"It's the perfect
stealth pathogen (means: no antibodies) that causes MS, Lupus,
excruciating headaches, Chronic Fatigue Syndrome, ALS, stroke,
dementia, etc," says a physician associated with Department of Energy,
Brookhaven, Long Island, Uconn, Yale, the
NIH, Allen Steere, etc,... And spirochetes for 100 years have been known
to target lymph nodes and destroy B cell germinal centers, permanently -
irreversibly. Go ahead and use PubMed and search for spirochetes and
lymph nodes (You
can do it!), to verify.
And while the CDC admits to 300,000
cases of "Lyme disease" annually, the falsified
Dearborn case definition ("only an HLA-linked hypersensitivity or
arthritis in a knee response") means only 15% of the cases are reportable,
which means there 2 million Lyme infection cases a year, half of whom
remain disabled (UCSF). That means there are 1 million
new cases of disability per year in America alone, and an untold number in
the greater world. The cryme of falsifying the disease definition and
description by CDC officers Alan Barbour and Barbara Johnson
has never been prosecuted because
this is America - Land of Oppression and Abuse, that jails and tortures
whistleblowers. The CDC claims the cyst or spheroplast form of
Borreliae are not viable, while
in 1964 wrote instructions for freeze-drying
your borrelia for later use as intact spirochetes (weaponizing).
And while all of this is
easily discoverable, not one single "MD" in America or any staff of the CDC
or NIH or any medical society will admit to it all publicly. None will
tell you that the OspA/LYMErix vaccine not only never prevented spirochetes
in any animal, it is the same fungal endotoxin that is responsible for
ruining the immune system and causing
post-sepsis syndrome, which is the real name and definition of Chronic
Fatigue Syndrome/ME or "Chronic Lyme." Certainly no "LLMDs" talk about
the mechanisms by which spirochetes cause disease or explain to you why
LYMErix, alone, caused the chronic, irreversible illness, with the
secondary, opportunistic infections, such as Candida, other fungi,
mycoplasma, etc., and especially the reactivated herpes viruses that are
ACTUALLY responsible for the MS, Lupus, etc outcomes.
Do they? And how
many "MDs" in America specialize in Infectious Diseases? You can see,
they're worthless. None even ask how LYMErix could have caused a "multi-system
disease indistinguishable from later presentations of Lyme disease"
- Mayo Clinic's former employee, David Persing.
Remember, people: The LAST thing you want to be known as
or remembered as, is as a COWARD.
Cowards are revolting, repulsive, disgusting, and grotesque. They are
the very lowest life forms. Even bathroom slime has more integrity
because it does not willingly try to sell itself as perfume or scented
body-wash. I am talking mainly about people with "MD" after their
Think of how many "doctors" were wrong about everything, how they did not
know about fungal-viral synergy, about how
fungal antigens cause immunosuppression, how this immunosuppression
plays a role in the Autism pandemic (kids
are GETTING the viruses, and not the "protection"). Think about
how in the last 10-15 years
psychiatry was debunked as hocus-pocus and how BigPharma is
worried that no one wants to be a psychiatrist out of "medical school" any
more (so who will push their bogus, brain-damaging "drugs?").
These facts - these truths we bring you that you can verify independently -,
very clearly have zero to do with people who have "MD" after their names.
"Doctors" are useless, all around. Their function is limited to
writing drug prescriptions, but most do not know what goes into a validating
a lab test, or are aware of the role of insurance companies writing
diagnostic and treatment "guidelines." Most "doctors" don't even know
MS and Lupus are caused by some combination of the herpesviruses, as are
most other illnesses and most cancers. They don't even know they can
use PubMed to search for this data and these associations!!
Now, what causes such stupidity? Arrogance, which is the result of
cowardice. 'The fear of appearing to be "less-than" the other guy.
How in the world could Lyme be a "Great
Imitator" causing all kinds of outcomes like ALS,
Lupus (Yale used to have a Lyme and
Lupus clinic, now Yale says Lupus is most likely due to Epstein-Barr),
and multiple sclerosis (NIH had an
MS-and-Lyme clinic, until they found out the fungal OspA or LYMErix vaccine
caused the MS outcome of Lyme - also due to reactivated latent herpesviruses),
cancer, ME/CFS, stroke, etc, if
spirochetes were not screwing up peoples' immune systems, permanently?
We patients have to explain and show this
data to you, because there really are no "doctors" in America.
