Greatest Imitator (OspA) Lay Explainer

[Kathleen]

http://www.actionlyme.org/GREATEST_IMITATOR_INTERVIEW.htm

QUESTIONER: Tell us about your background:

I actually do not want to talk about myself. Suffice it to say I
am: “A regular homegirl who put herself though homegirl state
college. KMD has a Bachelor’s degree in Chemistry from Southern CT
State Homegirl College (now, ‘University’) end of discussion.“

Chemistry, to me, is the most perfect use of human language – the
words mean only the pictures. Chemistry is the Physics of the Life
Sciences. What else is a young person, thinking of him/herself in the
future as an employed person, providing for self and family, going to
do with her/his life? The sum of what I learned by the time I was 20
said, “CHEMISTRY.” [I could not bring myself to pith (kill) a frog,
and the “Bac-T” labs stunk to high heaven... so I switched majors from
Environmental Biology.]

I worked at whole lot of different jobs after college and most of
the time, two or three $5/hour jobs at a time because it was the
recession of 1982 (I am 52) before getting my first lab job, then I
worked at Pfizer from around 1990 to 1999, mostly in an Analytical
Chemistry (Methods/Validations) service lab for all the Divisions. It
was all very rigorous and OSHA/FDA compliance-conscious. My co-
workers were all-around good people who I liked and enjoyed.
Absolutely nothing in my experience prepared me for what I saw in Lyme-
lab crime-land. I never expected such insanity to actually pass for
science.

Disclaimer - Were anyone to ask me if Lyme/LYMErix was a deliberate
bioweapons deployment I would say no. If you look at all of the
histories and publications of the ALD.com/IDSociety.org gang, not a
one of them is a real academic (except for Justin Radolf). I say, if
anything, the lack of prosecution over this fraud is Blackmail against
the US Government. I believe this is what so far prevents prosecution
for this Dearborn/Pam3Cys-immunosuppression outcomes fraud. And I
lean towards a conspiracy involving the insurance companies, because
that's actual evidence we have. That's the paper trail starting with
Edward McSweegan's Navy-trashing letter to Senator Barry Goldwater in
1986. We know who is a "supporter" of the ALDF.com and we know Kaiser-
Permanente is still at New York Medical College (Valhalla, NY),
training "MDs."

QUESTIONER: I believe readers need to have some clarification on what
a tripalmitoyl cysteine (Pam3Cys) is and does. Is Pam3Cys natural
occurring and/or synthetic?

KATHLEEN:

My first recommendation to the readers would be to have them go on the
YouTube and look for Khan Academy and watch his short videos on
immunology. They are invaluable. This will give people a background
in some of the terminology we will use. People must understand that
science is 3D. (Math is 2D and a tool, but math is not a science.
Usually the best mathematicians are not very excellent scientists.
What this means is that anyone with visual-spatial abilities, like
artists and auto-mechanics have an natural ability to be a scientist.)

My second admonition here, is to state that there is no other way to
approach understanding this, than to put the time into it. (I know
you know this, QUESTIONER. You put the time into it and came to
understand it.) Some Lyme victim/self-proclaimed activists we have
encountered who want this knowledge spoon-fed to them. When we don't
have the time to perform this individual service to people who have no
track record of LD performance of any significance, we endure all
kinds of insults - a very immature approach.

I have reason to believe that many Lyme victims are unfortunately on
mind-altering "pain" medications. Lyme victims on psychoactives
happens to be malpractice, since Lyme is already a brain disease. The
American Psychiatric Associations' "guidelines" on the treatment of a
delirium (demonstrated by SPECT scanning) is to treat medically,
first. That means all psychiatrists who are billing for the
"treatment" of "Lyme disease" have to be prescribing the anti-
meningitis drug ceftriaxone (and as we will see, antivirals), or they
could be charged by the medical boards or sued for malpractice.

I, for one, assert that I simply don't have the time or the energy to
spoon-feed this material to doubly-brain-damaged people who also have
some "Personality Disorder" issues probably as a result of their
psychoactives addictions. (I can expound upon the mechanisms of
addictions and brain damage... and also the mechanisms of thoughts
associated with such self-destruction perhaps at another time.)

As far as the evidently brain damaged behavior of psychiatrists who
malpractice treat Lyme as if it is a "mental illness" (? - means
"brain disease") well, here again we parse what exactly is
psychiatry? It's not a medical practice if they don't treat
medically. And it's not a moral/behavior judgment system if they
themselves are excluded from judgment or self-suggest they're some
sort of a superior being (deity), or perhaps they're "Nordics" or
"Pleiadians" or "Ascended Masters" - more highly evolved humans...

The Diagnostics and Statistical Manual is just that. Psychiatry, in
their un-wisdom and with their non-scientific training, have not
become aware that the frequency of a behavior (as demonstrated by
statistics), does not make a behavior right or wrong. Math
(statistics) is two-dimensional. It is a tool, not a science.
Science is 4-dimensional: the 3 dimensions of the physical world plus
time.

One would wonder if psychiatrists considered what would be the effect
on society of the sum of these these frequent, "normal" behaviors -
behaviors they endorsed through the process of statistically
demonstrating that they're "normal" or "common" or "everybody does
it?" As you can see, I strongly take issue with this morphing of the
subjective in the medical-legal world. Lawyers tend to be the same
sorts of personalities where the exclusion of the platform - the forum
- though which we determine the truth is not only rejected, but
violently rejected. The reason it is rejected, repelled, and despised
(as is all that I am about to reveal to you below), is because the
first premise within their disorder is that there is something special
about themselves - some special knowledge that they have (special,
secret knowledge being irresistible to humans being as old a story as
Adam and Eve) - that promotes them above others.

What would happen to psychiatrists if they engaged the logic that
psychiatry is not either a science or medicine - that they have no
more "expertise" as regards passing permanent, discriminatory
judgments on human lives, with the intent of having it perceived by
others that there is some predictive value in their subjective,
debased judgments, than the Ku Klux Klan?

Oddly, psychiatry is a belief system where everyone who is a
psychiatrist is allowed to hold to their own personal selection of
historically proposed theories - from behaviorism to biologic
psychiatry (the one promoted by BigPharma and BigInsurance) - the
selection of which they're also allowed to modify over time. Such a
thought process happens to be the definition of "psychosis." Yet,
psychiatry is the same gang who claim the religious to be psychotic
because psychiatry can't recognize spirit or the human will. They
don't recognize the difference between an animal and a human. It
wouldn't fit psychiatry's debased model of human-animalism for it to
be true that humans are able to predict outcomes - that others may
suffer - of their own behaviors or of their own collective behaviors
on society when ME! is at the center of one's universe.

How's that for intellectual sophistication? Psychiatry has proven
repeatedly that they're not interested in their own, nearly
exclusively, negative outcomes. ("I gotta take care of MEEeee,
First!!")

Too many people involved in "Lyme activism" or who are "the opposition
group" to the perpetrators of the Lyme crimes are no more than the
happy, smiling versions of the insurance company parasites of our
misery. They're the ones who also expect us Lyme victims to do all
the work: all the scientific work, all the fund-raising, all the
protests and petitions... because they're too busy seeing patients
(making money) to put an end to it all with a lawsuit or engaging the
Justice Department. The Connecticut Attorney General had to do that
for them. That ought to be an embarrassment to them, but I suppose
that when you're a Superior Human, you suffer no insults. ('I SIT as
A QUEEN AND I AM NOT A WIDOW, and will never see mourning.')

SIMPLE EXPLAINER; WHAT IS PAM3CYS:

Pam3Cys is OspA and HIV's gp120. It is the basic structure or the
molecule type or class. It was designed, apparently to be an analog of
E. coli's Lipid A, a toxin. It was designed as a synthetic toxin so
that bacteriologists/microbiologists had something to work with in a
lab, without extracting it from E. coli.

Pam3Cys BEHAVES as a chronic TLR2 agonist (especially as a result of
Chronic Lyme being chronic, by everyone's admission, shedding Osps as
Relapsing Fever organisms do), which results in 1) turning off the
immune system (immunosuppression) and 2) activates latent viruses like
Epstein-Barr, while tolerizing to fungal infections in the blood
(chronic fatigue).

KATHLEEN:
Answering "what is Pam3Cys, where does it come from?"

RADOLF, KOREANS, Pam3Cys ANTIBODIES IN HIV, SHAPE

From all the data we have, I believe OspA to be synthetic. Allow me
to explain why:

First of all, lipids cannot be recrystallized, so this disallows X-Ray
diffraction –scatter – studies to show OspA’s actual shape. Remember
that “Structure is Function;” at the molecular level, stuff is what it
does, and vice-versa. (We find later, that it appears one can apply
Mass-Spec to make assumptions about structure.)

We know from Mario Philipp (Tulane), that OspA is Pam3Cys. But what
is Pam3Cys?

KOREANS -

I first found the structure of Pam3Cys after searching the web and the
NIH database (MedLine, or PubMed) for years, from some Korean
Chemists, who, while describing the structure of – apparently, the HIV
vaccine candidate as Pam3 Cys – gave a structure for Pam3Cys. Here is
exactly what they said:

“We are currently using several mass spectral techniques to
characterize the amino acid sequence of the Pam3Cys envelope
glycoproteins of HIV-1 and the Simian Immunodeficiency Virus (SIV).
(17) Conventional FAB- [Fast Atom Bombardment –KMD] –MS using standard
matrices, like glycerol and dinitrobenzyl alcohol, is not particularly
effective for these molecules, largely due to their tendency to
aggregate.”

