Lyme section of the NINDS, and Yale used to
have a “Lyme and Lupus Clinic” before that became the criminal entity
“L2 Diagnostics,” led by none other than Robert Schoen of “we can’t tell
LYMErix apart from multisystem late Lyme” infamy.
(formerly at Yale) on Lyme and Lupus:
Reactivity of neuroborreliosis patients (Lyme disease)
to cardiolipin and gangliosides.
subset of patients (50%) with neuroborreliosis (Lyme disease)
showed IgG reactivity to cardiolipin in solid phase ELISA. In addition,
a subset of patients with neuroborreliosis (29%) and syphilis (59%) had
IgM reactivity to gangliosides with a Gal(beta 1-3) GalNac terminal
sequence (GM1, GD1b, and asialo GM1). Anti-ganglioside IgM antibodies
were significantly more frequent in these two groups of patients
compared to patients with cutaneous and articular Lyme disease,
primary antiphospholipid syndrome, systemic lupus erythematosus
and normal controls. Correlative evidence and adsorption experiments
indicated that antibodies to cardiolipin had separate specificities from
those directed against the gangliosides. IgM antibodies to Gal(beta 1-3)
GalNac gangliosides appeared to have similar specificities since these
were positively correlated and inhibitable by cross adsorption assays.
Given the clinical associations of patients with neuroborreliosis and
syphilis with IgM reactivity to gangliosides sharing the Gal(beta 1-3)
GalNac terminus, we suggest that these antibodies could represent a
response to injury in neurological disease or a cross reactive event
caused by spirochetes.”
Do you like the way Steere says there is such a thing as
neuroborreliosis? Now of course there is no such disease. In 2001 Mark
Klempner gave a talk about <whatever> at a hospital in Rhode Island in
which he was RECORDED as saying this about the Dearborn case definition:
"I just have one more question for Dr. Klempner. Um, being
that there are inadequacies, inaccuracies in the tesing methods,
seropositivity, etc, and the surveillance criteria that you used were
just that, surveillance. And the CDC recognizes that there are so many
more people that have Lyme disease who do not meet the CDC criteria.
What’s your feeling on what percentage of patients who have Lyme disease
because they have not met the criteria for diagnosis?"
"I, um, I think there are a number of inaccuracies in what you
just said. The CDC does not recognize
that there are patients who have, um, that are seropositive that don’t
meet seropositive criteria. What they say,
is that these are
the criteria. …"
CDC does not recognize anything that is not the Dearborn criteria.
And that is because they were the ones who falsified the case definition
on behalf of their own patent profiteering. It's all about the CDC
staff's and Yale's profiteering. But Dattwyler sees only one patient a year with only bad knees. And there
used to be a thing called Neuroborreliosis, but no more.
the Yale Lyme and Lupus gang say this about Lupus (and EBV):
Defective control of latent Epstein-Barr virus infection in systemic
“EBV infection is more common in patients with systemic lupus erythematosus
(SLE) than in control subjects, suggesting that this virus plays an
etiologic role in disease and/or that patients with lupus have impaired EBV-specific
immune responses…Patients with SLE had an approximately 40-fold increase
in EBV viral loads compared with controls, a finding not explained by
disease activity or immunosuppressive medications. The frequency of EBV-specific
CD69+ CD4+ T cells producing IFN-gamma was higher in patients with SLE
than in controls…These results demonstrate that patients with SLE have
defective control of latent EBV infection that probably stems from
altered T cell responses against EBV.”
Hotchkiss, Washington University, Saint Louis, MO:
wustl.edu discovers that
sepsis is like Chronic Lyme, in that the survivors of it are likely to
have survived via the immunosuppression (TLR2-agonist tolerance/Endotoxin
tolerance), but the result is the reactivation of latent viruses:
Dormant viruses re-emerge in patients with lingering sepsis, signaling immune
"Patients with lingering
sepsis had markedly higher levels of viruses detectable in the blood, compared
with the healthy controls and critically ill patients without sepsis. Among the
sepsis patients, for example, the researchers found that 53 percent had
Epstein-Barr virus, 24 percent had cytomegalovirus, 14 percent had
herpes-simplex virus, and 10 percent had human herpes simplex virus-7.