Think about it. All there are, are sleazebags, whores and greedy
douches. And they're all STUPID - which is the result of their
Pity. It's a pity that nowadays, we victims who figured out this 500
year old mystery of the Great Imitator,
are treated like trash across the board, by the US Government and all the
people in America with "MD" after their names. That's the best America
can do. Torture their victims. Think about it.
Who's ever thanked us? Who's ever admitted we were right, about Lyme
and OspA, formally?
NO ONE. None have the balls.
In America, in the near future - what's left of us when the rest
of the world abandons us to environmental and financial disasters (when
the rest of the world realizes they do not need us or our petrodollar
Monopoly money)-, the ones remembered for courage will not include any
"doctors." There will be no former "public servants," or cops, or
jail guards - no govt employees or sluts for the new world order - of
any kind, among us. No bureaucrats, no CEOs, no one who ever wore
a uniform or had a state or federal govt badge of any sort.
No employee of the military at any level.
Not a single person whose livelihood was dependent upon inflicting
suffering on others will be among us.
Why doesn't the CDC want you to know that Post-Lyme and
Chronic Fatigue/ME is really Post-SEPSIS-Syndrome?
Because the mechanisms of illness - acquired immune deficiency
particularly from the likes of TLR2-agonists or
fungal-antigen-bearing/shedding infections or even contamination of
childhood vaccines with the likes of a fungal antigen like LYMErix -, are
the same in Post-Sepsis and Vaccine-Damage Autism.
The reason the babies are actually
GETTING those live, attenuated, brain-tropic viruses from the vaccine vials
is due to immunosuppression and/or contamination causing the
The reason someone came up with the idea for a Rubella vaccine in the first
place was because Rubella causes the
neurodevelopmental brain damage we call
"Autism." Think about it. The kids are GETTING the VIRUSES and
they're all brain-tropic.
The Infectious Diseases Society of America says these vaccines are given too
many, too young, and are not properly vetted -
please see for
yourself, their exact language; the adverse events are a lot like sepsis
http://www.vimeo.com/truthcures <<< See all 3 videos, they are all
related, and you'll see - finally - that this is simple, and regarding
models of disease you know about and have seen before (dual infections and
The Autism pandemic is the result of babies getting the actual brain-tropic viruses that are in the vaccine
vials, either because those children are immunosuppressed or because
the vaccines are contaminated with the likes of fungal antigens like LYMErix.
Yes, the *ENTIRE* HHS.gov is that stupid. Add to that, everyone with
"MD" after their names. YES, ALL OF THEM are THAT
You have seen the MRIs of the heads of the ZIKA
brain damaged children in the news. The scientific literature says
Borna virus is the model for the "neurodevelopmental brain damage" we call
IDSA says vaccines are given too many, and too young, and none of them are
properly vetted, and this was true since the 1970s. The scientific
literature on those MMR qualifications shows those children were never
followed longer than a few days. The MMR vaccine qualifications were
even more criminal than the LYMErix stunt. Go look for yourself on
Pubmed. You'll do it if you give a sh*t about other people. But
if you don't, you won't bother.
It is the same with activism, in general.
If you are looking for the very simplest explainer
on the Lyme crymes, see the RICO
complaint already filed with the USDOJ. I was talking to
lawyers after all, so I had to really dumb it down.
Cryme Disease, the movie:
The fungal-ish OspA vaccine caused the
same post-sepsis, immunosuppression
disease as the one thrown out of the case definition at
Steere used a seronegative Lyme assay to assess chronic neuro Lyme, a
disease he later falsified and now claims
Steere recently claimed in a radio interview that (June 14, 2016) he
never knew Lyme caused a chronic neuro outcome. The CDC would
like to throw Allen Steere under the bus,... and Steere is trying to avoid
being thrown under the bus. Obviously not happening.
IF you are the kind of person
who wants a simple one-liner, single model, single, simple general idea
to explain something, this would be it (Dattwyler and Fauci, below).
OspA is a known immune-suppressor, not a "vaccine."