And here is their graphic, used without permission:

http://newjournal.kcsnet.or.kr/main/j_search/j_download.htm?code=B961118
1996; Characterization of Extremely Hydrophobic Immunostimulatory
Lipoidal Peptides by Matrix Assisted Laser Desorption Ionization Mass
Spectrometry

Note their claim, here. in their “Figure 1”:

“The structure of… Pam3Cys… showing the modified cysteine [has an S
for sulfur in this amino acid-KMD with and N-palmitoyl ester [the
lower string of carbons-KMD] and a dipalmitoylglyceryl moiety [the top
2 lipid strings-KMD] connected via a thio [means sulfur again-KMD]
ether linkage [means sulfur instead of oxygen as an excuse for an
“ether”-KMD] linkage. This amino acid is placed at the N-terminus of
the synthetic peptide."

So, what that means to me is that the series of amino acids slopped
together (where it says “peptide” or the "R" group) is what they were
after, while matter-of-factly explaining what Pam3Cys is,
structurally. The Korean scientists claimed to have obtained these
manufactured Pam3Cys-HIV-SIV-peptides from San Antonio, Texas,
Southwest Research Foundation for Biomedical Research (SRFBR).

What that means:

1) The amino-acid sequence from the "R" end of Pam3Cys is different
between HIV gp120 and OspA. No big deal there. The protein end is
not very immunogenic. It is the cysteine core and the hyperlipidity
that "scares" the immune system. The immune system seems to not like
fat, slimey bugs. (At least not until they're tolerized to them,
which we will see was the essence of the "Lyme Disease" crime, and
brings in the question of biofilms.)

2) OspA/Pam3Cys/HIV gp120 sticks to itself, which is probably
responsible for the Western Blot smudging and “multiple reactive
species” the Lyme criminals (Sigal, Persing and Schoen) found when
they reported the truth about their unreadable Western Blots in the
OspA vaccination trials. These people actually could not read their
Western Blots in any of the OspA vaccine trials (LYMErix or
ImmuLyme). The vaccine junk was probably not properly micellized by
the carriers.

3) It looks to me like they’re saying Pam3Cys, the synthetic analog of
the E. coli Lipid A or the Braun lipoprotein (1983) is in the modified
HIV and SIV antigens supplied to them by SRFBR. (There is also an HIV
antibody study to support that this might be the structure, which I
discuss further on in this answer.)

The Korean scientists said, “We are currently using several mass
spectral techniques to characterize the amino acid sequence of the
Pam3Cys envelope glycoproteins of HIV-1 and the Simian
Immunodeficiency Virus (SIV). (17)"

It's not clear whether the Koreans are talking about a vaccine for HIV
which has Pam3Cys in it, or the original, "SIV and HIV gp120," because
they added in the Simian Immune Deficiency Virus, apparently, when one
would suppose researchers like those at SRFBR would not have an
interest in deploying a monkey AIDS vaccine. It becomes even more
confusing when we later see that 1) antibodies are usually pretty
specific, and 2) there is a strongly positive result among AIDS
victims to a Pam3Cys version of this antigen when used as an antibody
test.

Anthony Fauci, the head of NIAID (National Institute of Allergy and
Infectious Disease), has twice admitted that he doesn't know what he's
doing or talking about - once in the NEJM in August, 2008, and once on
the Washington Post online video series "On Leadership." (This kind
of incompetence at the highest "Government" level is less amazing now,
thanks to Wikileaks.)

What is the ancient history of these kinds of fungal antigens and
immunosuppression?

The science goes back at least to the 1950s. Raymond Dattwyler, et
al, references these earlier studies and immunosuppression from fungal
antigens in his 1988 "Modulation of NK Cell Activity" and
"Seronegative Lyme T-Cell Proliferation Assay" papers. He also
references this histoplasmo business, which was a bug either sold or
given to Saddam Hussein in the 1980s by the USA as "Dual -Use"
organisms. (It's fascinating stuff and quite popular, my website
statistics tell me.)

I would venture that we all re-examine what we knew about the cellular
immunity oddities revealed in the late 1980s and early 1990s, before
the "American Lyme Disease Foundation (ALDF.com) was founded at the
financially floundering New York Medical College in Valhalla, NY.,
where Kaiser-Permanente now has a starring role in writing the MD
training modules. (They actually have "Kaiser-Permanente" stamped on
the bottom of their MD-training modules.)

The Infectious Diseases Society of America in 1989 was a much
different entity than it is today. They even changed the name of
their journal from "Infectious Disease Reviews." Re-Disclaimer: I am
a Pharma chemist, not an immunologist or pathologist, but I know a lab
slight-of-hand when I see one, because methods validations was my
specialty - study design and Methods and Materials should not be
overlooked in these crooks' shenanigans. That said, I would like to
steal a compelling snippet from Wikipedia (which I use, in addition to
Khan Academy and other sources, and not as sci-med bible but needs to
be cross-checked):

FROM WIKIPEDIA:
http://en.wikipedia.org/wiki/T_cell
Natural killer

Natural killer T cells (NKT cells) are a special kind of lymphocyte
that bridges the adaptive immune system with the innate immune system.
Unlike conventional T cells that recognize peptide antigen presented
by major histocompatibility complex (MHC) molecules, NKT cells
recognize glycolipid antigen presented by a molecule called CD1d. Once
activated, these cells can perform functions ascribed to both Th and
Tc cells (i.e., cytokine production and release of cytolytic/cell
killing molecules). They are also able to recognize and eliminate some
tumor cells and cells infected with herpes viruses.

Compare to:

1988, Raymond Dattwyler, et al,
"Modulation of natural killer cell activity by Borrelia burgdorferi.
[PubMed 3056196]"

"However, this does not explain the significantly decreased NK
cytotoxic ability of these patients' PBL. It is possible that this
inhibitor of NK activity is the result of a recruitment of inactive NK
cells expressing CD16+. Leu-7- cells have cytotoxic activity (26).
Alternatively, the decrease in NK activity may be due to a direct
effect of the B. burgdorferi organism or its products on the NK cell.
It has been reported that LPS isolated from Salmonella has the ability
to inhibit the bacterial augmentation of activated killer cells while
leaving endogenous NK. It is also possible that B. burgdorferi
produces a toxin that is responsible for the inhibition. An adenylate
cyclase toxin can be extracted from Bordetella that will increase cAMP
levels when added to NK cells, resulting in an inhibition of NK
activity without killing the NK effector cells.(27)"
http://www.ncbi.nlm.nih.gov/pubmed/3056196

Ie., Cells normally tasked to eradicate cells infected with herpes
viruses have, according to Ray Dattwyler, et al, may have been
somewhat chemically inhibited after exposure to, possibly a Bb
"toxin."

If you see all the "Related" and "Cited by" articles on PubMed for
this Dattwyler-Modulation article on PubMed, you will find that none
of the ALDF.com cited it. However, the NK-cell Activity Modulation
study by Dattwyler et al, basically ran at the same time as the
Seronegative T Cell Assay that Dattwyler and Volkman developed for the
same reason (Seronegative Lyme disease. Dissociation of specific T-
and B-lymphocyte responses to Borrelia burgdorferi; PubMed ID:
3054554]. They knew seronegative, chronic neurologic Lyme victims
were the sickest. In 1990 Allen Steere performed a review called
Chronic Neurologic Manifestations of Lyme Disease; PubMed ID: 2172819,
using this Dattwyler Seronegative T Cell Proliferation Assay to
include people who were sick with Lyme in the study.

Also, at the 1994 FDA Lyme Vaccines Meeting, Raymond Dattwyler said of
seronegative Lyme victims:
Page 49 of the transcripts:

DR. OBRIEN: I was concerned about your last slide where you said
there was a poor correlation between seronegative response and
clinical disease. And as I heard you to say, some people who mount
better responses get worse disease. Did I hear you say that?

DR. DATTWYLER: No, no. I said the reverse. The better responses
tended to have a better response. And I should clarify where this is
from. This is from antibiotic treatment trials of erythema migrans,
in which individuals given an antibiotic regimen which was not optimal
- we didn't know what was optimal at the time - 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.

It turns out that fungal antigen induced immune-suppression is
described by Dattwyler, et al, in the Seronegative Lyme assay article:
"This disorder in these seronegative patients reflected a dissociation
between T-cell and B-cell immune responses, in which the cell mediaed
arm of the immune response was intact yet the humoral portion of the
response appeared to be blunted. This diminished antibody response is
in contrast to the T-cll anergy commonly observed in several chronic
infections (e.g., infection with Mycobacteria leprae or M. marinum,
filariasis, and some chronic fungal infections 29-33)."

Apparently not aware of the structure/function of the likes of the
fungal antigen OspA, Dattwyler was wrong to say Lyme/Borreliosis did
not belong in the Mycoplasma/Mycobacteria/chronic fungal infection/
immune-suppression classes.