"These viruses generally
don’t lead to significant illness in people who are healthy but can cause
problems in patients who are immune-suppressed. "
FULL JOURNAL REPORT, snippet:
Reactivation of Multiple Viruses in Patients with Sepsis
is the host's non-resolving inflammatory response to infection that leads to
organ dysfunction , . A current controversial hypothesis postulates that
if sepsis pursues a protracted course, it progresses from an initial primarily
hyper-inflammatory phase to a predominantly immunosuppressive state –.
Experimental therapeutic approaches in sepsis have almost exclusively focused on
blocking early inflammation or host-pathogen interaction and failed –.
Recently, immuno-adjuvant therapies that boost host immunity, e.g., GM-CSF and
interferon-γ, have been successful in small clinical trials thereby supporting
the concept that reversing immunosuppression in sepsis is a plausible strategy
to improve outcome , . However, several issues have limited this
approach including lack of consensus that immunosuppression is a clinically
important phenomenon , , . Also, difficulty in identifying patients
with impaired immunity as well as determining optimal timing for administration
pose significant challenges to pursuing this approach . While immuno-adjuvant
therapies might improve sepsis survival if administered during the later
immunosuppressive phase, these agents might worsen outcome if given during the
early hyper-inflammatory phase , . Thus, a means to distinguish these two
contrasting phases of sepsis is needed not only to verify the hypothesis that
sepsis progresses to an immunosuppressive state but also to guide use of
potential agents which boost immunity.
viruses such as cytomegalovirus are normally held in abeyance by cellular
and immune surveillance mechanisms which if impaired, for example by
immunosuppressive medications, often result in viral reactivation, replication,
and virally-mediated tissue injury –. Sepsis impairs innate and adaptive
immunity by multiple mechanisms including apoptosis-induced depletion of immune
effector cells and induction of T-cell exhaustion thereby possibly predisposing
to viral reactivation and dissemination –. …”
Q. Medvedev and Cross-Tolerance;
Medvedev talking about Immunosuppression
from Post-Lyme and Post-LYMErix Sepsis (TLR2-agonists or Pam3Cys is OspA or shed
IRAK4 kinase activity is not required for induction of endotoxin tolerance but
contributes to TLR2-mediated tolerance
endotoxin tolerance following the initial “cytokine storm” phase of sepsis is
thought to protect the host from an overexuberant immune response and tissue
damage but at the same time, may render the host immunocompromised and more
susceptible to secondary infection [18,–20]. ...
"Reprogramming  of
TLR4 signaling in endotoxin-tolerant monocytes and macrophages does not occur as
a result of decreased TLR4 expression but involves altered recruitment, tyrosine
phosphorylation, and K63-linked polyubiquitination of proximal receptor-adapter-kinase
complexes [22,–27] and induction of negative regulators IRAK-M, SHIP1, and A20
[24, 25, 28]. Although a few studies have sought to dissociate kinase and
adapter functions of IRAK4 in IL-1R/TLR signaling, albeit with conflicting
results [13,–16, 29,–31], it is unclear how IRAK4 kinase activity affects
induction of TLR2 and TLR4 homo- and heterotolerance. To address these
questions, we used IRAK4KDKI mice to determine the impact of kinase deficiency
of IRAK4 on the induction of TLR tolerance. Our data showed comparable induction
of endotoxin tolerance in WT or IRAK4KDKI PMs and BMDMs, as judged by attenuated
MAPK phosphorylation, inhibited expression of proinflammatory cytokines and
chemokines, and up-regulation of negative TLR regulators, A20 and IRAK-M.