We are not about to prove that OspA is a triacyl lipoprotein also called a
basic Pam3Cys molecule type, is fungal, is a more serious endotoxin than
LPS, a TLR2/TLR1 agonist, and that other spirochetal lipoproteins are
triacylated, if not Pam3Cys exactly. We can assume anyone knows how to use
the National Library of Medicine or else the United States and European
patent databases or even just pull the one arm of one-armed information
bandit named Google and discover that, for instance, State University of New
York, Stony Brook’s, Raymond Dattwyler has a patent for an inhalation form
It, the OspA in Dattwyler’s OspA patent, is intended to attenuate (lessen,
or dampen) any suffocating inflammatory response people might suffer from
the likes of the dual infections of, for example, influenza and pneumonia,
such as what happened in the 1918 Spanish Flu epidemic [FAUCI]. During that
pandemic, the healthy people succumbed to the secondary pneumonia. That is,
the strong, mucus-y inflammatory response is what killed 20+ million people
back then. They choked to death. (One infection invites another, this is
Let’s just go ahead and have a look
at what Raymond Dattwyler says about OspA as Pam3Cys and how inhaling a
fungal antigen like this, OspA or Pam3Cys or a triacyl lipoprotein might
tolerize you against the deadly pneumonia part of Pandemic
LIVE BACTERIAL VACCINE
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).
NIAID's Chief Anthony Fauci on the 'monia part of 1918
being what causes people to choke to death -- it was inflammatory response
in the lungs to the fungal-ish pneumonia:
Predominant role of bacterial pneumonia as a cause of death in pandemic influenza:
implications for pandemicinfluenza preparedness.
Despite the availability of published data on 4 pandemics that
have occurred over the past 120 years, there is little modern
information on the causes of death associated with influenza pandemics.
relevant information from the most recent influenza pandemic
that occurred during the era prior to the use of antibiotics,
the 1918-1919 "Spanish flu"
pandemic. We examined lung tissue sections obtained during 58
autopsies and reviewed pathologic and bacteriologic data from
109 published autopsy series that described 8398 individual
postmortem samples we examined from people who died of influenza during
1918-1919 uniformly exhibited severe changes indicative of
bacterial pneumonia. Bacteriologic and histopathologic results
from published autopsy series clearly and consistently
implicated secondary bacterial pneumonia caused by common upper
respiratory-tract bacteria in most influenza fatalities.
The majority of deaths in the
1918-1919 influenza pandemic
likely resulted directly from secondary bacterial pneumonia
caused by common upper respiratory-tract bacteria. Less
substantial data from the subsequent 1957 and 1968 pandemics are
consistent with these findings. If severe pandemic influenza is
largely a problem of viral-bacterial copathogenesis, pandemic
planning needs to go beyond addressing the viral cause alone
(e.g., influenza vaccines
and antiviral drugs). Prevention, diagnosis, prophylaxis, and
treatment of secondary bacterial pneumonia, as well as
stockpiling of antibiotics and bacterial vaccines, should also
be high priorities for pandemic planning.
So, if OspA was obviously something that causes
too-much inflammation-and-then-immunosuppression (endotoxin tolerance), it
could not have been a vaccine. And if OspA was not a vaccine, then
certain people not only lied it onto the market, they falsified the Dearborn
case definition to leave out the 85% of us who do not have a genetic
background for a tendency to have Rheumatoid Arthritis (HLAs).
So, IF you are the kind of person who
wants a simple one-liner, single model, single, general idea to explain
something, this would be it. OspA is a known immune-suppressor, not a
"vaccine." It does the OPPOSITE of what vaccines are intended to do,
which is produce antibodies. It is a more severe endotoxin than LPS.
"TLR2 mediates inflammatory responses to a wide variety of lipidated
microbial components, including bacterial lipoproteins, atypical
lipopolysaccharides, and lipomannans (26–28).
Among these microbial agonists,
bacterial lipoproteins are by far the most potent
See the rest of the videos here:
Crymes on Vimeo
ONLY IN the United States of
you see the likes of the
Edward McSweegan and
Durland Fish, not knowing
spirochetes were their own
phylum (are not regular "bacteria"), are relapsing fever
organisms, that the
nature of the relapse
was antigenic variation (vaccines would do no good), and that the
McSweegan-Fish gang never even asked what
(fungal, TLR2/1 agonist, causes permanent immunosuppression, never could have been a
vaccine). The CDC deployed the stupid
and cowardly Allen Steere who
Rheumatology to avoid VietNam
(there are no old ladies who need aspirin among deployed US combat forces),
probably because he was known to be too stupid to ask any questions about
ticks or spirochetes.
What is the simplest way to explain that the
ALDF dot com / Yale / CDC Lyme cabal
threw out of the Dearborn, "2-tiered" "case definition" the
very same disabling, chronic neurologic, "New
Great Imitator" disease that was caused by the
fungal toxin, Pam3Cys or OspA?