This phenomenon of seronegative victims being the sickest was later re-
confirmed by Wormser and Klempner who in 2005 published a study
basically reclaiming the association Allen Steere made between
seropositivity and specific HLAs, over which the gang was sued in a
class action - the non-disclosure that the Allen Steere version of HLA-
linked hypersensitivity-Lyme disease (falsified at the October 1994
CDC Dearborn, MI Conference and Allen Steere alone in Europe, intended
to redefine "Lyme disease" to just the hypersensitivity or arthritis
response) - and, as Wormser and Klempner claimed, these Steere-
hypersensitivity/seropositive patients: "generally feel well aside
from their arthritis symptoms" [PubMed ID: 16107953; "A case-control
study to examine the HLA haplotype associations in posttreatment
chronic Lyme disease" At the 1998 Vaccine Committee Meeting Vijay
Sikand said the arthritis patients were immune competent and could
make enough antibodies to fight off the disease (like rabbits do).

Otherwise, we have to deal with the Negative Data Rule, where people
who wish to create a scientific world view around an intended
financial or bioweapons product or goal see to it that none of the
obvious "Next-Question"? science is funded. The Negative Data Rule
has all kinds of outcomes and consequences, so I won't go into it.
Let it suffice to say Yale Pathology Department participated in or
referenced the autopsies of 3 babies who died of Congenital Lyme in
the 1980s. Today, the entity sued by the Connecticut Attorney
General, Richard Blumenthal, in an AntiTrust lawsuit - some of whom
are employed by Yale - blatantly deny any such thing ever occurred
(Eugene Shapiro, Under Our Skin documentary, Open Eye Pictures).

There's nothing in the DSM-IV for people who have MD degrees but who
will knowingly say any old thing that is not true to fund their own or
their gang's commercial enterprise, like psychiatry and their infamous
"ghost-writer" relationship with BigPharma. (How many psychiatrists
work in labs with mice and rats and microscopes and gene expression
arrays? None.) I would call it a DSM-IV Personality Disorder like
Lyme-Victim-Abuse-by-DSM-IV-Personality-Disordered-Psychotics-
Masquerading-As-MDs.

This Dattwyler-NK-Epstein-Barr business - the potential compromise to
the very cells we expect to deal with un-latent Epstein-Barr (NK) and
what we see in reports explaining the phenomena of
1) "Epstein-Barr-like immortalized cells" in Lyme victims (Duray,
1989, 1992),
2) the significant increase in replication of Epstein-Barr co-cultured
with Lyme spirochetes (Hulinska, 2003, "Association with lymphoblasts
and internalization of B. garinii by tube phagocytosis increased
replication of viruses more successfully than B. afzelii and chemical
inductors"), and as we will see later,
3) "Ligands for TLR2 or TLR7/8 or whole bacteria had a weaker but
still superadditive effect on [EBV-KMD] B-cell transformation." (Isra,
et al, 2010)
- concerns me. One would think such research would be funded. But,
the Negative-Data Rule-and-the-NIH is another one of those American
social/moral ills that prolong world-wide misery. They oughtta have a
DSM-IV for social diseases like "the U. S. Department of Health and
Human Services."

Radolf and Chemistry:

Next (Number 2), now consider: We cannot recrystalize a lipid to see
its real shape by X-Ray Diffraction studies. [But apparently it can
be blown up (Mass Spec).] Therefore:

Justin Radolf (now at UConn, and who, regardless of having falsely
stated that chronic Lyme does not cause ALS in a newspaper letter-to-
the-editor, is a very good scientist – probably the best in Lyme
Medical Cryme world), in 1990 performed experiments to determine that
he thinks Pam3Cys is actually “TRI-PALMITOYL CYSTEINE” (meant to be
read as an image, a shape) by allowing spirochetes to uptake H3 (heavy
hydrogen isotope) radiolabeled palmitate and then he was able to break
(dissolve) it off again, intact. Let me tell reveal exactly what he
said:

From that 1990 Radolf Abstract (Immunogenic Integral Membrane Proteins
of Borrelia burgdorferi Are Lipoproteins, PubMed ID 2318538):

“The OspA and OspB antigens were radioimmunoprecipitated from
[3H]palmitate-labeled detergent-phase proteins with monoclonal
antibodies, and [3H]palmitate was recovered unaltered from these
proteins after sequential alkaline and acid hydrolyses. The combined
results provide formal confirmation that the major B. burgdorferi
immunogens extracted by Triton X-114 are lipoproteins.”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC258571/pdf/iai00052-0147.pdf

in the text of that 1990 Radolf report:

“Similar biochemical analyses of the other 3H-lipid-labeled B.
burgdorferi proteins were not performed. However, it is reasonable to
assume that these molecules also contain covalently attached fatty
acids, particularly since they remained radiolabeled after boiling in
SDS and electrophoresis in SDS-polyacrylamide gels. Further
biochemical analyses of these other borrelial lipoproteins are
necessary to determine whether fatty acids are linked to some of them
in ratios other than those described for conventional bacterial
lipoproteins. In addition to lipoproteins with typical 2:1 ester to-
amide linkages, T. pallidum appears to contain at least one, the 47-
kDa immunogen, with unconventional lipid linkages (18, 19). Putative
unconventional lipoproteins in Mycoplasma caprkicolum have also been
described (25)."

The logical thing to do is to look at Radolf's references in that
report to see what experiments support his statement that
"unconventional lipid linkages and lipoproteins are found in
spirochetes and mycoplasma."

Additionally, if T. pallidum has an OspA-like antigen in it, that
negates the principle that "Lyme Disease" ("burgdorferi") = Relapsing
Fever + Pam3Cys. (Perhaps Dattwyler could look into that, too.)

Does the syphilis spirochete have a TLR2/1 agonist in it?

Says Radolf in 2005: Lipoprotein-dependent and -independent immune
responses to spirochetal infection.
"Nevertheless, we believe that our results can be extrapolated to
syphilis given the abundance of lipoproteins in both T. pallidum and
B. burgdorferi, the stereotypical nature of responses to these TLR2/1-
dependent agonists in vitro and in vivo (42, 50, 51, 53, 54, 61),
corroborated further herein using OspC-L and 17-L, and the similar
histopathological abnormalities induced by these two pathogens (24,
49)."
http://www.ncbi.nlm.nih.gov/pubmed/16085913
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1182186/?tool=pubmed

Thirdly, we have seen that HIV patients have antibodies against
Pam3Cys – a curiosity, since we think of HIV/Pam3Cys as an immune-
suppression disease:

1988, re HIV and Pam3Cys; Distinction between HIV-1 and HIV-2
infection using novel synthetic lipopeptide conjugates as antigens in
enzyme immunoassays [PubMed 2464607].
“A novel immunoassay technique using synthetic lipopeptide (Pam3Cys-
Ser) linked to immunodominant peptide domains of HIV-1 and HIV-2
envelope proteins as an antigen adsorbent has been developed.
Attachment of peptides to microtiter plates can be considerably
improved with this method by employing the hydrophobic properties of
lipopeptide. From the sera of 121 HIV-1 infected patients 117 reacted
with Pam3Cys-Ser-[HIV-1(598-609)cyclic disulfide]. Five of 5 HIV-2
positive sera were positive with Pam3Cys-Ser-[HIV-2(593-603)cyclic
disulfide]. Control sera failed to react with these conjugates.”
http://www.ncbi.nlm.nih.gov/pubmed/2464607

What does that mean? I don't know. I can only speculate that those
were early HIV patients.

Note: we no longer refer to “disease” as a result of “inflammation”
thanks to HIV and LYMErix Disease. Hopefully I will be able to
explain why here.

Fourth, "The Braun Lipoprotein" (the original synthesis of Pam3Cys);
1983; (PubMed, ID#6347861); Synthesis of the mitogenic S-[2,3-
bis(palmitoyloxy)propyl]-N-palmitoylpentapeptide from Escherichia coli
lipoprotein

"The N-terminal pentapeptide of the lipoprotein from the outer
membrane of Escherichia coli was obtained by coupling S-[2,3-
bis(palmitoyloxy)-(2RS)-propyl]-N-palmitoyl-(R)-cysteine to O-tert-
butylseryl-O-tert-butyl-seryl-asparaginyl-alanine tert-butyl ester
followed by deprotection with trifluoroacetic acid. The tetrapeptide
was built up from alanine tert-butyl ester with N-9-
fluorenylmethyloxycarbonyl protected amino acids. S-[2,3-
Bis(palmitoyloxy)propyl]-N-palmitoylcysteine was obtained from N,N'-
dipalmitoylcystine di-tert-butyl ester via reduction to the thiol, and
S-alkylation with racemic 3-bromo-1,2-propanediol followed by
esterification with palmitic acid in the presence of
dicyclohexylcarbodiimide/dimethylaminopyridine and deprotection with
trifluoroacetic acid. The compounds were characterized unequivocally
by 13C-NMR and mass spectra. The diastereomers of S-[2,3-
bis(palmitoyloxy)propyl]-N-palmitoylcysteine tert-butyl ester with
opposite configuration at the propyl-C-2 atom could be separated on a
silica-gel column.
http://www.ncbi.nlm.nih.gov/pubmed/2464607

Okay, now run the whole thing backwards and/or sideways for yourself:

1) 1983, some German scientists wanted to create an analog of the E
coli Lipid A (there are weird lipids that attract a smart guy like
Radolf). They came up with Pam3Cys. (What one does is then use the
"Related Articles" feature on MedLine to see what uses this E coli
Lipid A analog, Pam3Cys thing had.) 2) Radolf came up with it, too,
in Borrelia, using radiolabeled palmitate. 3) Korean Chemists blew up
the synthetic HIV gp120 and SIV gp120 (?), apparently, and ) HIV
victims overwhelmingly have antibodies to Pam3Cys.