Notably, IRAK4 kinase activity was found to be a prerequisite for conferring
inhibition of LPS-inducible JNK and p38 MAPK activation following prior exposure
to Pam3Cys. These results represent the first systematic analyses of the
role of IRAK4 kinase activity in TLR homo- and heterotolerance and pave the way
for improved understanding of how IRAK4 kinase dysregulation may underlie
immunocompromised states in late sepsis."
R. Remember Pam3Cys is the basic molecule of LYMErix or OspA and others
shed by Borrelia:
is critical for the induction of Pam3CSK4-tolerance in monocytic THP-1 cells.
"A20 functions to
terminate Toll-like receptor (TLR)-induced immune response, and play important
roles in the induction of lipopolysacchride (LPS)-tolerance. However, the
molecular mechanism for Pam3CSK4-tolerance is uncertain. Here we report
that TLR1/2 ligand Pam3CSK4 induced tolerance in monocytic THP-1 cells. The
pre-treatment of THP-1 cells with Pam3CSK4 down-regulated the induction of
pro-inflammatory cytokines induced by Pam3CSK4 re-stimulation. Pam3CSK4
pre-treatment also down-regulated the signaling transduction of JNK, p38 and NF-κB
induced by Pam3CSK4 re-stimulation. The activation of TLR1/2 induced a rapid
and robust up-regulation of A20, suggesting that A20 may contribute to the
induction of Pam3CSK4-tolerance. This hypothesis was proved by the observation
that the over-expression of A20 by gene transfer down-regulated Pam3CSK4-induced
inflammatory responses, and the down-regulation of A20 by RNA interference
inhibited the induction of tolerance. Moreover, LPS induced a significant
up-regulation of A20, which contributed to the induction of cross-tolerance
between LPS and Pam3CSK4. A20 was also induced by the treatment of THP-1
cells with TNF-α and IL-1β. The pre-treatment with TNF-α and IL-1β partly
down-regulated Pam3CSK4-induced activation of MAPKs. Furthermore, pharmacologic
inhibition of GSK3 signaling down-regulated Pam3CSK4-induced A20 expression,
up-regulated Pam3CSK4-induced inflammatory responses, and partly reversed
Pam3CSK4 pre-treatment-induced tolerance, suggesting that GSK3 is involved
in TLR1/2-induced tolerance by up-regulation of A20 expression. Taken
together, these results indicated that A20 is a critical regulator for
TLR1/2-induced pro-inflammatory responses."
TLR2/1-induced tolerance or LYMErix or Lyme tolerance
is a thing, like Endotoxin Tolerance, only worse, since so far it
is not reversible. In other words, IDSA and the CDC have no idea
what they are talking about, and this concerns every major disease, if
not every disease.
S. Poland, 2013, The influence of toll-like receptor stimulation
on expression of EBV lytic genes.
"Epstein-Barr virus (EBV) establishes latency in the resting memory
It has been recently suggested that maintenance of chronic infection is
dependent on periodic reactivation. Although the stimuli for EBV
reactivation in vivo during natural infections are largely unknown,
there is evidence indicating that heterologous infections could trigger
herpesviruses reactivation. The purpose of this work was to identify the
influence of Toll-like receptors stimulation on EBV replication in EBV
latently infected Burkitt lymphoma cells (P3HR-1, Raji and Namalwa). The
cells were stimulated with
Pam3CSK4 (synthetic triacylated lipoprotein),
PolyI:C (synthetic analog of dsRNA), LPS (lipopolysaccharide from E.coli),
measles virus (MeV) and PMA (phorbol myristate acetate). Non-stimulated
cells (NS) served as control. EBV expression was investigated at mRNA
level for three viral lytic genes: BZLF1 (immediate early, ZEBRA), BALF2
(early, EA) and BcLF1 (late, VCA). Additionally, the effect of
stimulation on NF-kBp65 and inflammatory cytokines (IL-lb, IL-6, IL-8,
IL-10, IL-12p70, and TNF) was investigated. Stimulation of TLRs led to
limited changes in EBV expression manifesting as increase of ZEBRA at
mRNA level in cells treated with PolyI:C and Pam3CSK4. Stimulation with
PolyI:C, Pam3CSK4 and LPS also lead to considerable increase of
NF-kBp65, while increased levels of inflammatory cytokines were observed
for IL-8, TNF and IL-6 in cells treated with PMA and MeV.
