"The Science Escapes Us" - IDSA = Plum Stupid
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Mort Zuckerman
Oct 15, 2010, 12:16:00 PM10/15/10
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Subject: "The Science Escapes Us" - IDSA = Plum Stupid
Date: Oct 15, 2010 12:08 PM
Poor Sam Donta:
http://www.nature.com/news/2010/101014/full/news.2010.542.html?s=news_rss
Still dealin wid IDSA's lying tards.
I propose a new model
based on the IDSA evidence:
http://www.actionlyme.org/20101014_PLUMSTUPID.doc
http://groups.google.com/group/scilyme2/browse_thread/thread/3cdbfda70dcbe34?hl=en
Dx: “We Don’t Know What You Have (the science escapes us)”
Rx: “Put da Lyme in da coconut, den you feel betta”
Thanks and Have a Nice Day ☺
-- Yale, CDC & Big KP
Now that it has been proven (1, 2, 3), re-proven (4, 5) and re-re-
proven (6, 7) once again and in recent history, that indeed “Lyme
Disease (8, 9)” is a chronic, un-eradicable infection primarily of the
central nervous system, formerly, formally serologically known as
Relapsing Fever (10, 11, 12), and that long term intravenous
antibiotic treatment generally results in relief-but-then-relapse (3,
5), one wonders, “Where do we go from here?”
The first order of business is the clarification of falsified antibody
testing for “Lyme Disease.”
In 1992 Allen Steere went to Germany, with, as he claimed,
“The group 1 strain of B. burgdorferi, G39/40, used in this study and
in the previous study of US patients was isolated from an Ixodes
damini tick in Guilford, Connecticut 921). The group 2 strain, FRG
[Federal Republic of Germany], was isolated from Ixodes ricinus near
Cologne (21). The group 3 strain, IP3, was isolated from Ixodes
persulcatus near Leningrad (23). All three strains used in this study
were high passage isolates, which were classified by Richard Marconi
(Rocky Mountain Laboratory, Hamilton, MT) using 16S ribosomal RNA
sequence determination as described (11, 24). The recombinant
preparations of OspA and OspB used in this study were purified
maltose-
binding protein-Osp fusion proteins derived from group 1 strain B31
(25). The fusion proteins contained the full-length OspA or OspB
sequence without the lipid moiety or the signal sequence -" illegal,
plasmid-dropping, antigen-and-antibody dropping, “high passage
strains” and OspA and B with no lipids attached (not likely to produce
antibodies), resulting in the new, 1994, Centers for Disease Control
(CDC), “case definition” of “Lyme Disease” (8, 9).
At the Dearborn, MI, Consensus Conference regarding the
“standardization” of Western Blotting for “Lyme Disease,” the invited
labs assessed Steere’s scientifically fraudulent proposal for a new
diagnostic standard for Lyme from 8% to 28% accurate (detected % of
known cases).
Independently, Gary Wormser at New York Medical College (NYMC)
assessed the Steere proposal in 1993 as: “Overall, 51 of 59 (86%)
convalescent-phase serum specimens were reactive by IB, 35 of which
were interpreted as positive: 26 based on IgM criteria, 8 based on
both IgG and IgM criteria, and 1 based on IgG criteria,” or 8 out of
59 patients were positive for Steere’s Dearborn proposal in IgG. Or,
15% accurate (13).
With this Steere/Germany standard the two OspA vaccines (ImmuLyme and
LYMErix) were allegedly assessed for safety and efficacy (14,15),
which meant 85% of known cases would be thrown out of consideration,
which, hypothetically, was the game plan all along. Later we found
out that the Western Blots in OspA vaccinated people were not readable
due to multiple reactive species or generalized darkening of the
Western Blot strips, rendering any potential bands that would
demonstrate illness/Lyme breakthrough in vaccinated persons,
undecipherable (16, 17).
That leaves us with the years 1992 to the present, almost 2011,
completely wasted.
In terms of research dollar-years and lives we’re now back at Square
One, wondering what is to be done with the testing for “Lyme Disease,”
and even more importantly, what do we call a “case” of “Lyme Disease”
once the millions of people who were misdiagnosed in the Lyme-OspA
scam process and have gone on to chronic illness?
We know from scientifically valid biomarkers of illness
(scientifically valid in the sense that valid methods were used to
assess the markers or signs that a person suffered real illness or
health irregularities), the true and correct DNA and RNA methods to
determine chronic infections status, and especially the prominent
question of “seronegativity” being associated with the greatest
apparent suffering. In 1994 at the meeting of the Food and Drug
Administration regarding potential Lyme vaccines, Raymond Dattwyler
(SUNY-Stony Brook) noted that “the ones that failed to mount a
vigorous immune response tended to do worse, clinically. So, there was
an inverse correlation between the degree of serologic response and
the outcome.”
In 2005, Mark Klempner (Boston University) and Gary Wormser (NYMC)
reported that the arthritis cases and seroposivity tended to be
associated with Allen Steere’s alleged haplotypes over which
SmithKline was sued in a class action after the Yale-owned LYMErix
trial (18): “Patients generally feel well aside from their arthritis
symptoms.”
In 1988, Raymond Dattwyler published that he wondered about
seronegative “Lyme” and the suppression of NK cells (19), and he
wondered enough to come up with a new assay to determine if exposure
to Lyme and a lowered immunological response (20). His new assay was
called “Seronegative Lyme disease. Dissociation of specific T- and B-
lymphocyte responses to Borrelia burgdorferi.” Later, Allen Steere
used this same seronegative “Lyme” assay and determined that 4/9 of
his lab workers had been exposed to Borrelia (21).
The question was why.
We know from the previous history of Relapsing Fever (before the era
of Allen Steere, et al), that antigenic variation was the nature of
the relapse, and that spirochetes become host- and tissue- adapted.