I don't know what this means. We just know that behaviorally - in in
vitro studies - folks wanted to come up with a mimic for a toxin (E
coli's) to use in experiments with cells. Makes sense.

THEREFORE, here is my PRECONCLUSION:

Pam3Cys (the structural backbone or the molecule type or class) seems
to bind antibodies from HIV, SIV and is LYMErix or OspA. It appears
to be synthetic; it has been examined chemically and behaviorally.

In FAB-MS, what was sent to the Koreans from U.S. scientists seems to
be Pam3Cys (the blown up fragments reconstruct or point to a structure
based on a database of previously blown up molecules) and as such
would be a problem in a vaccine-vial and delivered as a vaccine in
free OspA form. [I just don’t think it happened. People were
injected with amorphous clumps of OspA fat blobs. Many people had
“vascular injury” - vascular adverse events - in the OspA trials
(Schoen). Naturally.]

A lot of people have tried to determine what these antigens are,
exactly. Some lipoproteins may be unique. Regardless of what we know
and can know about OspA’s structure, we know how it behaves in cells.
It is a toll-like-receptor-2 (TLR2/1) agonist. That means it is
managed by TLR2/1, or two of the 10 or so known antigen-handlers of
the immune system. (NOTE: Mouse TLR2 is not the same as human TLR2
and agonism of mouse TLR2 gave different results than human TLR2
agonism; we can’t use any mouse studies in “Lyme Disease.”)

WE KNOW: Pam3Cys or HIV gp120 or OspA is tri- (means 3) - acylated -
(fat strings attached by a say, COOH acid group) – lipoprotein, so it
is managed by TLR1/2. Di (2) acyl (fatty acid group) lipoproteins
appear to be managed by TLR2 and 6. So, you see where I am going:
Structure determines Function, or, by its FUNCTION, maybe we can tell
what it looks like. FUNCTIONALLY, to humans, OspA/Pam3Cys did a lot
of damage because of its downstream effects and because we’re auto-
vaccinated with this stuff if we have Chronic Lyme, due to spirochetal
blebbing or the shedding of OspA-blebs as part of these organisms’
“immune evasion strategies” (Alan Barbour, 1996, The Scientist).
That is, one of the bug’s strategies would have been to have the likes
of OspA antigens not recognized by human immune cells, via the chronic
agonism of TLR2.

And that brings us to the main event: What happens as a result of the
down-regulation of normal immune functioning caused by TLR2 agonists?
What does Pam3Cys do?

Stuff does what it is and is what it does at the molecular/atomic
level. This is because interactions between molecules occur as a
result of atomic forces and electron density and diffusion.
Therefore, there was never any getting around what exactly OspA was/
did or what HIV gp120 is/does without appearing to be a totally
idiotic excuse for a scientist, since this is General Chemistry 101.
How the Lyme criminals were able to rely on not a single MD in America
having remembered a nanogram of science from Pre-Med should be an
anthropological study performed by the U.S. National Institute of
Mental Health. But that's like giving a buzzard a scholarship to the
Art Students League.

We find that the perpetrators of the Lyme crimes say one thing in
their digestion of their own reports for public consumption, but their
journal publications and patents almost 100% of the time, reveal the
complete opposite.

The true big picture of "Chronic Lyme" is advanced immunological
ageing. Lyme victims often claim to feel like they're 100 years old.
That's accurate.

Allow me to apologize for simply quoting scientists. I would rather
hear it directly from the source, unfiltered.

Number 1) Radolf, 2001 (no antibodies after repeated exposure to
Pam3Cys/TLR2-agonists) Toll-Like Receptor 2-Dependent Inhibition of
Macrophage Class II MHC Expression and Antigen Processing by 19-kDa
Lipoprotein of Mycobacterium tuberculosis1 [PubMed ID: 11441098]

”Inhibition of MHC-II Ag processing by either MTB bacilli or purified
MTB 19-kDa lipoprotein was dependent on Toll-like receptor (TLR) 2 and
independent of TLR 4. Synthetic analogs of lipopeptides from Treponema
pallidum also inhibited Ag processing. Despite the ability of MTB 19-
kDa lipoprotein to activate microbicidal and innate immune functions
early in infection, TLR 2-dependent inhibition of MHC-II expression
and Ag processing by MTB 19-kDa lipoprotein during later phases of
macrophage infection may prevent presentation of MTB Ags and decrease
recognition by T cells. This mechanism may allow intracellular MTB to
evade immune surveillance and maintain chronic infection.”
http://www.jimmunol.org/cgi/content/full/167/2/910

No antibodies are produced after a time as a result of TLR2 agonism.
In this case, he was talking about tuberculosis. There are no less
that 54 science groups who referenced that report in PubMed, so I will
leave it up to the reader to follow up, but will record, next, this
most recent one by Clifford V. Harding, Mycobacterium tuberculosis and
TLR2 agonists inhibit induction of type I IFN and class I MHC antigen
cross processing by TLR9 [PubMed ID 20660347]:

"...Inhibition of the response to one TLR by another may affect the
ultimate response to pathogens like M. tuberculosis that express
agonists of multiple TLRs, including TLR2 and TLR9. This mechanism may
contribute to immune evasion and explain why IFN-alpha/beta provides
little contribution to host immunity to M. tuberculosis. However,
downregulation of certain TLR responses may benefit the host by
preventing detrimental excessive inflammation that may occur in the
presence of persistent infection."
http://www.ncbi.nlm.nih.gov/pubmed/20660347

Repeating for emphasis: "downregulation of certain TLR responses
may benefit the host by preventing detrimental excessive inflammation
that may occur in the presence of persistent infection."

(What they're talking about, basically, is tolerance to prevent
toxic shock or septic shock occurs as a result of chronic shedding of
Pam3Cys-type, TLR2/1 agonists toxins like OspA. We will see that it
is not possible that OspA could have been a vaccine. This is probably
why SmithKline and Yale came up with the story that "OspA antibodies
disinfected ticks," rather than fought off spirochetes in humans,
which is the normal way vaccines are intended to work. We know for
sure they were not able to read their Western Blots in OspA vaccinated
humans because Schoen and Persing admitted it in a journal article in
1995 [PubMed ID: 8968914] and in their RICO patent [US Patent No
6,045,804] in 1995-1996. Persing and Sigal admitted it again later in
2000 [PubMed ID: 10913394]. The vaccines were falsely qualified.
That's the reason for ALDF/IDSA's aggression against all of their
victims. OspA gave people the New Great Imitator outcomes, as you will
see.)

Number 2) Ray Dattwyler, 1988, when developing the Seronegative Lyme
T-Cell Assay:

”The disorder in these seronegative patients reflected a dissociation
between T-cell and B-cell response, in which the cell-mediated
response was intact yet the humoral portion of the response to B.
burgdorferi appeared to be blunted. This diminished antibody response
is in contrast to the T-cell anergy commonly observed in several
chronic infections (Mycobacterium lepri or M. marinum, filariasis, and
some chronic fungal infections 29-33).”
http://www.ncbi.nlm.nih.gov/pubmed/3054554

(There is a scientific history that reveals fungal antigen-related
immunosuppression.)

Number 3) Wormser, 2000; "Modulation of lymphocyte proliferative
responses by a canine Lyme disease vaccine of recombinant outer
surface protein A (OspA)[PubMed ID 10865170]":
The modulation of human lymphocyte proliferative responses was
demonstrated with a recombinant outer surface protein A (OspA) vaccine
preparation for the prevention of Borrelia burgdorferi infection.
After exposure to either the unaltered vaccine preparation or OspA
prepared in saline, normal lymphocyte responses to the mitogens
concanavalin A, phytohemagglutinin-M or pokeweed mitogen, or the
antigen BCG were consistently reduced. Whole cell extracts of B.
burgdorferi also modulated immune responses but required a much
greater quantity of protein than needed for the OspA preparation. The
magnitude of modulation was directly dependent on the quantity of
OspA. OspA interferes with the response of lymphocytes to
proliferative stimuli including a blocking of cell cycle phase
progression. Future studies designed to delete the particular region
or component of the OspA molecule responsible for this effect may lead
to improved vaccine preparations.
http://www.ncbi.nlm.nih.gov/pubmed/10865170

(Gary Wormser has reason to believe there is an immunosuppression
outcome related to TLR2-agonism, like Chronic Lyme and OspA
vaccination.)

Numbers 4 - 12 - "EBV-like transformed cells"/Anti-Apoptosis:

4) Duray, in IDSA's 1989 journal: Clinical pathologic correlations of
Lyme disease [PubMed 2614170]:
“Frank signs of meningeal irritation herald stage II illness,
reflected by an increase of CSF lymphocytes and plasma cells and
moderate increases in total protein in CSF [9,16,17]. Immature B
cells can also be seen in the spinal fluid. These cells can appear
quite atypical- not unlike transformed of neoplastic lymphocytes.
Although it is known that spirochetes can be isolated from spinal
fluid, they are not recovered in all cases.”
http://www.ncbi.nlm.nih.gov/pubmed/2814170

Who referenced this article where Duray discusses transformed B-cells?
http://www.ncbi.nlm.nih.gov/pubmed?db=pubmed&cmd=link&linkname=pubmed_pubmed_citedin&uid=2814170

Lenny Sigal, Alan Barbour, Andrew Pachner, CDC's Duane Gubler, CDC's
Barbara Johnson* and Joe Piesman,* , Norgard and Radolf.