They knew OspA vaccination causes
neurologic, immunosuppression disease before the Oct 1994
Dearborn, Michigan fake consensus conference ever took place (chronology
In order for it to be prosecuted as
criminal case you have to show they knew ahead of time that there was
this problem with their "vaccine" choice and that they CHANGED the
testing definition after that, such as to leave out the chronic
neurologic Lyme definition - the very disease caused by the fungal OspA vaccines.
This is from June, 1993, by Alan Barbour and
They said this ˄ BEFORE the CDC's Dearborn-"Let's-Leave-Out-the-Chronic-Neurologic-Form-of-the-Disease-Which-Is-Also-Caused-by-OspA-Injection-Alone"
fake consensus conference took place (Oct, 1994). So, these
criminals would have known there was a problem with OspA injections making
people sick. After all, OspA is a fungal endotoxin, TLR2/1-agonist.
The current, 1994, "Dearborn" case definition only detects the 15% of cases, only the late-, HLA-linked- arthritis cases, no early cases, and then
these CDC (vaccine patent holding) criminals say
this late manifestation needs no treatment. The truth is that chronic
neurologic disease is mainly caused by immunosuppression, reactivated
Epstein-Barr and cross tolerance to other infections, or, technically, is
post-sepsis syndrome or a kind of a B cell AIDS (see the
In this criminal case, you have to show to the
DOJ that they
diagnostic criteria from an older one that allowed more people to be
1990 CDC version).
If the DOJ does not respond, clearly this was a bioweapon accident of some
The circumstantial scientific,
epidemiological evidence from
Plum Island as the original outbreak area says so. (Do
the Russians know by now? They knew in 2006. The Chinese, a year
later. Site stats.)
The US press cant handle it, and no
one has ever written about it in any book.
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.
And it turns out that Lyme and Syphilis as "Great Imitators" are
really Great Detonators of latent viruses and general immunosuppression -
also known as post-sepsis syndrome. It turns out that Pam3Cys (OspA),
a triacyl lipopeptide, is a functional mimic of E. coli's Lipid A, a serious
fungal (TLR2/1-agonist) ENDOTOXIN. Think about that. The CDC
wanted to inject everyone with several blobs of bathroom scum. And
that's what happens with a tick bite, too.
"For months after infection, those germinal centers fail to produce the
specific cells — memory B cells and antibody-producing plasma cells —
that are crucial for producing lasting immunity. In effect, the bacteria
prevent the animal’s immune system from forming a “memory” of the
invading bacteria and launching a protective immune response against
"The researchers found that following Borrelia
this process even prevented induction of strong immune responses
to an influenza infection."
Cadavid on Septic Spirochetes:
"Finally, spirochetal lipoproteins have more prominent
pro-inflammatory effects compared to other bacterial lipoproteins and
synthetic lipopeptides (28)."
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
Gary Wormser on OspA causing immunosuppression (which means it was the
opposite of a "vaccine"):
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.”
Donald H. Marks - an OspA vaccine trial administrator -
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's VooDoo Somatoformia – as well as cancer. Cancer
is in the Subimmune class, at the other end of the immunity spectrum
from Autoimmunity. 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 in these chronic, waste-basket
diseases. 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
5.) 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....”
Who else says OspA alone is responsible for the immunosuppression with brain inflammation that is characteristic of "Chronic Lyme?"
6.) THE NIH (Martin and Marques):
burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral
blood monocytes but differentially regulates HLA-class II expression
spirochete Borrelia burgdorferi is the agent of Lyme disease, which causes
central nervous system manifestations in up to 20% of patients. We
investigated the response of human brain microglial cells, glial
progenitors, neurons, astrocytes, as well as peripheral blood monocytes to
stimulation with B. burgdorferi. We used oligoarrays to detect changes in
the expression of genes important for shaping adaptive and innate immune
responses. We found that stimulation with B. burgdorferi lysate increased
the expression of Toll-like receptors (TLRs) 1 and 2 in all cell types
except neurons. However, despite similarities in global gene profiles of
monocytes and microglia, only microglial cells responded to the stimulation
with a robust increase in HLA-DR, HLA-DQ, and also coexpressed CD11-c, a
dendritic cell marker. In contrast, a large number of HLA-related
molecules were repressed at both the RNA and the protein levels in
stimulated monocytes, whereas secretion of IL-10 and TNF-alpha was strongly
induced. 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.