This meant that persons who had missed the opportunity for early
diagnosis and treatment would not have the Dearborn “case definition”
of “late, OspA-hypersensitivity, specific HLA-linked, Lyme Arthritis”
in “early Lyme,” would be left to his/her peril in finding a competent
MD who had been exposed in pre-medicine undergraduate study to a
course in genetics. These organisms are taxonomically classified by
differences in flagellin. The best way to detect Lyme with antibody
testing is via all-borrelial-specific anti-flagellin antibody
detection, because flagellin is not a variable antigen. The group
who perfected and patented the anti-Borrelia- burgdorferi specific
flagellin method was Yale’s Erol Fikrig and Richard Flavell in 1991
(22, 23). Why this test was not used to assess Fikrig and Flavell’s
OspA vaccine patent, LYMErix, is anyone’s guess.
Regardless of this State of Nonsense (Connecticut), …
People wonder what to make of the serious illness they suffer as a
result of “Lyme” and LYMErix vaccination, which appeared to be similar
(24). In 1995, David Persing and Yale’s Robert Schoen patented a
method wherein they, the winners, would be in receipt of all the
government funding and also a national monopoly on the - as they hoped
and intended - post-OspA-vaccinated United States:
“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…. ” (25, 26). And they,
most of all, would have access to all the potentially patentable
goodies in the national blood with this monopoly on testing.
Further investigations into the outcomes of other lipoprotein/fungal
vaccines revealed a similar outcome to that observed in the un-
reported LYMErix adverse events patients, resulting in the January
2001 FDA hearing on the matter and the class action lawsuits. Adverse
events were only reported to the FDA by the vaccines trails
administrators if they were of the arthritis kind, since “arthritis
only” had become the new “case definition” at the 1994 Dearborn
”conference.” When Dennis Parenti of SmithKline reported that there
were only two neurological adverse events to LYMErix at the 2000 Lyme
Disease Foundation Conference in Hartford, CT, several physicians and
attendees immediately got up and walked out of the conference room,
while the rest groaned.
The functional results of OspA vaccination were, we hypothesize, not
dissimilar from the results of structurally similar vaccine antigens
that are managed by TLR2:
“These results are consistent with a model in which the presence of
the 19-kD protein [of Mycobacteria tuberculosis] has a detrimental
effect on the efficacy of vaccination with live mycobacteria.” (27)
“Synthetic analogs of lipopeptides from Treponema pallidum also
inhibited Ag [antigen] processing.”
(28)
“the immunosuppressive effect is dependent on glycosylated and
acylated 19-kDa lipoprotein [of Mycoplasma tuberculosis] 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 activation. (29)
“Thus, tolerance to LPS and mycobacterial components cannot be
attributed solely to a decrease in TLR/MD-2 expression levels,
suggesting inhibition of expression or function of other signaling
intermediates 2002, Induction of bacterial lipoprotein tolerance is
associated with suppression of toll-like receptor 2 expression.”(30)
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. (31)
And, we know that:
[((2003) Borrelia burgdorferi-induced tolerance as a model of
persistence via immunosuppression.]
“If left untreated, infection with Borrelia burgdorferi sensu lato may
lead to chronic Lyme borreliosis. It is still unknown how this
pathogen manages to persist in the host in the presence of competent
immune cells. It was recently reported that Borrelia suppresses the
host's immune response, thus perhaps preventing the elimination of the
pathogen (I. Diterich, L. Härter, D. Hassler, A. Wendel, and T.
Hartung, Infect. Immun. 69:687-694, 2001). Here, we further
characterize Borrelia-induced immunomodulation in order to develop a
model of this anergy. We observed that the different Borrelia
preparations that we tested, i.e., live, heat-inactivated, and
sonicated Borrelia, could desensitize human blood monocytes, as shown
by attenuated cytokine release upon restimulation with any of the
different preparations. Next, we investigated whether these Borrelia-
specific stimuli render monocytes tolerant, i.e. hyporesponsive,
towards another Toll-like receptor 2 (TLR2) agonist, such as
lipoteichoic acid from gram-positive bacteria, or towards the TLR4
agonist lipopolysaccharide. Cross-tolerance towards all tested stimuli
was induced. Furthermore, using primary bone marrow cells from TLR2-
deficient mice and from mice with a nonfunctional TLR4 (strain C3H/
HeJ), we demonstrated that the TLR2 was required for tolerance
induction by Borrelia, and using neutralizing antibodies, we
identified interleukin-10 as the key mediator involved. Although
peripheral blood mononuclear cells tolerized by Borrelia exhibited
reduced TLR2 and TLR4 mRNA levels, the expression of the respective
proteins on monocytes was not decreased, ruling out the possibility
that tolerance to Borrelia is attributed to a reduced TLR2 expression.
In summary, we characterized tolerance induced by B. burgdorferi,
describing a model of desensitization which might mirror the
immunosuppression recently attributed to the persistence of Borrelia
in immunocompetent hosts”. (32)
“Next, we investigated whether these Borrelia-specific stimuli render
monocytes tolerant, i.e. hyporesponsive, towards another Toll-like
receptor 2 (TLR2) agonist, such as lipoteichoic acid from gram-
positive bacteria, or towards the TLR4 agonist lipopolysaccharide.
Cross-tolerance towards all tested stimuli was induced.”
Epstein-Barr’s activity regarding TLR2:
(2007) Epstein-Barr virus induces MCP-1 secretion by human monocytes
via TLR2.