* CDC officers whose European patents also demonstrate that they know
there are 2 kinds of Lyme: 1) the Allen Steere-, HLA-linked
hypersensitivity response, and 2) the normal people.

5) Duray at the 1992, ALDF.com's Cold Spring Harbor Conference:

"On occasion, these atypical-appearing large lymphocytes have been
misinterpreted in biopsy by several laboratories as cells of a
malignant lymphoma or leukemia. Bb antigens, then, may stimulate
growth of immature lymphocytic suibsets in some target organs, as well
as in the cerebrospinal fluid (Szyfelbein and Ross 1988). Usual
bacterial infections do not produce such lymphocytic infiltrates in
tissue. These immunoblastoid cells in Bb infections at times resemble
those found in Epstein-Barr virus infections. Does Bb reactivate
latent virus infections in tissues? Do some tick inocula harbor
simultaneous infectious agents (ixodid ticks can harbor Rickettsiae,
Babesia microti, and Ehrlichia bacteria, in addition to Bb), producing
multi-agent infections in some hosts? Further studies can clarify
these issues by mans of tissue-based molecular probe analysis." -
Paul Duray, NCI, NIH, Ft. Detrick, at the 1992 Cold Spring Harbor
ALDF.com conference, published in Steven Schutzer's 1992 book, "Lyme
Disease, Molecular and Immunologic Approaches."

6) 2000, Gross, et al, "In vitro Brucella suis infection prevents the
programmed cell death of human monocytic cells."

”Analysis of Brucella-infected monocytes revealed specific
overexpression of the A1 gene, a member of the bcl-2 family implicated
in the survival of hematopoietic cells. Brucella infection also
rendered macrophage-like cells resistant to Fas ligand- or gamma
interferon-induced apoptosis, suggesting that Brucella infection
protected host cells from several cytotoxic processes occurring at
different steps of the immune response. The present data clearly show
that Brucella suis modulated the monocyte/macrophage's apoptotic
response to the advantage of the pathogen, thus preventing host cell
elimination. This might represent a strategy for Brucella development
in infected hosts.”
http://www.ncbi.nlm.nih.gov/pubmed/10603407

In the body of the full text report:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC97140/?tool=pubmed
INTRO:
"In recent years, it has become obvious that programmed death (or
apoptosis) of cells of the monocytic lineage may be relevant for local
immune responses against microorganisms (26, 31). Several bacterial
organisms, such as Shigella flexneri (47), Legionella pneumophilia
(35), Yersinia enterocolitica (41), Bordetella pertussis (20),
Actinobacillus actinomycetemcomitans (18), Listeria monocytogenes
(40), and Salmonella enterica serovar Typhimurium (27), promote the
destruction of monocytic phagocytes by apoptosis, thus circumventing
the first line of defense of the immune system. Surviving bacteria
infect neighboring cells and disseminate to other tissues, often
epithelial cells. Recently, it was reported that some intracellular
bacteria that preferentially infect monocytic phagocytes have a
totally opposite strategy and protect their host against apoptosis.
Mycobacterium tuberculosis, which was reported to promote alveolar
macrophage apoptosis (19, 22), and Mycobacterium bovis were shown to
inhibit spontaneously occurring apoptosis in human monocytes (9, 24),
possibly by inducing tumor necrosis factor alpha (TNF-α) production.
Furthermore, HeLa cells infected with the obligate intracellular
bacteria chlamydiae are resistant to apoptosis triggered by exogeneous
stimuli (12), and Rickettsia rickettsii prevents the programmed cell
death of endothelial cells (7). Molloy et al. showed that apoptosis of
BCG-[Tuberculosis- KMD] infected macrophages kills intracellular
mycobacteria (30).
"It was thus postulated that inhibition of host cell apoptosis
benefits the intracellular pathogen because it protects it against
immune attacks from the outside. This could favor an optimal
multiplication of intracellular bacteria (7, 9, 12, 24)."

(So, we can't say that it isn't commonly known that intracellular
pathogens like Borreliae deploy mechanisms of stealth, and that one of
those mechanisms is inhibition of apoptosis. The reader should go
ahead and follow up on the references and see what are the updates to
this area of research. It is not discussed at all by the Infectious
Diseases Society of America, the NIH or the CDC, allowing other
nations' scientists to take the ball and run with it.)

7) 2003, Hulinska, et al; "Interaction of Borrelia burgdorferi sensu
lato with Epstein-Barr virus in lymphoblastoid cells. [PubMed
12630667]"

”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.
http://www.ncbi.nlm.nih.gov/pubmed/12630667

"Association with lymphoblasts and internalization of B. garinii by
tube phagocytosis increased replication of viruses more successfully
than B. afzelii and chemical inductors."

Of course, "WHY??" That ▲ would freak me right out if I was a
scientist. Which I am so it does. (I can't speak for ILADS.org or
IDSociety.org. Or the AMA. Or the DHHS.)

In a related, more recent study, Hulinska hypothesizes:
"In conclusion, induction of EBV lytic cycle in lymphoblastoid cells
causes increased oxidative stress in the host cells within 48 h, a
process that could be involved in malignant transformations." from:
"Induction of Epstein-Barr virus (EBV) lytic cycle in vitro causes
oxidative stress in lymphoblastoid B cell lines" [PubMed ID:
190782543]
http://www.ncbi.nlm.nih.gov/pubmed/19082543

8) 2010, April, Iskra, et al, "Toll-like receptor agonists
synergistically increase proliferation and activation of B cells by
epstein-barr virus." [PubMed 20089650]:
"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."
http://www.ncbi.nlm.nih.gov/pubmed/20089650

9) 2004; Gerlic, Horowitz, et al, "Mycoplasma fermentans inhibits
tumor necrosis factor alpha-induced apoptosis in the human
myelomonocytic U937 cell line" [PubMed ID: 15286682]:
"Mycoplasma fermentans (M. fermentans) was shown to be involved in the
alteration of several eukaryotic cell functions (i.e. cytokine
production, gene expression), and was suggested as a causative agent
in arthritic diseases involving impaired apoptosis. We investigated
whether M. fermentans has a pathogenic potential by affecting tumor
necrosis factor (TNF)alpha-induced apoptosis in the human
myelomonocytic U937 cell line. A significant reduction in the TNF
alpha-induced apoptosis (approximately 60%) was demonstrated upon
either infection with live M. fermentans or by stimulation with non-
live M. fermentans. To investigate the mechanism of M. fermentans
antiapoptotic effect, the reduction of mitochondrial transmembrane
potential (DeltaPsim) and the protease activity of caspase-8 were
measured. In the infected cells, the reduction of DeltaPsim was
inhibited (approximately 75%), and an approximately 60% reduction of
caspase-8 activity was measured. In conclusion, M. fermentans
significantly inhibits TNFalpha-induced apoptosis in U937 cells, and
its effect is upstream of the mitochondria and upstream of caspase-8."
http://www.ncbi.nlm.nih.gov/pubmed/15286682

9) 2002, Garth Nicolson, "High frequency of systemic mycoplasmal
infections in Gulf War veterans and civilians with Amyotrophic Lateral
Sclerosis (ALS)" [PubMed ID:
"We also found that ALS patients have some of the signs and symptoms
seen in a variety of chronic illness patients, consistent with their
having mycoplasmal infections that are also found in these patients.
18-20, 28, 29 Similar to chronic mycoplasma infections, 21-23, 27-29
enteroviruses [EBV, Cytomegalovirus, HHV - KMD] have also been found
in patients with chronic myocarditis and chronic fatigue. 31 It is
interesting that both enteroviruses and mycoplasmas have the capacity
to cause slow, persistent infections that can eventually result in
cellular dysfunction and eventually cell death, and mycoplasmal
infections have been implicated in infectious neurological diseases
17, 28"

[And he goes on to say, it seems that mycoplasma plus viruses plus
other co-factors create this outcome. This is what I found, too,
independently. For instance, the minute I first saw a graphic of
mycoplasma adherence to red blood cells, I instantly knew that that
would effect osmotic potential and the ability to transfer oxygen.
Search using the term Eperythrozoon (note: "Ep - erythro -"). Many
scientists, upon further research, agree that this could be the
outcome of mycoplasma in the blood: oxygen transport and RBC
metabolism problems. This is what I am claiming the evidence suggests
is responsible for Chronic Fatigue. Garth Nicolson had published such
a hypothesis at least a good 6 years earlier. Probably more. I
recommend people read his full text article and look at all of his
references, too.]

10) 2004, Zhang, Lo, et al, "Mycoplasma fermentans infection promotes
immortalization of human peripheral blood mononuclear cells in
culture." [PubMed ID 153314490]
"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. http://www.ncbi.nlm.nih.gov/pubmed/15331449

("The in vitro findings would be of relevance to lymphoproliferative
disorders that occurred in patients with immune suppression.")