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
Luft in 1989, in IDSA's own "journal," saying "treatment
fails in half the cases." And the OspA vaccine caused the same
systemic disease, say the crooks, themselves. See the
Occam's Razor report for who says so.
Steere was at this 1994 FDA meeting:
DATTWYLER: "-- the ones that (sic) failed to mount a vigrous immune response tended to do worse. So, there is an inverse correlation between the degree of serologic response and the outcome.
"So, individuals with a poor immune response tend to have worse disease."
1994 FDA Meeting Transcripts where Ray Dattwyler tells the FDA Vaccine Committee that the
patients with low or no antibodies are the sickest: http://www.actionlyme.org/Dattwyler_Luft_DNA_in_CSF.htm
Ray Dattwyler (SUNY-SB) says in 1988 that exposure to Lyme or even just its supernatants (OspA-like molecules) turn off the NK cell activity (or is immunosuppressive):
"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 organism.
"The inhibition is directly attributable to the organism or its supernatants (data not shown)."
From: Modulation of natural killer cell activity by Borrelia
Department of Pathology, State University of New York, Stony
PMID: 3056196 [PubMed - indexed for
Ann N Y Acad Sci. 1988;539:103-11.
Dattwyler on Seronegative Lyme and how that is like fungal diseases:
DOWNLOAD THE FULL TEXT of Dattwyler talking about seronegative, neuroLyme,
Lyme is like Jeopardy! Ask the right question: "Something that
causes a 'multi-system disease' and is
IDSA's own 'New Great Imitator.'"
The answer is, "What is OspA?"
UCSF says Lyme and LYMErix-Disease are a diseases of
immunosuppression, and they say that half the Lyme/tick bite victims
remain ill and are not cured with antibiotics
Feb 12, 2016:
“Early Lyme disease prior to antibiotic therapy was characterized by marked
upregulation of Toll-like receptor signaling but lack of activation of
the inflammatory T-cell apoptotic and B-cell developmental pathways seen in
other acute infectious syndromes,” wrote the study’s authors. “Six
months after completion of therapy, Lyme disease patients were found to have
31 to 60% of their pathways in common with three different immune-mediated
chronic diseases. No differential gene expression signature was observed
between Lyme disease patients with resolved illness to those with persistent
symptoms at six months post-treatment.”
See more below from UC Davis, and in the
Occam's Razor report. The Great
Imitator is EBV, the Great Initiator is the fungal antigen OspA, shed by
spirochetes - their own phylum, and not regular "bacteria" -
on blebs, says the NIH.
America is a really stupid country, when you consider that nearly every
disease is an outcome of the first immune disordered step - inhibition of
apoptosis of infected B cells.
Look at the experience of Lewis Bull, East Lyme, CT,
back in the OspA "vaccines" trials days (late 1990s) to see exactly what
these evil bastards of the CDC (Barbour, Johnson, Steere) had planned from
the beginning to do with LYMErix - "multisystem
(read: "sepsis")," Chronic Fatigue Syndrome-like - outcomes.
'Says it all.
University of California, Davis, says the
Steere, Gary Wormser, Edward McSweegan, et al
must be lying their faces off:
and LYMErix cause permanent immunosuppression or is like a B cell AIDS.
Lyme is not an "inflammatory," "autoimmune disease," it is the
Great Initiator of latent viruses, as
a fungal antigen shedder, SPIROCHETE (its own phylum). Fungal antigens
like triacyl lipopeptides (OspA) have always been known to cause
immunosuppression. The complete opposite of an "autoimmune" or
"inflammatory" disease. The only
will be signs of nerve and brain degradation in the cerebral spinal fluid;
no antibodies in the blood.
exactly is OspA?
“I did not get the vaccine so this does not concern me.” Oh,
yes, you got the vaccine. Everyone with Lyme got LYMErix. Here is what
LYMErix is, and how this "vaccine-was-the-disease" works:
This is image is of Pam3Cys
or OspA. What is variable is the protein end "("peptide"), but what is
immunogenic (seen as an invader to the immune system) are the fatty acids or
acyl groups and the very electronegative cysteine core:
Pam3Cys is 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.
Cadavid and the NIH say these shed
vesicles or blebs go to the brain and
In other words, the NIH is saying that thanks to exposure to shed blebs
with TLR2/1 agonists like OspA on them, the HLA molecules will be
downregulated and that you will make no antibodies. This
mechanism is mimicked elsewhere, in other fungal diseases models. It
is also CALLED endotoxin tolerance.
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.
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