“Epstein-Barr virus (EBV) is a gammaherpesvirus infecting the majority
of the human adult population in the world. TLR2, a member of the
Toll-
like receptor (TLR) family, has been implicated in the immune
responses to different viruses including members of the herpesvirus
family, such as human cytomegalovirus, herpes simplex virus type 1,
and varicella-zoster virus. In this report, we demonstrate that
infectious and UV-inactivated EBV virions lead to the activation of
NF-
kappaB through TLR2 using HEK293 cells cotransfected with TLR2-
expressing vector along with NF-kappaB-Luc reporter plasmid. NF-kappaB
activation in HEK293-TLR2 cells (HEK293 cells transfected with TLR2)
by EBV was not enhanced by the presence of CD14. The effect of EBV was
abrogated by pretreating HEK293-TLR2 cells with blocking anti-TLR2
antibodies or by preincubating viral particles with neutralizing anti-
EBV antibodies 72A1. In addition, EBV infection of primary human
monocytes induced the release of MCP-1 (monocyte chemotactic protein
1), and the use of small interfering RNA targeting TLR2 significantly
reduced such a chemokine response to EBV. Taken together, these
results indicate that TLR2 may be an important pattern recognition
receptor in the immune response directed against EBV infection.” (33)
And we know that:
“Yale researcher Stephen Barthold, a veterinarian and professor of
comparative medicine who developed the first mouse model of Lyme
disease, studies the expression of B. burgdorferi surface proteins
throughout various stages of the spirochete’s life cycle. He finds
that during the early stages of infection, B. burgdorferi avoids
immune detection by decreasing its expression of surface proteins or
cloaking its expressed surface proteins under a layer of slime. "It's
using some sort of stealth-bomber-type mechanism," he says. Or, using
another diversionary tactic called blebbing, the spirochete can pinch
off bits of its membrane in order to release its surface proteins
Explains Barbour: "It’s like a bacterial Star Wars defense program,"
in which released surface proteins might intercept incoming host
antibodies keeping the spirochete safe from immunological
attack.” (34)
which is what we call the auto-vaccination with OspA - the immune-
suppressing fungal antigen, known also, structurally, as Pam3Cys
(35).
In short, “Lyme Disease” is chronic and seronegative because it is
chronic, or chronically shedding variable (Relapsing Fever-esque)
outer surface lipoproteins like OspA, or, as Alan Barbour states in
his US Patent #6,719,983:
“2.1 Methods of Treatment
”An important aspect of the invention is the recognition that Borrelia
VMP-like sequences recombine at the vls site, with the result that
antigenic variation is virtually limitless. Multiclonal populations
therefore can exist in an infected patient so that immunological
defenses are severely tested if not totally overwhelmed. Thus there is
now the opportunity to develop more effective combinations of
immunogens for protection against Borrelia infections or as preventive
inoculations such as in the form of cocktails of multiple antigenic
variants based on a base series of combinatorial VMP-like antigens.”
“antigenic variation is virtually limitless. Multiclonal populations
therefore can exist in an infected patient so that immunological
defenses are severely tested if not totally overwhelmed.”
What are the other functional outcomes of the chronic agonism of TLR2
– the one that manages triacyl lipopeptides like OspA or Pam3Cys that
render the immune system overwhelmed, not to mention persons late in
the disease who do not serologically (antibodies) react to antigen
from spirochetes fresh out of a tick due to antigen variation,… not to
mention the diminution of antibody production due to chronic TLR2
agonism?
Says Paul Duray of the National Cancer Institute and Ft. Detrick
(hint, hint):
"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." (36)
The lymphocytes of these chronic “Lyme” victims look like Epstein-Barr
transformed cells.
In 2003, Hilinska et al report in “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.” (37)
One of the characteristics of chronic neurologic “Lyme” is that it is
called an “aseptic meningitis” (38, 39, 40).
This is, of course, while the German Multiple Sclerosis expert Roland
Martin had been recruited by the National Institute of Health to
research the association between “Lyme” and Multiple Sclerosis.(41,
42). Martin went home once he found out that OspA-induced
immunosuppression was the likelier reason “Lyme” was mistaken for
Multiple Sclerosis or vice versa.
DISCLAIMER: We Lyme victims did not dream up this nonsense. We only
report it.
Could the co-TLR2 agonists (inducing tolerance and a lack of
antibodies) Epstein-Barr and Borreliosis be simply responsible for: “
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?”(36) ?
It is common knowledge that 95% of the adult population in Western
cultures has been exposed to Epstein-Barr and its common similar
herpes viruses. Hypothetically, there is a mouse herpesvirus
(gamma2herpes) that to our knowledge has not been investigated
regarding transmission to other hosts via ticks. We’re not privileged
to know much about what happens on Plum Island. We only know there is
a “Plum Island” strain of mycoplasma, and that Yale’s Durland Fish
experimented with trying to get African Swine Fever virus to “take” to
local hard-bodied ticks at that Not-Bioweapons/Just-Helping laboratory
(43, 44).
However, something that might have been discovered 10 or 15 years
sooner had not certain persons associated with Yale and New York
Medical College made an agreement with Kaiser-Permanente (45) to sell
a vaccine against a disease they suddenly decided doesn’t actually
cause any illness (and the world is flat, the moon made of green
cheese, and all hospitals are going to become brothels because it’s
cheaper and therefore cost-effective to deploy self-alleged MDs who
never perform any scientifically valid rule-outs before making
theoretical diagnostic assumptions based on “projection,” rather than
bog down the likes of the actual laboratories with the fancy machinery
that serves no purpose other than to take up space and look shiny,
just like the misguided folks at Silly NASA…).
“Epstein-Barr virus (EBV) efficiently drives proliferation of human
primary B cells in vitro, a process relevant for human diseases such
as infectious mononucleosis and posttransplant lymphoproliferative
disease. Human B-cell proliferation is also driven by ligands of Toll-
like receptors (TLRs), notably viral or bacterial DNA containing
unmethylated CpG dinucleotides, which triggers TLR9. Here we
quantitatively investigated how TLR stimuli influence EBV-driven B-
cell proliferation and expression of effector molecules. CpG DNA
synergistically increased EBV-driven proliferation and transformation,
T-cell costimulatory molecules, and early production of interleukin-6.
CpG DNA alone activated only memory B cells, but CpG DNA enhanced EBV-
mediated transformation of both memory and naive B cells. Ligands for
TLR2 or TLR7/8 or whole bacteria had a weaker but still superadditive
effect on B-cell transformation. Additionally, CpG DNA facilitated the
release of transforming virus by established EBV-infected
lymphoblastoid cell lines. These results suggest that the
proliferation of EBV-infected B cells and their capability to interact
with immune effector cells may be directly influenced by components of
bacteria or other microbes present at the site of infection.--
Toll-like receptor agonists synergistically increase proliferation and
activation of B cells by epstein-barr virus. (46)
We know that “Lyme” is associated with the production of Amyotrophic
Lateral Sclerosis (in 47% of the ALS cases in Lyme-endemic areas) (47)
and Multiple Sclerosis (48). And we know that ALS is associated with
mycoplasmal infection (tolerance to TLR2 agonists), and, MS, and
apparently “Lyme” is associated with Epstein-Barr virus or something
like it (Duray).