11) (2007) "The inhibitory effect of Mycoplasma fermentans on tumour
necrosis factor (TNF)-alpha-induced apoptosis resides in the membrane
lipoproteins." [PubMed ID 16889623]
"To investigate the mechanism of M. fermentans antiapoptotic effect,
the reduction of mitochondrial transmembrane potential (delta psi m)
was measured. M. fermentans total proteins LPMf and MALP-2, but not
AqMf, inhibited the reduction of delta psi m. In addition, M.
fermentans total proteins LPMf and MALP-2, but not AqMf, downregulated
the formation of active caspase-8 [caspases are auto-kill enzymes-
KMD]. NF-kappaB was transactivated in cells treated with M. fermentans
lipoproteins, and was essential for host cell survival, but not for
the inhibition of TNFalpha-induced apoptosis by LPMf. Our results
suggest that the inhibitory effect exerted by M. fermentans on
TNFalpha-induced apoptosis in U937 cells is due to the membrane
lipoproteins of these bacteria."
http://www.ncbi.nlm.nih.gov/pubmed/16889623

[Autism epidemic hint: Recall that the Johns Hopkins physician who's
daughtersuffered the typical brain damage acquired from vaccination
had a "mitochondrial defect." I suggest that common local, even
household fungi can have this effect: should a child be vaccinated in
this immunosuppressed state with live attenuated and not heat-killed
viruses, one wonders how these vaccines can have their desired
effect. You vaccinate a kid who is already struggling with this
preservation of aberrant cells business and viola! They can't handle
the viruses. One wonders if acquiring subclinical cases of the
diseases these vaccines allegedly prevent - the "R" in "MMR" stands
for Rubella, a vaccine given to prevent congenital autism - is what is
meant by "SSPE" (subacute, sclerosing pan-encephalitis) as an adverse
event warned of in these vaccines' monographs. Ask the mothers. Did
the babies have the clinical signs of encephalitis? Seems to me they
did (screaming, high temps, etc).]

More news on fungal-viral syngery at:
"Interactions between bacterial pathogens and mitochondrial cell death
pathways" [PubMed ID: 20818415]
http://www.nature.com/nrmicro/journal/v8/n10/full/nrmicro2421.html
Nature Reviews Microbiology 8, 693-705 (October 2010) | doi:10.1038/
nrmicro2421
"The modulation of host cell death pathways by bacteria has been
recognized as a major pathogenicity mechanism. Among other strategies,
bacterial pathogens can hijack the cell death machinery of host cells
by influencing the signalling pathways that converge on the
mitochondria. In particular, many bacterial proteins have evolved to
interact in a highly specific manner with host mitochondria, thereby
modulating the decision between cell life and death. In this Review,
we explore the intimate interactions between bacterial pathogens and
mitochondrial cell death pathways."

I am suggesting that it is possible that the Pam3Cys/sticky fungal
antigens shed by these organisms, particular Borrelia, adhere to the
mitochondrial membranes, disrupting the machinery, in the same way
that mycoplasma adhere to red blood cells, disrupting osmotic
potential, causing clinical signs of anemia (chronic fatigue) without
a detectable loss of oxygen/hemoglobin.

12) 1999: "Mycoplasmal infections prevent apoptosis and induce
malignant transformation of interleukin-3-dependent 32D hematopoietic
cells." [PubMed 10567525]
”In comparison, live Mycoplasma fermentans or M. penetrans infection
for 4 to 5 weeks induced malignant transformation of 32D cells.”
http://www.ncbi.nlm.nih.gov/pubmed/10567525

So. We know EBV and mycoplasmal lipid induce malignant
transformations. If you don't know it, go ahead and look it up for
yourself. But read the science, not someone else's interpretation of
it.

Number 13) 1998, Philipp, The immunosuppressive cytokine IL-10:
"Borrelia burgdorferi stimulates the production of interleukin-10 in
peripheral blood mononuclear cells from uninfected humans and rhesus
monkeys." [PubMed 9598735]
"Thus, the lipid moiety is essential in the induction of IL-10 in
these PBMC. B. burgdorferi M297, a mutant strain that lacks the
plasmid that encodes OspA and OspB, also induced IL-10 gene
transcription in PBMC, indicating that this phenomenon is not causally
linked exclusively to OspA and its lipid moiety. These results
demonstrate that B. burgdorferi can stimulate the production of an
antiinflammatory, immunosuppressive cytokine in naive cells and
suggest that IL-10 may play a role both in avoidance by the spirochete
of deleterious immune responses and in limiting the inflammation that
the spirochete is able to induce."
http://www.ncbi.nlm.nih.gov/pubmed/9596735

When I gave a scientific presentation supplying 30 pages of
documentation to all 15 members of the FDA Vaccine Committee hearing
on LYMErix on January 31, 2001, I mentioned this IL-10 induction
report by Mario Philipp and also the Dattwyler NK cell activity
diminution report when I claimed that while LYMErix vaccination could
not give people Lyme disease, it seems to be causing a chronic Lyme-
like outcomes as a result of the immune-dysregulation it causes. And
here we are today, saying the exact same thing, 10 years later...

What you are seeing happening is the confluence of science in Chronic
Fatigue Syndrome, Gulf War Syndrome, vaccines' damage, and bioweapons
conspiracy theory - as reported by Congress ( in "UNITED STATES DUAL-
USE EXPORTS TO IRAQ AND THEIR IMPACT OF PERSIAN GULF WAR VETERANS, May
25, 1994") - by researchers who have been marginalized in their own
fields. The truth is overlapping. And overwhelming.

Number 14) In 2004, Schroder et al, "Lipopolysaccharide binding
protein binds to triacylated and diacylated lipopeptides and mediates
innate immune responses." [PubMed ID:15294986]
"TLR-2 is known to form heterodimers with either TLR-1 or -6, and
MALP-2 has been identified to interact with TLR-2/TLR-6 heterodimers
(28). In contrast, triacylated lipopeptides have been shown to be
recognized via TLR-2/TLR-1 (29).

"Moreover, we obtained several lines of evidence that CD14 is also
involved in cellular responses to triacylated and diacylated
lipopeptides. In confirmation of prior studies, lipopeptides displayed
a pattern of recognition via TLR-2 in differential combinations with
TLR-1 and -6 related to their different degree in acylation.

"Lipoproteins and lipopeptides bearing the Pam2Cys or Pam3Cys motif
are abundant among pathogens of the respiratory tract, such as
Mycoplasma pneumonia and Mycobacterium tuberculosis. Our own previous
studies have revealed that major cell wall components of Streptococcus
pneumoniae and Staphylococcus aureus [MRSA-KMD] causing pneumonia, are
also recognized by LBP (31, 48). Thus, recognition of molecular
patterns by LBP may be an important step in the initiation of a host
response during pneumonia. In addition, our data suggest that LBP, by
recognizing lipoproteins, may also play a role in chronic or cyclic
infections: With the exception of Mycoplasma-caused pneumonia,
clinically important pathogens carrying lipoproteins represent causes
of slow, cyclic or chronic infectious diseases, e.g., Lyme disease or
tuberculosis. Even mycoplasm pneumonia, although frequent in children,
is often afebrile and self-limiting in contrast to pneumonia caused by
other pathogens (61). Our data suggest that recognition of these slow-
acting microorganisms may also be accomplished by LBP. Synthetic
lipopeptides have been the basis for broad vaccine development lately
for a wide variety of diseases including HIV, malaria, CMV, and HSV
(reviewed in Ref. 16). Understanding of the molecular mechanisms of
host recognition of lipopeptides and lipoproteins in more detail may
further help to further improve these innovative strategies.
http://www.jimmunol.org/content/173/4/2683.long

Again: "With the exception of Mycoplasma-caused pneumonia, clinically
important pathogens carrying lipoproteins represent causes of slow,
cyclic or chronic infectious diseases, e.g., Lyme disease or
tuberculosis... Synthetic lipopeptides have been the basis for broad
vaccine development lately for a wide variety of diseases including
HIV..."

Translation: You may not want to make a vaccine out of these types of
molecules because...

Number 15) "Tolerance Induced by the Lipopeptide Pam3Cys Is Due to
Ablation of IL-1R-Associated Kinase-11"

"As expected, Mono Mac 6 cells that were precultured without Pam3Cys
(naive cells) gave a strong intracellular TNF signal after Pam3Cys
stimulation (Fig. 4, second panel). By contrast, when the cells were
precultured in the presence of the low Pam3Cys dose, followed by
Pam3Cys (10 µg/ml) stimulation for 5 h, then there was no
intracellular TNF expression observed (Fig. 4, fourth panel). This
demonstrates that the cells have become tolerant to Pam3Cys
stimulation. In an average of three experiments, the Pam3Cys-induced
TNF expression was 8.5 ± 0.9 channels in the naive cells, and it was
reduced to 0.1 ± 0.7 channels in tolerant cells (p < 0.05)."

"NF-κB is a crucial transcription factor for the regulation of TNF
gene expression. LPS tolerance has been shown to act via NF-κB, either
by reduced mobilization or by shifting to p50p50 homodimers."

"We then studied IRAK-1 during Pam3Cys tolerance. As shown in Fig. 10,
upper panel, IRAK-1 protein was strongly expressed in naive cells. In
Pam3Cys-tolerant cells, however, no signal for IRAK-1 was detectable."

In the present study, CD14 and TLR2 showed strong and moderate cell
surface expression in tolerant cells, respectively. This indicates
that Pam3Cys tolerance does not act by down-regulating these cell
surface receptors, but we have not studied expression of TLR1, which
is the partner for TLR2 in Pam3Cys signaling (35). In a study by
Nomura et al. (36), murine macrophages tolerant to LPS failed to stain
with an Ab that recognizes the complex of TLR4 and MD-2, which
suggests that these molecules are down-regulated or that they do not
interact anymore. Currently, we cannot exclude the possibility that,
in Pam3Cys tolerance, there is a disruption of the interaction of the
TLR1, TLR2, and CD14 receptor components.