In conclusion, the results of our experiments support the suggestion
that TLRs stimulation with microbial ligands influences EBV virus
T. Clifford Harding and Justin Radolf
on the downregulation of MHC or HLA molecules, resulting in
immunosuppression or lack of antibodies from exposure to the likes of
OspA covered blebs:
Toll-like receptor 2-dependent inhibition of macrophage class II MHC
expression and antigen processing by 19-kDa lipoprotein of Mycobacterium
tuberculosis (MTB) induces vigorous immune responses, yet persists
inside macrophages, evading host immunity. MTB bacilli or lysate was
found to inhibit macrophage expression of class II MHC (MHC-II)
molecules and MHC-II Ag processing. This report characterizes and
identifies a specific component of MTB that mediates these inhibitory
effects. The inhibitor was extracted from MTB lysate with Triton X-114,
isolated by gel electroelution, and identified with Abs to be MTB 19-kDa
lipoprotein. Electroelution- or immunoaffinity-purified MTB 19-kDa
lipoprotein inhibited MHC-II expression and processing of both soluble
Ags and Ag 85B from intact MTB bacilli. Inhibition
of MHC-II Ag processing by either MTB bacilli or purified MTB 19-kDa
lipoprotein was dependent on Toll-like receptor (TLR) 2 and independent
of TLR 4. Synthetic
analogs of lipopeptides from Treponema pallidum also inhibited Ag
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
are 4 examples from the literature of how Epstein-Barr also can be
seronegative via the same mechanism of downregulation of
antigen-presenting molecules or downregulation of HLA molecules (shows
antigen so that B cells can make antibodies) or the MHC or “Major
Histocompatibility Class” of cell components (all the same thing):
Down-regulation of MHC class II expression through inhibition of CIITA
transcription by lytic transactivator Zta during Epstein-Barr virus
immune modulation in EBV infection
"Dysregulation of EBV-specific immune responses is also characteristic
of EBV-associated autoimmune diseases such as rheumatoid arthritis (RA)
and systemic lupus erythematosus (SLE). CTL response to EBV infection
has been well documented since the discovery of EBV . However,
significant progresses in characterizing individual viral proteins
involved in evasion of the T cell-mediated adaptive immune response have
only been made in the last decade [12-16]. For
example, the functional homologue of human IL10, BCRF1, elicits CD8+ T
cell responses, and can be processed and presented to CD8+ CTLs through
a TAP-independent pathway ."
lytic cycle of Epstein-Barr virus is associated with decreased
expression of cell surface major histocompatibility complex class I and
class II molecules.
Epstein-Barr virus evasion of CD8(+) and CD4(+) T cell immunity via
concerted actions of multiple gene products.
"Evidence is accumulating that this paradoxical situation is the result
of actions of multiple viral gene products, inhibiting discrete stages
of the MHC class I and class II antigen presentation pathways.
Immediately after initiation of the lytic cycle, BNLF2a prevents
peptide-loading of MHC class I molecules through inhibition of the
Transporter associated with Antigen Processing, TAP. This will reduce
presentation of viral antigens by the large ER-resident pool of MHC
class I molecules. Synthesis of new MHC class I molecules is blocked by
BGLF5. Viral-IL10 causes a reduction in mRNA levels of TAP1 and
bli/LMP2, a subunit of the immunoproteasome. MHC class I molecules
present at the cell surface are downregulated by BILF1. Also the antigen
presenting capacity of MHC class II molecules is severely compromised by
multiple EBV lytic gene products, including gp42/gH/gL, BGLF5, and
vIL-10. In this review, we discuss how concerted actions of these EBV
lytic proteins result in highly effective interference with CD8(+) and
CD4(+) T cell surveillance, thereby providing the virus with a window
generation of viral progeny.”