We know that 90% of Chronic Fatigue patients found out they had “Lyme
Disease” when finally assessed by a reputable laboratory – one not
like Quest Diagnostics, which uses strain B31, the non-neurotropic,
non-OspC-bearing, non-band-23-producing strain (49). We hypothesize
that since it is known that mycoplasmal infections in the blood
disrupt the osmotic potential in erythrocytes (disrupt the transfer of
oxygen), and metabolism (these things need to be fed, after all) (50,
51), and since there has been reported a high association to
mycoplasmal infections in Chronic Fatigue and Gulf War Illness victims
(52, 53), that the tolerance to TLR2 agonists Lyme/LYMErix results in
tolerance to mycoplasma in the blood (Chronic Fatigue) with no
relative antibody production (28).
“Lyme” also produces a Lupus-like syndrome (54), and recently (and
formerly, formally associated with Allen Steere) was linked by the
Allen-Steere-Lupus-Lyme group (now known as the biotech spin-off, “L2-
Diagnostics”) with Epstein-Barr (55).
We hypothesize that due to the induction of tolerance to TLR2 agonists
like fungal or mycoplasmal antigens (Pam3Cys or OspA blebbing or
vaccination) interrupting Epstein-Barr latency,
Chronic infection or colonization by mycoplasma(s) could gradually and
significantly alter many biologic properties of mammalian host cells
in culture, including induction of malignant transformation. We
examined effects of Mycoplasma fermentans infection on the continuing
survival and immortality of human peripheral blood mononuclear cells
(PBMCs) from healthy blood donors. Without specific supplemental
growth factors, human PBMCs normally die rapidly, with few cells other
than macrophages/monocytes surviving after 2 weeks in cultures. Only
occasional Epstein-Barr virus (EBV)-positive B lymphocytes would
continue to proliferate and undergo spontaneous immortalization. Our
present study revealed that infection of human PBMCs in culture with
the incognitus and PG18 strains of M fermentans, but surprisingly not
with some other strains tested in parallel, markedly enhanced the rate
of EBV-positive B lymphocytes to undergo immortalization (74% vs 17%).
Compared with spontaneously immortalized PBMCs, the PBMCs immortalized
in cultures infected with the mycoplasmas often had prominent
karyotype changes with chromosomal loss, gain, or translocations.
Furthermore, many of these immortalized B lymphocytes were found to be
monoclonal in nature. The in vitro findings would be of relevance to
lymphoproliferative disorders that occurred in patients with immune
suppression. The mycoplasma-mediated promotional effect in cell
immortalization and its potential clinical implications warrant
further study. --2004; Blood; Mycoplasma fermentans infection promotes
immortalization of human peripheral blood mononuclear cells in
culture.
(56)
the induction of chronic Lyme results in the un-latency of Epstein-
Barr. Says one researcher,
Regulation and dysregulation of Epstein-Barr virus latency:
implications for the development of autoimmune diseases.
Epstein-Barr virus (EBV) is a human herpesvirus hiding in a latent
form in memory B cells in the majority of the world population.
Although, primary EBV infection is asymptomatic or causes a self-
limiting disease, infectious mononucleosis, the virus is associated
with a wide variety of neoplasms developing in immunosuppressed or
immunodeficient individuals, but also in patients with an apparently
intact immune system. In memory B cells, tumor cells, and
lymphoblastoid cell lines (LCLs, transformed by EBV in vitro) the
expression of the viral genes is highly restricted. There is no virus
production (lytic viral replication associated with the expression of
all viral genes) in tight latency. The expression of latent viral
oncogenes and RNAs is under a strict epigenetic control via DNA
methylation and histone modifications that results either in a
complete silencing of the EBV genome in memory B cells, or in a cell-
type dependent usage of latent promoters in tumor cells, germinal
center B cells, and LCLs. Both the latent and lytic EBV proteins are
potent immunogens and elicit vigorous B- and T-cell responses. In
immunosuppressed and immunodeficient patients, or in individuals with
a functional defect of EBV-specific T cells, lytic EBV replication is
regularly activated and an increased viral load can be detected in the
blood. Enhanced lytic replication results in new infection events and
EBV-associated transformation events, and seems to be a risk factor
both for malignant transformation and the development of autoimmune
diseases. One may speculate that an increased load or altered
presentation of a limited set of lytic or latent EBV proteins that
cross-react with cellular antigens triggers and perpetuates the
pathogenic processes that result in multiple sclerosis, systemic lupus
erythematosus (SLE), and rheumatoid arthritis. In addition, in SLE
patients EBV may cause defects of B-cell tolerance checkpoints because
latent membrane protein 1, an EBV-encoded viral oncoprotein can induce
BAFF, a B-cell activating factor that rescues self-reactive B cells
and induces a lupus-like autoimmune disease in transgenic mice. (57)
It could be that it’s actually OspA-induced Epstein-Barr that is the
“New Great Imitator.”
And that the Yale-Plum-Permanentes are the Greatest Great-Imitators.
Of either physicians or scientists.
Still, where do we go from here?
“We don’t know.” First, we have to deal with the sugarplum fairy-
dancing cocoanut-heads, masquerading as “MDs” and “scientists” - doing
perpetual, eternal lapses and re-lapses between the green cheese moon
and the flat earth on the dot guv dime because they haven’t the plain
old regular nuts to admit that they knew all along - and from the
beginning, 1992, when Allen Steere went to Europe with his “high
passage” plasmid-dropping spirochete strains and “recombinant OspA-B
with the no-lipid attached” to come up with a “diagnostic standard”
for “Lyme” that ended up none of the two “primary immunodominant
antigens” represented - that OspA was not a vaccine.
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Department of Medicine, New England Medical Center, Boston,
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Golenbock DT, Vogel SN.
Department of Microbiology and Immunology, Uniformed Services
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Hovav AH, Mullerad J, Davidovitch L, Fishman Y, Bigi F, Cataldi A,
Bercovier H.