"Taken together, our findings demonstrate that in the same type of
cell two different mechanisms of tolerance can coexist: 1) induction
of p50 homodimers for LPS/TLR4 signals, and 2) depletion of IRAK-1
protein for Pam3Cys/TLR2 signals. This indicates that it may be of
importance to the host to ensure down-regulation of TNF and to prevent
the detrimental effects of excessive amounts of this cytokine after
repeated stimulation, i.e., during a persistent bacterial infection
that will involve engagement of more than one type of TLR."

What that means is that this is a mechanism, perhaps, to shield the
mammal from toxic shock.

What it all means - the sum of all of these reports - is that LYMErix
could never have been a vaccine, and the same is true for all
molecules of this same class - TLR2/1 agonists - like the Tuberculosis
and probably the HIV non-vaccines.

It means that the chronic agonism of TLR2 by Lyme and other organisms
like it, will produce no antibodies late in the disease, or are
stealth (Radolf).

It means that all such studies based on antibodies such as ones to
rule out what's infecting Chronic Fatigue victims need to be thrown
out. (We can talk more about this some other time re the bad guy's
"Primers Shell Game" or their "Lyme is a Persistent Infection"
articles. Or we can talk about the cyst form, biomarkers, and valid
methods of detection, since these topics are all part of their
deliberately fraudulent diagnostics.)

It means that OspA appears to have been designed to be an E coli
toxin. We don't know how OspA in triplicate seems to be HIVgp120.
(We can only wonder about Plum Island and how far back this thing was
known to be an immune suppressor, but on the other hand, Radolf tells
us the syphilis spirochete also has an OspA-like antigen in it.)

It also means the lies Yale and SmithKline told about LYMErix had a
detrimental effect on our understanding of everything from Lupus to
Multiple Sclerosis to ALS to Cancer to HIV to Tuberculosis... all of
modern man's plagues.

Yale et al, LIED about the very fact that "Lyme" is not an
"inflammatory disease," but a diseases-set related to mutations in B-
cells, immunosuppression, the activation of viruses and belonging to
the Initiators of the Opportunistics, like AIDS. A disease that
induces a Pandora's Box of others, without the trace of antibodies.
"The perfect stealth pathogen." A perfect bioweapon, the Trojan
Horse.

QUESTIONER: I have seen you say, OpsA is a Pam3Cys and it can be
applied to the optic nerve to regenerate the nerve itself. This was
done in the UK by (I will quote the study and docs here).

KATHLEEN: Yeah, that's a weird one. But not so weird when you
understand that these types of antigens inhibit apoptosis. Remember
that lithium acts as a calcium antagonist in calmodulin (changing
membrane potential and therefore is an inhibitor of apoptosis in
response to injury or, say poison from a stroke). This is the reason
people thought there was something in the spring water that gave it
Fountain of Youth properties. There was. Lithium.

But lithium also promotes BCL2-class molecules which inhibit
apoptosis. You can have a genetic "defect" of, say a duplicated,
reversed transcription of a BCL-2 like gene, and end up with one of
those "nerve overgrowth syndromes" seen in people chromosome 15
abnormalities. Why? Because reverse duplications can result in the
over-expression of the gene.

These fungal antigens inhibit apoptosis as a survival strategy and we
end up at the same time, apparently, activating latent enteroviruses.
We could call it fungal-viral synergy. Plenty of researchers see this
now. I suspect Yale (Joe Craft) sees this now regarding what's
happening in Lyme-Lupus. I quoted Garth Nicolson on this because he
was one of the earlier pioneers of "Get the cotton picken science
straight and nevermind the psychiatric voodoo." People in the field
are now more commonly using the term "dysimmunity" over autoimmunity
because dysimmunity dys-implies that the infectious organism is gone.
'No longer there. [We don't say that any more (autoimmunity), because
you can't use antibody studies to determine whether or not someone is
suffering an infection. This is what LYMErix Disease taught us.]

What is the mechanism of inhibition of apoptosis? For Tb-like
antigens (Pam3Cys), "In conclusion, M. fermentans significantly
inhibits TNFalpha-induced apoptosis in U937 cells, and its effect is
upstream of the mitochondria and upstream of caspase-8."

and more recently:
"These results may be attributed to the reduction in phosphorylation
of the mitogen-activated protein kinase (MAPK), p38, and the
transcription factor NFkappaB, as well as to an increase in the
expression of the suppressors of cytokine signaling (SOCS)-1 and -3
proteins in LPS-pretreated mast cells."

And of course, the ever infamous EBV which is notorious for
transforming cells, or "keeping them alive nearly forever so that they
can be used in lab studies."

Other data on this "use Pam3Cys topically on injured optic nerves"
business (all very dramatic in my opinion):
2010; "Stimulation of axon regeneration in the mature optic nerve by
intravitreal application of the toll-like receptor 2 agonist
Pam3Cys" [PubMed 19661221]:
RESULTS: Intravitreal injection of Pam(3)Cys, as lens injury (LI),
induced the upregulation of ciliary neurotrophic factor and glial
fibrillary acidic protein expression in retinal glia accompanied by
the activation of the JAK/STAT3 pathway in RGCs. As a consequence,
RGCs switched to a regenerative state, indicated by a significant
upregulation of GAP43 expression and increased neurite outgrowth of
RGCs in culture. Repeated intravitreal Pam(3)Cys application in vivo
induced neuroprotective effects and caused stronger axon regeneration
in the injured optic nerve than observed after LI.
http://www.ncbi.nlm.nih.gov/pubmed/19661221

again, "RGCs switched to a regenerative state, indicated by a
significant upregulation of GAP43 expression and increased neurite
outgrowth of RGCs in culture"

Another one:
"Neuroprotective and axon growth-promoting effects following
inflammatory stimulation on mature retinal ganglion cells in mice
depend on ciliary neurotrophic factor and leukemia inhibitory
factor." [PubMed 19906980]
"In conclusion, the results of the present study support the
hypothesis that astrocytes are the major source of factors mediating
the neuroprotective and axon regeneration-promoting effects of
inflammatory stimulation in the eye. Furthermore, they provide
additional confirmatory evidence for CNTF being a direct key mediator
of these beneficial effects and identify LIF as another significant
contributing factor."
http://www.ncbi.nlm.nih.gov/pubmed/19906980

Bottom Line: They don't really know why.

QUESTIONER: Help us understand if OspA is a toxin how can it be a good
thing at the same time?

KATHLEEN: OspA is a toxin because as I showed earlier, it was meant
to be a mimic of E. coli Lipid A, which is a toxin. According to
Allen Steere, et al, OspA is a toxin for people who have his Dearborn-
HLA-Farce haplotypes

However Steere has admitted in the journals (but not to the public),
that he treats Lyme with long term, repeated antibiotics, and that he
thinks Lyme/LYMErix Disease is a disease of immune-dysregulation/
suppression. Let me quote those articles of his:

2006, Allen Steere; "Therapy for Lyme arthritis: strategies for the
treatment of antibiotic-refractory arthritis." [PubMed ID: 17009226]
"Unless a patient has concomitant neurologic abnormalities, a 1-month
course of oral doxycycline or amoxicillin is recommended (Figure 3).
Most patients experience resolution of arthritis during the course of
such therapy. However, if there is mild residual joint swelling, we
repeat the oral antibiotic regimen for another 30 days, even though
the arthritis usually resolves without further therapy (7). In our
experience ['knowing about the "target imbalance' or the fact that
these genes/Osps undergo antigenic variation, rendering flagellin or
the intragenic spacer RNAs the only sane ones to us, and playing the
DNA/RNA shell game - using the wrong DNA/RNA to look for Lyme in
humans, but using the right DNA or RNA to look for spirochetes in
ticks to patent- KMD], no patient who received IV therapy had
persistence of B burgdorferi DNA in joint fluid or synovial tissue or
recurrent attacks of arthritis [which is, of course, a lie, See
PubMed: 8769624- KMD]. Hence, if patients have moderate to severe
joint swelling after a 1-month course of oral antibiotics, IV
ceftriaxone (2 gm/day) for an additional month is appropriate. If
arthritis persists and PCR results remain positive, we re-treat with
oral antibiotics for an additional month, even though PCR results may
remain positive in joint fluid for several weeks after the eradication
of spirochetes (24, 41)."
http://onlinelibrary.wiley.com/doi/10.1002/art.22131/full

This of course does make any sense because IV cef (means "head")
triaxone is for meningitis. It should surprise no one that Allen
Steere might think the brain is the knee because his associate, Steven
Malawista recommended throwing out "complicating variables like the
brain-brain-barrier" altogether. What can you say to that nonsense?