Therefore, never use antibody testing to show an association between an
illness and an infectious disease.
says the chronic agonism of TLR2/1 by these lipoproteins also inhibit
TLR7/9 function (manages the viruses like EBV); people want to know how
Lyme and LYMErix activate EBV, besides that being about what happens
commonly, in all general immunosuppression such as Humira and Stelara
and post-transplant patients who acquired EBV-induced lymphoma, which we
will get to:
signaling depletes IRAK1 and inhibits induction of type I IFN by TLR7/9.
“Pathogens may signal through multiple TLRs with synergistic or
antagonistic effects on the induction of cytokines, including type I IFN
(IFN-I). IFN-I is typically induced by TLR9, but not TLR2. Moreover, we
previously reported that TLR2 signaling by Mycobacterium tuberculosis or
other TLR2 agonists inhibited TLR9 induction of IFN-I and
IFN-I-dependent MHC-I Ag cross processing. The current studies revealed
that lipopeptide-induced TLR2 signaling inhibited induction of
first-wave IFN-α and IFN-β mRNA by TLR9, whereas induction of
second-wave IFN-I mRNA was not inhibited. TLR2 also inhibited induction
of IFN-I by TLR7, another MyD88-dependent IFN-I-inducing receptor, but
did not inhibit IFN-I induction by TLR3 or TLR4 (both Toll/IL-1R
domain-containing adapter-inducing IFN-β dependent, MyD88 independent).
The inhibitory effect of TLR2 was not dependent on new protein synthesis
or intercellular signaling. IL-1R-associated kinase 1 (IRAK1) was
depleted rapidly (within 10 min) by TLR2 agonist, but not until later
(e.g., 2 h) by TLR9 agonist. Because IRAK1 is required for
TLR7/9-induced IFN-I production, we propose that TLR2 signaling induces
rapid depletion of IRAK1, which impairs IFN-I induction by TLR7/9.
This novel mechanism, whereby TLR2 inhibits IFN-I induction by TLR7/9,
may shape immune responses to microbes that express ligands for both
TLR2 and TLR7/TLR9, or responses to bacteria/virus coinfection.”
The Stelera and Humira and other mab (monoclonal antibody) commercials
all seen them. They warn particularly against fungal infections,
against taking immune suppressing drugs like steroids, and that there is
a risk of Lymphoma. Well, what causes Lymphoma?
600 articles. Could be a thing. A thing like, you know the Chronic
Fatigue Syndrome patients who ended up with cancer, and who were then
treated with Rituximab and to-everyone’s-surprise-except-us…
is so convinced LYMErix causes immunosuppression he proposes to use it
in combination with a virus for an inhalation form something we proposed
years ago, given the pandemic flu of 1918 killed people due to the
secondary infection, the mycobacteria, or flumonia. It only killed
healthy people, remember, people with strong immune responses.
Therefore, he thinks it could be an inoculum or a tolerizer against the
serious septic shock event (but in the lungs) that results in death or
near death for the post-sepsis survivors of Lyme and LYMErix:
lipidation/processing reaction has been described for the intact OspA
gene of B. burgdorferi. The primary translation product of the
full-length B. burgdorferi OspA gene contains a hydrophobic N-terminal
sequence, of 16 amino acids, which is a substrate for the attachment of
a diacyl glyceryl to the sulflhydryl side chain of the adjacent cysteine
(Cys) residue (at position 17). Following this attachment, cleavage by
signal peptidase II and the attachment of a third fatty acid to the
N-terminus occurs. The completed lipid moiety, a
tripalmitoyl-S-glycerylcysteine modification, is termed Pam3Cys
(or is sometimes referred to herein as Pam(3)Cys or Pam3Cys). It has
been suggested that the lipid modification allows membrane localization
of proteins, with polypeptide portions exposed as immune targets. In
addition to serving as targets for the immune response, Pam3Cys-modified
proteins, such as OspA, have been reported to act as potent inflammatory
stimulants though the toll-like 2 receptor mechanism (TLR2).