Department of Clinical Microbiology, Faculty of Medicine, The Hebrew
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Diterich I, Rauter C, Kirschning CJ, Hartung T.
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KMDickson
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Subject: "The Science Escapes Us" - IDSA = Plum Stupid
Date: Oct 15, 2010 12:08 PM
Poor Sam Donta:
http://www.nature.com/news/2010/101014/full/news.2010.542.html?s=news_rss
Still dealin wid IDSA's lying tards.
I propose a new model
based on the IDSA evidence:
http://www.actionlyme.org/20101014_PLUMSTUPID.doc
http://groups.google.com/group/scilyme2/browse_thread/thread/3cdbfda70dcbe34?hl=en
Dx: “We Don’t Know What You Have (the science escapes us)”
Rx: “Put da Lyme in da coconut, den you feel betta”
Thanks and Have a Nice Day ☺
-- Yale, CDC & Big KP
Now that it has been proven (1, 2, 3), re-proven (4, 5) and re-re-
proven (6, 7) once again and in recent history, that indeed “Lyme
Disease (8, 9)” is a chronic, un-eradicable infection primarily of the
central nervous system, formerly, formally serologically known as
Relapsing Fever (10, 11, 12), and that long term intravenous
antibiotic treatment generally results in relief-but-then-relapse (3,
5), one wonders, “Where do we go from here?”
The first order of business is the clarification of falsified antibody
testing for “Lyme Disease.”
In 1992 Allen Steere went to Germany, with, as he claimed,
“The group 1 strain of B. burgdorferi, G39/40, used in this study and
in the previous study of US patients was isolated from an Ixodes
damini tick in Guilford, Connecticut 921). The group 2 strain, FRG
[Federal Republic of Germany], was isolated from Ixodes ricinus near
Cologne (21). The group 3 strain, IP3, was isolated from Ixodes
persulcatus near Leningrad (23). All three strains used in this study
were high passage isolates, which were classified by Richard Marconi
(Rocky Mountain Laboratory, Hamilton, MT) using 16S ribosomal RNA
sequence determination as described (11, 24). The recombinant
preparations of OspA and OspB used in this study were purified
maltose-
binding protein-Osp fusion proteins derived from group 1 strain B31
(25). The fusion proteins contained the full-length OspA or OspB
sequence without the lipid moiety or the signal sequence -" illegal,
plasmid-dropping, antigen-and-antibody dropping, “high passage
strains” and OspA and B with no lipids attached (not likely to produce
antibodies), resulting in the new, 1994, Centers for Disease Control
(CDC), “case definition” of “Lyme Disease” (8, 9).
At the Dearborn, MI, Consensus Conference regarding the
“standardization” of Western Blotting for “Lyme Disease,” the invited
labs assessed Steere’s scientifically fraudulent proposal for a new
diagnostic standard for Lyme from 8% to 28% accurate (detected % of
known cases).
Independently, Gary Wormser at New York Medical College (NYMC)
assessed the Steere proposal in 1993 as: “Overall, 51 of 59 (86%)
convalescent-phase serum specimens were reactive by IB, 35 of which
were interpreted as positive: 26 based on IgM criteria, 8 based on
both IgG and IgM criteria, and 1 based on IgG criteria,” or 8 out of
59 patients were positive for Steere’s Dearborn proposal in IgG. Or,
15% accurate (13).
With this Steere/Germany standard the two OspA vaccines (ImmuLyme and
LYMErix) were allegedly assessed for safety and efficacy (14,15),
which meant 85% of known cases would be thrown out of consideration,
which, hypothetically, was the game plan all along. Later we found
out that the Western Blots in OspA vaccinated people were not readable
due to multiple reactive species or generalized darkening of the
Western Blot strips, rendering any potential bands that would
demonstrate illness/Lyme breakthrough in vaccinated persons,
undecipherable (16, 17).
That leaves us with the years 1992 to the present, almost 2011,
completely wasted.
In terms of research dollar-years and lives we’re now back at Square
One, wondering what is to be done with the testing for “Lyme Disease,”
and even more importantly, what do we call a “case” of “Lyme Disease”
once the millions of people who were misdiagnosed in the Lyme-OspA
scam process and have gone on to chronic illness?
We know from scientifically valid biomarkers of illness
(scientifically valid in the sense that valid methods were used to
assess the markers or signs that a person suffered real illness or
health irregularities), the true and correct DNA and RNA methods to
determine chronic infections status, and especially the prominent
question of “seronegativity” being associated with the greatest
apparent suffering. In 1994 at the meeting of the Food and Drug
Administration regarding potential Lyme vaccines, Raymond Dattwyler
(SUNY-Stony Brook) noted that “the ones that failed to mount a
vigorous immune response tended to do worse, clinically. So, there was
an inverse correlation between the degree of serologic response and
the outcome.”
In 2005, Mark Klempner (Boston University) and Gary Wormser (NYMC)
reported that the arthritis cases and seroposivity tended to be
associated with Allen Steere’s alleged haplotypes over which
SmithKline was sued in a class action after the Yale-owned LYMErix
trial (18): “Patients generally feel well aside from their arthritis
symptoms.”
In 1988, Raymond Dattwyler published that he wondered about
seronegative “Lyme” and the suppression of NK cells (19), and he
wondered enough to come up with a new assay to determine if exposure
to Lyme and a lowered immunological response (20). His new assay was
called “Seronegative Lyme disease. Dissociation of specific T- and B-
lymphocyte responses to Borrelia burgdorferi.” Later, Allen Steere
used this same seronegative “Lyme” assay and determined that 4/9 of
his lab workers had been exposed to Borrelia (21).
The question was why.
We know from the previous history of Relapsing Fever (before the era
of Allen Steere, et al), that antigenic variation was the nature of
the relapse, and that spirochetes become host- and tissue- adapted.