1996, Allen Steere, "Detection of Borrelia burgdorferi DNA by
polymerase chain reaction in cerebrospinal
fluid in Lyme neuroborreliosis." [PubMed ID 8769624]:

"of 73 patients with Lyme arthritis who were untreated or treated
with short courses of oral antibiotics before testing, 70 (96 percent)
had positive PCR results. In contrast, of 19 patients who received
either parenteral antibiotics or long courses of oral antibiotics,
only 7 (37 percent) had positive test results after treatment
(P<0.001). In the 29 patients for whom serial samples were available,
all pretreatment samples were positive."
http://www.ncbi.nlm.nih.gov/pubmed/8769624

Not wanting to miss out on all the Lyme/LYMErix Disease immune-
suppression fun, Allen Steere came up with his own imaginary version
of it (Dec, 2010):

"Role of adrenomedullin in Lyme disease. [PubMed ID 20921145]:
"Borrelia burgdorferi stimulates a strong inflammatory response during
infection of a mammalian host. To understand the mechanisms of immune
regulation employed by the host to control this inflammatory response,
we focused our studies on adrenomedullin, a peptide produced in
response to bacterial stimuli that exhibits antimicrobial activity and
regulates inflammatory responses by modulating the expression of
inflammatory cytokines. Specifically, we investigated the effect of B.
burgdorferi on the expression of adrenomedullin as well as the ability
of adrenomedullin to dampen host inflammatory responses to the
spirochete. The concentration of adrenomedullin in the synovial fluid
of untreated Lyme arthritis patients was elevated compared with that
in control osteoarthritis patient samples. In addition, coculture with
B. burgdorferi significantly increased the expression of
adrenomedullin in RAW264.7 macrophages through MyD88-,
phosphatidylinositol 3-kinase (PI3-K)-, and p38-dependent signaling
cascades. [Check, yeah, we covered that; happened years ago, KMD]
Furthermore, the addition of exogenous adrenomedullin to B.
burgdorferi-stimulated RAW264.7 macrophages resulted in a significant
decrease in the induction of proinflammatory cytokines. Taken
together, these results suggest that B. burgdorferi increases the
production of adrenomedullin, which in turn negatively regulates the
B. burgdorferi-stimulated inflammatory response.
http://www.ncbi.nlm.nih.gov/pubmed/20921145

Ahh, I see. It was this mystery compound all along, adrenomedullin.
Let me guess, we, the Hysterics, actually psychologically induced this
mystery adreno thing, and that was the reason all along you thought
you saw an association between hysteria and the chronic Lyme
outcomes. For which you asked for grant money to determine the
seronegative aspects of. And to study the neurologic outcomes of.
And in which you found spirochetes in the dead-bodies and brains of
people you treated numerous times (1994). And among whom you found a
nitric oxide marker of degenerative brain disease. These people whose
brains need to be thrown out. Yes, Allen Steere, we was trickin you
all long. And "stalking" you in Albany while you were at Tufts in
Boston, after we had already proven the entire crime to the FDA
Vaccine Committee in Bethesda 5 months earlier (2001). And while you
were hiding in your high-security T cell freezers... looking like a
ghost. Depressed. A victim of "internet cult" VooDoo.
Yes, indeed, Allen. We do indeed have magical powers. We made the
entire DHHS and State Department an international pariah because we
had your pin head to experiment with <smiley face>.

QUESTIONER: What about how Epstein-Barr and how that causes mutations
- The New Great Imitator Outcomes. The type Paul Duray was talking
about?

KATHLEEN: Yeah, that's important stuff. I wonder about that myself,
now that I have recently acquired (within the last 3 months) a copy of
the full text of the Garth Nicolson-Mycoplasma-Gulf War Illness
report. Recall that Sam Donta was given an 8 million dollar grant to
treat Gulf War Illness with doxycycline because he thought he was
treating Mycoplasma. (Compliance problems resulted in no data; we all
understand compliance problems - at least I do.)

A lot of people seem to be unfamiliar with Donta's past work. That
has much to do with certain Lyme activists groups vilifying him
because, as they claim, he "doesn't know what he is talking about -
doesn't treat the coinfections." What these, apparently, Naturally-
Peerless Reviewers of Donta's don't understand is that his protocols
do, in fact, treat all the coinfections. And the ones we were slow to
learn about, obviously - the mycoplasma in Lyme. Or the chronic
stealth mycoplasma who made a home in us, thanks to OspA or Borrelia.

One of the reasons Paul Duray was interesting to me was because he
also worked for the US Military (Donta's study was obviously
coordinated with the VA). Duray worked with Stephen Hatfill at Fort
Detrick . Yet here is this high-level man, high-level in the National
Cancer Institute at Fort Detrick (hint, hint), a top US pathology
expert, who had been giving the Lyme criminal gang (I know you're
going to edit that out) all the clues all along. From 1989 to 1992,
when things totally fell apart for us, because Allen Steere had
decided he was working for insurance companies (his father worked for
BigInsurance). That mystified me. Why would it not be interesting to
the Lyme cryme gang that "these could be mistaken for leukemia or
Epstein-Barr infected cells."

To answer your question, really, would be quite lengthy, and at that,
like the Pam3Cys-Growth Factor question regarding regenerating optic
nerves... I am not sure it is all known how, mechanistically, fungi
and EBV result in immortalizations.

Consider this - one of the meningitis organisms:

2010, March (BU, where Mark Klempner - who assured Donta was booted
out of the same place - lives now furthering his bumbling in South
Boston, making the residents nervous because this bumbling liar is a
now CDC bioweaponeer); "Meningococcal porin PorB prevents cellular
apoptosis in a toll-like receptor 2- and NF-kappaB-independent
manner." PubMed ID:
"Meningococcal porin PorB is an inhibitor of apoptosis induced via the
intrinsic pathway in various cell types. This effect is attributed to
prevention of mitochondrial depolarization and of subsequent release
of proapoptotic mitochondrial factors. To determine whether apoptosis
is globally inhibited by PorB, we compared the intrinsic and extrinsic
pathways in HeLa cells. Interestingly, PorB does not prevent extrinsic
apoptosis induced by tumor necrosis factor alpha plus cycloheximide,
suggesting a unique mitochondrial pathway specificity. Several
intracellular factors regulated by NF-kappaB, including members of the
Bcl-2 family and of the inhibitor of apoptosis (IAP) family, play
major roles in controlling apoptosis, and some of them are thought to
contribute to the antiapoptotic effect of the gonococcal porin, PIB.
However, most of the members of the Bcl-2 family and the IAP family
are not induced by meningococcal PorB in HeLa cells, with the
exception of Bfl-1/A1. Interestingly, PorB does not induce NF-kappaB
activation in HeLa cells, likely due to a lack of Toll-like receptor 2
(TLR2) expression in these cells. Bfl-1/A1 expression is also
regulated by CBF1, a nuclear component of the Notch signaling pathway,
independent of NF-kappaB activation. Since HeLa cells are protected by
PorB from intrinsic apoptosis events, regardless of TLR2 and NF-kappaB
expression, the possibility of a contribution of alternative signaling
pathways to this effect cannot be excluded. In this paper, we describe
an initial dissection of the cascade of cellular events involved in
the antiapoptotic effect of PorB in the absence of TLR2.
http://www.ncbi.nlm.nih.gov/pubmed/20028813
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2825956/?tool=pubmed

"Some examples of bacteria that inhibit apoptosis are Chlamydia (20,
22, 79), Shigella flexneri (11), Brucella (28), Porphyromonas
gingivalis (56, 58), Neisseria meningitidis, and Neisseria gonorrhoeae
(4, 23, 31, 42, 50, 55, 62, 65, 73). Our group and other workers have
reported that live N. meningitidis and purified meningococcal porin
inhibit apoptosis (15, 49, 50, 62, 75), potentially via multiple
mechanisms. While meningococcal infection induces NF-κB-mediated
upregulation of antiapoptotic genes, purified PorB and PorB from live
bacteria directly interact with mitochondria and modulate their
membrane potential, preventing release of cytochrome c.N. gonorrhoeae
and purified gonococcal porin PIB induce NF-κB-mediated upregulation
of antiapoptotic genes (4, 5, 23, 33, 55, 65), which could also
contribute to prevention of apoptosis."

It seems that pathogens reliably, almost, deploy strategies that not
only ensure their own survival in human hosts, but tend to invite
others. "Lyme" is not limited to burgdorferi and its ticks' co-
infections. "Lyme" and the criminal enterprise that put out Pam3Cys
as vaccines gave us a new view of human illness. Rather than stimulus-
response (antigen-antibodies), we now know a human to be a sum of
their exposures, and that sum is somewhat dependent on the sequence in
which a person becomes infected with each infection.

We learned that all results based on antibody testing for the last 50
years have to be thrown out.

The whole sci-med world has been turned upside down because of this
Pam3Cys business. The NIH found out the hard way that LYMErix was not
a vaccine when they tried it as an HIV vaccine, it appears to me.
They really were embarrassed and let me quote Anthony Fauci on that
(2008, NEJM):
2008, Aug, "An HIV vaccine--challenges and prospects." PubMed ID:
18753644
"The failure of the first T-cell vaccine to affect the risk of
infection or viral levels has led to a reexamination of the direction
of the HIV-vaccine field and, in particular, of the balance between
fundamental-discovery research and more empirical development efforts.
Since an empirical approach is less compelling for HIV than for other
human viruses, from which it differs so fundamentally, this
reexamination has pointed to a need to emphasize fundamental questions
of HIV-vaccine discovery and discovery-related research.5

"a need to emphasize fundamental questions of HIV-vaccine discovery
and discovery-related research"

Fundamentally, I don't think the DHHS could care less about the
scientific truth. I don't think the United States takes any stand
whatsoever on Truth.