Dattwyler says OspA is Pam3Cys and is a TLR2 agonist. So far, he is the
only one who has openly admitted LYMErix never could have been an
injectable vaccine. Or said what it was. HHS.gov claims to not know.
Yale says they do not know what OspA is (it was their vaccine, LYMErix),
the CDC said they do not know what OspA is, Paul Auwaerter said he does
not know what OspA is, NIH Director Francis Collins did not know, NIAID
director Anthony Fauci did not know, and IDSA refused to reply to our
emails or phone calls.
take this here vaccine. We don’t know what it, OspA, is. And just about no one
has this disease it prevents. And when they do, like Wormser and Klemper
said, the people only have arthritis and no other symptoms.
”Thanks and have a nice day.
”--- CDC, IDSA, Yale, et al.”
It being empirically
observed that Lyme helps activate EBV:
Interaction of Borrelia
burgdorferi sensu lato with Epstein-Barr virus
in lymphoblastoid cells.
”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.”
It being empirically observed that the Lyme Criminals observed that Lyme
Borrelia burgdorferi-induced tolerance as a model of persistence
Here they are citing it:
(Auwaerter, Fish, Krause, Radolf)
Mario Philipp (Tulane) has for years said
OspA was associated with the production of the immunosuppressive
cytokine, IL-10 (this was mentioned to the FDA by Dickson, Jan 31, 2001)
The latest one is this:
”It has been
established that interleukin-10 (IL-10)
inhibits inflammatory cytokines produced by macrophages in response to
Borrelia burgdorferi or its lipoproteins.
The mechanism by which IL-10 exerts
this anti-inflammatory effect is still unknown. Recent findings indicate
that suppressors of cytokine signaling (SOCS) proteins are induced by
cytokines and Toll-like receptor (TLR)-mediated stimuli, and in turn
they can down-regulate cytokine and TLR signaling in macrophages.
Because it is known that SOCS are induced by IL-10 and
that B. burgdorferi and its lipoproteins most likely interact via TLR2
or the heterodimers TLR2/1 and/or TLR2/6, we hypothesized that SOCS are
induced by IL-10 and
B. burgdorferi and its lipoproteins in macrophages and that SOCS may
mediate the inhibition by IL-10 of
concomitantly elicited cytokines. We report here that mouse J774
macrophages incubated with IL-10 and
added B. burgdorferi spirochetes (freeze-thawed, live, or sonicated) or
lipidated outer surface protein A (L-OspA)
augmented their SOCS1/SOCS3 mRNA and protein expression, with SOCS3
being more abundant. Pam(3)Cys, a synthetic lipopeptide, also induced
SOCS1/SOCS3 expression under these conditions, but unlipidated OspA was
ineffective. Neither endogenous IL-10 nor
the translation inhibitor cycloheximide blocked SOCS1/SOCS3 induction by
B. burgdorferi and its lipoproteins, indicating that the expression of
other genes is not required. This temporally correlated with the IL-10-mediated
inhibition of the inflammatory cytokines IL-1beta, IL-6, IL-12p40,
IL-18, and tumor necrosis factor alpha. Our data are evidence to suggest
that expression of SOCS is part of the mechanism of IL-10-mediated
inhibition of inflammatory cytokines elicited by B. burgdorferi and its
At the same time,
Epstein-Barr is known to have a human homolog of IL-10. To review, EBV
has a mimic of the human BCL2, anti-apoptosis gene, a human homolog of
human interleuken 10, and as you have seen in this report, Epstein-Barr
downregulates the MHC or antigen-presenting cells and may be
antibody-negative or seronegative in active disease. These could be 3
reasons EBV contributes to so many cancers – in the Subimmune Class of
diseases -, as well as its well-known association to Autoimmune diseases
(Great Imitator ones, like MS and Lupus and even some evidence that EBV
is associated with Rheumatoid arthritis – search PubMed using RA and DNA
and EBV and not antibodies).