This meant that persons who had missed the opportunity for early
diagnosis and treatment would not have the Dearborn “case definition”
of “late, OspA-hypersensitivity, specific HLA-linked, Lyme Arthritis”
in “early Lyme,” would be left to his/her peril in finding a competent
MD who had been exposed in pre-medicine undergraduate study to a
course in genetics. These organisms are taxonomically classified by
differences in flagellin. The best way to detect Lyme with antibody
testing is via all-borrelial-specific anti-flagellin antibody
detection, because flagellin is not a variable antigen. The group
who perfected and patented the anti-Borrelia- burgdorferi specific
flagellin method was Yale’s Erol Fikrig and Richard Flavell in 1991
(22, 23). Why this test was not used to assess Fikrig and Flavell’s
OspA vaccine patent, LYMErix, is anyone’s guess.
Regardless of this State of Nonsense (Connecticut), …
People wonder what to make of the serious illness they suffer as a
result of “Lyme” and LYMErix vaccination, which appeared to be similar
(24). In 1995, David Persing and Yale’s Robert Schoen patented a
method wherein they, the winners, would be in receipt of all the
government funding and also a national monopoly on the - as they hoped
and intended - post-OspA-vaccinated United States:
“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…. ” (25, 26). And they,
most of all, would have access to all the potentially patentable
goodies in the national blood with this monopoly on testing.
Further investigations into the outcomes of other lipoprotein/fungal
vaccines revealed a similar outcome to that observed in the un-
reported LYMErix adverse events patients, resulting in the January
2001 FDA hearing on the matter and the class action lawsuits. Adverse
events were only reported to the FDA by the vaccines trails
administrators if they were of the arthritis kind, since “arthritis
only” had become the new “case definition” at the 1994 Dearborn
”conference.” When Dennis Parenti of SmithKline reported that there
were only two neurological adverse events to LYMErix at the 2000 Lyme
Disease Foundation Conference in Hartford, CT, several physicians and
attendees immediately got up and walked out of the conference room,
while the rest groaned.
The functional results of OspA vaccination were, we hypothesize, not
dissimilar from the results of structurally similar vaccine antigens
that are managed by TLR2:
“These results are consistent with a model in which the presence of
the 19-kD protein [of Mycobacteria tuberculosis] has a detrimental
effect on the efficacy of vaccination with live mycobacteria.” (27)
“Synthetic analogs of lipopeptides from Treponema pallidum also
inhibited Ag [antigen] processing.”
(28)
“the immunosuppressive effect is dependent on glycosylated and
acylated 19-kDa lipoprotein [of Mycoplasma tuberculosis] 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 activation. (29)
“Thus, tolerance to LPS and mycobacterial components cannot be
attributed solely to a decrease in TLR/MD-2 expression levels,
suggesting inhibition of expression or function of other signaling
intermediates 2002, Induction of bacterial lipoprotein tolerance is
associated with suppression of toll-like receptor 2 expression.”(30)
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. (31)
And, we know that:
[((2003) Borrelia burgdorferi-induced tolerance as a model of
persistence via immunosuppression.]
“If left untreated, infection with Borrelia burgdorferi sensu lato may
lead to chronic Lyme borreliosis. It is still unknown how this
pathogen manages to persist in the host in the presence of competent
immune cells. It was recently reported that Borrelia suppresses the
host's immune response, thus perhaps preventing the elimination of the
pathogen (I. Diterich, L. Härter, D. Hassler, A. Wendel, and T.
Hartung, Infect. Immun. 69:687-694, 2001). Here, we further
characterize Borrelia-induced immunomodulation in order to develop a
model of this anergy. We observed that the different Borrelia
preparations that we tested, i.e., live, heat-inactivated, and
sonicated Borrelia, could desensitize human blood monocytes, as shown
by attenuated cytokine release upon restimulation with any of the
different preparations. Next, we investigated whether these Borrelia-
specific stimuli render monocytes tolerant, i.e. hyporesponsive,
towards another Toll-like receptor 2 (TLR2) agonist, such as
lipoteichoic acid from gram-positive bacteria, or towards the TLR4
agonist lipopolysaccharide. Cross-tolerance towards all tested stimuli
was induced. Furthermore, using primary bone marrow cells from TLR2-
deficient mice and from mice with a nonfunctional TLR4 (strain C3H/
HeJ), we demonstrated that the TLR2 was required for tolerance
induction by Borrelia, and using neutralizing antibodies, we
identified interleukin-10 as the key mediator involved. Although
peripheral blood mononuclear cells tolerized by Borrelia exhibited
reduced TLR2 and TLR4 mRNA levels, the expression of the respective
proteins on monocytes was not decreased, ruling out the possibility
that tolerance to Borrelia is attributed to a reduced TLR2 expression.
In summary, we characterized tolerance induced by B. burgdorferi,
describing a model of desensitization which might mirror the
immunosuppression recently attributed to the persistence of Borrelia
in immunocompetent hosts”. (32)
“Next, we investigated whether these Borrelia-specific stimuli render
monocytes tolerant, i.e. hyporesponsive, towards another Toll-like
receptor 2 (TLR2) agonist, such as lipoteichoic acid from gram-
positive bacteria, or towards the TLR4 agonist lipopolysaccharide.
Cross-tolerance towards all tested stimuli was induced.”
Epstein-Barr’s activity regarding TLR2:
(2007) Epstein-Barr virus induces MCP-1 secretion by human monocytes
via TLR2.
“Epstein-Barr virus (EBV) is a gammaherpesvirus infecting the majority
of the human adult population in the world. TLR2, a member of the
Toll-
like receptor (TLR) family, has been implicated in the immune
responses to different viruses including members of the herpesvirus
family, such as human cytomegalovirus, herpes simplex virus type 1,
and varicella-zoster virus. In this report, we demonstrate that
infectious and UV-inactivated EBV virions lead to the activation of
NF-
kappaB through TLR2 using HEK293 cells cotransfected with TLR2-
expressing vector along with NF-kappaB-Luc reporter plasmid. NF-kappaB
activation in HEK293-TLR2 cells (HEK293 cells transfected with TLR2)
by EBV was not enhanced by the presence of CD14. The effect of EBV was
abrogated by pretreating HEK293-TLR2 cells with blocking anti-TLR2
antibodies or by preincubating viral particles with neutralizing anti-
EBV antibodies 72A1. In addition, EBV infection of primary human
monocytes induced the release of MCP-1 (monocyte chemotactic protein
1), and the use of small interfering RNA targeting TLR2 significantly
reduced such a chemokine response to EBV. Taken together, these
results indicate that TLR2 may be an important pattern recognition
receptor in the immune response directed against EBV infection.” (33)
And we know that:
“Yale researcher Stephen Barthold, a veterinarian and professor of
comparative medicine who developed the first mouse model of Lyme
disease, studies the expression of B. burgdorferi surface proteins
throughout various stages of the spirochete’s life cycle. He finds
that during the early stages of infection, B. burgdorferi avoids
immune detection by decreasing its expression of surface proteins or
cloaking its expressed surface proteins under a layer of slime. "It's
using some sort of stealth-bomber-type mechanism," he says. Or, using
another diversionary tactic called blebbing, the spirochete can pinch
off bits of its membrane in order to release its surface proteins
Explains Barbour: "It’s like a bacterial Star Wars defense program,"
in which released surface proteins might intercept incoming host
antibodies keeping the spirochete safe from immunological
attack.” (34)
which is what we call the auto-vaccination with OspA - the immune-
suppressing fungal antigen, known also, structurally, as Pam3Cys
(35).
In short, “Lyme Disease” is chronic and seronegative because it is
chronic, or chronically shedding variable (Relapsing Fever-esque)
outer surface lipoproteins like OspA, or, as Alan Barbour states in
his US Patent #6,719,983:
“2.1 Methods of Treatment
”An important aspect of the invention is the recognition that Borrelia
VMP-like sequences recombine at the vls site, with the result that
antigenic variation is virtually limitless. Multiclonal populations
therefore can exist in an infected patient so that immunological
defenses are severely tested if not totally overwhelmed. Thus there is
now the opportunity to develop more effective combinations of
immunogens for protection against Borrelia infections or as preventive
inoculations such as in the form of cocktails of multiple antigenic
variants based on a base series of combinatorial VMP-like antigens.”
“antigenic variation is virtually limitless. Multiclonal populations
therefore can exist in an infected patient so that immunological
defenses are severely tested if not totally overwhelmed.”
What are the other functional outcomes of the chronic agonism of TLR2
– the one that manages triacyl lipopeptides like OspA or Pam3Cys that
render the immune system overwhelmed, not to mention persons late in
the disease who do not serologically (antibodies) react to antigen
from spirochetes fresh out of a tick due to antigen variation,… not to
mention the diminution of antibody production due to chronic TLR2
agonism?
Says Paul Duray of the National Cancer Institute and Ft. Detrick
(hint, hint):
"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." (36)
The lymphocytes of these chronic “Lyme” victims look like Epstein-Barr
transformed cells.
In 2003, Hilinska et al report in “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.” (37)
One of the characteristics of chronic neurologic “Lyme” is that it is
called an “aseptic meningitis” (38, 39, 40).
This is, of course, while the German Multiple Sclerosis expert Roland
Martin had been recruited by the National Institute of Health to
research the association between “Lyme” and Multiple Sclerosis.(41,
42). Martin went home once he found out that OspA-induced
immunosuppression was the likelier reason “Lyme” was mistaken for
Multiple Sclerosis or vice versa.
DISCLAIMER: We Lyme victims did not dream up this nonsense. We only
report it.
Could the co-TLR2 agonists (inducing tolerance and a lack of
antibodies) Epstein-Barr and Borreliosis be simply responsible for: “
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?”(36) ?
It is common knowledge that 95% of the adult population in Western
cultures has been exposed to Epstein-Barr and its common similar
herpes viruses. Hypothetically, there is a mouse herpesvirus
(gamma2herpes) that to our knowledge has not been investigated
regarding transmission to other hosts via ticks. We’re not privileged
to know much about what happens on Plum Island. We only know there is
a “Plum Island” strain of mycoplasma, and that Yale’s Durland Fish
experimented with trying to get African Swine Fever virus to “take” to
local hard-bodied ticks at that Not-Bioweapons/Just-Helping laboratory
(43, 44).
However, something that might have been discovered 10 or 15 years
sooner had not certain persons associated with Yale and New York
Medical College made an agreement with Kaiser-Permanente (45) to sell
a vaccine against a disease they suddenly decided doesn’t actually
cause any illness (and the world is flat, the moon made of green
cheese, and all hospitals are going to become brothels because it’s
cheaper and therefore cost-effective to deploy self-alleged MDs who
never perform any scientifically valid rule-outs before making
theoretical diagnostic assumptions based on “projection,” rather than
bog down the likes of the actual laboratories with the fancy machinery
that serves no purpose other than to take up space and look shiny,
just like the misguided folks at Silly NASA…).
“Epstein-Barr virus (EBV) efficiently drives proliferation of human
primary B cells in vitro, a process relevant for human diseases such
as infectious mononucleosis and posttransplant lymphoproliferative
disease. Human B-cell proliferation is also driven by ligands of Toll-
like receptors (TLRs), notably viral or bacterial DNA containing
unmethylated CpG dinucleotides, which triggers TLR9. Here we
quantitatively investigated how TLR stimuli influence EBV-driven B-
cell proliferation and expression of effector molecules. CpG DNA
synergistically increased EBV-driven proliferation and transformation,
T-cell costimulatory molecules, and early production of interleukin-6.
CpG DNA alone activated only memory B cells, but CpG DNA enhanced EBV-
mediated transformation of both memory and naive B cells. Ligands for
TLR2 or TLR7/8 or whole bacteria had a weaker but still superadditive
effect on B-cell transformation. Additionally, CpG DNA facilitated the
release of transforming virus by established EBV-infected
lymphoblastoid cell lines. These results suggest that the
proliferation of EBV-infected B cells and their capability to interact
with immune effector cells may be directly influenced by components of
bacteria or other microbes present at the site of infection.--
Toll-like receptor agonists synergistically increase proliferation and
activation of B cells by epstein-barr virus. (46)
We know that “Lyme” is associated with the production of Amyotrophic
Lateral Sclerosis (in 47% of the ALS cases in Lyme-endemic areas) (47)
and Multiple Sclerosis (48). And we know that ALS is associated with
mycoplasmal infection (tolerance to TLR2 agonists), and, MS, and
apparently “Lyme” is associated with Epstein-Barr virus or something
like it (Duray).