Since this is such
an important topic, how do fungal antigens activate IL-10 and what role
does such a phenomenon cause disease should be studied:
In the next topic,
THE LIST, several of those authors show mechanisms by which fungal
antigens suppress the immune response, such as Harding and Medvedev.
We, ActionLyme and the Society for Advancement of Scientific
Hermeneutics (SASH), have been reporting this phenomenon starting in
early 2004, when we discovered lipoproteins like LYMErix inhibit
apoptosis – making it reminiscent of what BCL2 class molecules do, and
that “EBV-immortalized B cells” is basically the same thing Duray saw in
the cerebral spinal fluid of chronic neurologic Lyme victims.
Since the whistle was blown at the FDA (mentioning Philipp and IL-10 and
Dattwyler and his “Inhibition of NK cell activity” as shown above, from
exposure to borrelial lipids) in January, 2001:
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf , the
question has been for us, what causes this synergy? We know from
Baumgarth and Barthold (THE LIST) and others, that Borrelia live in B
cells and so does Epstein-Barr, and they both prefer the lymph nodes.
We know that the sticky Pam3Cys molecules adhere to intracellular
components membranes, including mitochondria (CDC even says so, as you
have seen in this report).
THE LIST: Here
we have compiled a list of researchers who say and show that something
like OspA never could have been a vaccine, as a TLR2/1-agonist, causing
immunosuppression (observed and mechanisms):
be about spirochetes and biofilms and co-infections (Oh, My!) if
LYMErix vaccination caused the exact same systemic and neurologic
disease as Lyme. These are scientists who know what they are talking
about regarding Lyme/spirochetes and OspA as immunosuppressive.
Notice that none of
the Lyme "non-profits" tell you what Lyme and Lyme cryme is all about.
They do not want anything to change. They are happy about all the
people who die from Lyme disease as long as their "CEOs" make several
hundred thousand dollars a year for doing nothing but being blowhard
We will be attacked
for this report as we always are; people will say this is “So-and-So’s
science,” when it is no science the ActionLyme and SASH groups have
themselves discovered in a lab and reported in the journals. We welcome
all such comments on the science to be directed towards the authors of
all of these reports. We have even provided a form letter for the
self-alleged Lyme activists who “help people” to send to those
researchers at the end of this summary of the science.
NIH's Martin and Marques
NIH's "Lyme and MS" Division find that OspA-ish lipopropteins shed by
borrelia all the time cause
humoral immunosuppression with brain inflammation)
Justin Radolf on what else has OspA-sorta in it:
Radolf saying OspA causes immunosuppression:
Ray Dattwyler, et al (SUNY-SB)
Here is the form letter for the
anti-science rebuttal-ists associated with ILADS.org and the fake
non-profits like lymedisease.org, NatCapLyme, “MayDay,” etc.
We the undersigned take issue with your racist, bully, “science”
and find it offensive. Rather than using our tax dollars for
your fancy big-word-saying (we have read this hundreds of times
and we still don't get it, which means you are a bully), kindly
say words like “awareness” and “support,” and talk about how
famous you are for giving referrals to LLMDs.
How in the world can we advance our causes and raise money for
Lyme research, cars, misc. expenses, restaurants, hairdos, and
travel to protest events and for signs that say, “IDSA you’re
bad, do your homework,” etc., when you are sowing all this
confusion with words no one understands.
Everyone is entitled to their opinion. Ours is equal to yours.
To Wit: NASA has asked us to advise on rocket propulsion, and
General Motors consults with us on many other important matters
regarding how cars can move apparently by themselves on the
roads and this is well-known. We have spoken in front of
Congress about how we speak in front of Congress, many times.
You may frame a copy of this if you like since it contains our
Oh, and you need a translator.
Dedicated to Chelsea Hildebrand and the other young people who
have lost their lives to Lyme.