We know that 90% of Chronic Fatigue patients found out they had “Lyme
Disease” when finally assessed by a reputable laboratory – one not
like Quest Diagnostics, which uses strain B31, the non-neurotropic,
non-OspC-bearing, non-band-23-producing strain (49). We hypothesize
that since it is known that mycoplasmal infections in the blood
disrupt the osmotic potential in erythrocytes (disrupt the transfer of
oxygen), and metabolism (these things need to be fed, after all) (50,
51), and since there has been reported a high association to
mycoplasmal infections in Chronic Fatigue and Gulf War Illness victims
(52, 53), that the tolerance to TLR2 agonists Lyme/LYMErix results in
tolerance to mycoplasma in the blood (Chronic Fatigue) with no
relative antibody production (28).
“Lyme” also produces a Lupus-like syndrome (54), and recently (and
formerly, formally associated with Allen Steere) was linked by the
Allen-Steere-Lupus-Lyme group (now known as the biotech spin-off, “L2-
Diagnostics”) with Epstein-Barr (55).
We hypothesize that due to the induction of tolerance to TLR2 agonists
like fungal or mycoplasmal antigens (Pam3Cys or OspA blebbing or
vaccination) interrupting Epstein-Barr latency,
Chronic infection or colonization by mycoplasma(s) could gradually and
significantly alter many biologic properties of mammalian host cells
in culture, including induction of malignant transformation. We
examined effects of Mycoplasma fermentans infection on the continuing
survival and immortality of human peripheral blood mononuclear cells
(PBMCs) from healthy blood donors. Without specific supplemental
growth factors, human PBMCs normally die rapidly, with few cells other
than macrophages/monocytes surviving after 2 weeks in cultures. Only
occasional Epstein-Barr virus (EBV)-positive B lymphocytes would
continue to proliferate and undergo spontaneous immortalization. Our
present study revealed that infection of human PBMCs in culture with
the incognitus and PG18 strains of M fermentans, but surprisingly not
with some other strains tested in parallel, markedly enhanced the rate
of EBV-positive B lymphocytes to undergo immortalization (74% vs 17%).
Compared with spontaneously immortalized PBMCs, the PBMCs immortalized
in cultures infected with the mycoplasmas often had prominent
karyotype changes with chromosomal loss, gain, or translocations.
Furthermore, many of these immortalized B lymphocytes were found to be
monoclonal in nature. The in vitro findings would be of relevance to
lymphoproliferative disorders that occurred in patients with immune
suppression. The mycoplasma-mediated promotional effect in cell
immortalization and its potential clinical implications warrant
further study. --2004; Blood; Mycoplasma fermentans infection promotes
immortalization of human peripheral blood mononuclear cells in
culture.
(56)
the induction of chronic Lyme results in the un-latency of Epstein-
Barr. Says one researcher,
Regulation and dysregulation of Epstein-Barr virus latency:
implications for the development of autoimmune diseases.
Epstein-Barr virus (EBV) is a human herpesvirus hiding in a latent
form in memory B cells in the majority of the world population.
Although, primary EBV infection is asymptomatic or causes a self-
limiting disease, infectious mononucleosis, the virus is associated
with a wide variety of neoplasms developing in immunosuppressed or
immunodeficient individuals, but also in patients with an apparently
intact immune system. In memory B cells, tumor cells, and
lymphoblastoid cell lines (LCLs, transformed by EBV in vitro) the
expression of the viral genes is highly restricted. There is no virus
production (lytic viral replication associated with the expression of
all viral genes) in tight latency. The expression of latent viral
oncogenes and RNAs is under a strict epigenetic control via DNA
methylation and histone modifications that results either in a
complete silencing of the EBV genome in memory B cells, or in a cell-
type dependent usage of latent promoters in tumor cells, germinal
center B cells, and LCLs. Both the latent and lytic EBV proteins are
potent immunogens and elicit vigorous B- and T-cell responses. In
immunosuppressed and immunodeficient patients, or in individuals with
a functional defect of EBV-specific T cells, lytic EBV replication is
regularly activated and an increased viral load can be detected in the
blood. Enhanced lytic replication results in new infection events and
EBV-associated transformation events, and seems to be a risk factor
both for malignant transformation and the development of autoimmune
diseases. One may speculate that an increased load or altered
presentation of a limited set of lytic or latent EBV proteins that
cross-react with cellular antigens triggers and perpetuates the
pathogenic processes that result in multiple sclerosis, systemic lupus
erythematosus (SLE), and rheumatoid arthritis. In addition, in SLE
patients EBV may cause defects of B-cell tolerance checkpoints because
latent membrane protein 1, an EBV-encoded viral oncoprotein can induce
BAFF, a B-cell activating factor that rescues self-reactive B cells
and induces a lupus-like autoimmune disease in transgenic mice. (57)
It could be that it’s actually OspA-induced Epstein-Barr that is the
“New Great Imitator.”
And that the Yale-Plum-Permanentes are the Greatest Great-Imitators.
Of either physicians or scientists.
Still, where do we go from here?
“We don’t know.” First, we have to deal with the sugarplum fairy-
dancing cocoanut-heads, masquerading as “MDs” and “scientists” - doing
perpetual, eternal lapses and re-lapses between the green cheese moon
and the flat earth on the dot guv dime because they haven’t the plain
old regular nuts to admit that they knew all along - and from the
beginning, 1992, when Allen Steere went to Europe with his “high
passage” plasmid-dropping spirochete strains and “recombinant OspA-B
with the no-lipid attached” to come up with a “diagnostic standard”
for “Lyme” that ended up none of the two “primary immunodominant
antigens” represented - that OspA was not a vaccine.
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Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi,
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Georgilis K, Peacocke M, Klempner MS.
Department of Medicine, New England Medical Center, Boston,
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