Lyme Crymes, the Movie
(Randy Sykes and Simsbury TV)
Cryme Disease video playlist
Bad Ass Cryme Blog
(Vaccine Injury, Connecting the Dots, pdf)
141219_post-sepsis Rituximab (again)
Pandora: ME/CFS related to
Follow the Lyme/LYMErix
Scam in the order it occurred, below:
Older data on the incurability of Relapsing Fever
1986, McSweegan trashes Navy for $$$ for
1988, Dattwyler & about immune-suppressing, seronegative Lyme
1990, CDC: "Diagnose Lyme as if it was Relapsing
Allen Steere "NeuroLyme won't
test positive," 1990.
CDC officer Allen Steere falsifies testing in
1992, CDC patents with
SmithKline show 2 kinds of Lyme
Barbour and Fish slam Neurologic Lyme victims.
Compare the 2 kinds of Lyme in the RICO
1994, FDA LYMErix Meeting
CDC's Dearborn Booklet .pdf
CDC's invitation to participate in Dearborn
Dearborn, Who Said What?
Igenex, Harris, Dearborn .pdf
Evidence Lyme criminals knew
LYMErix produced the same "multisystem disease" as "Chronic Lyme"
LYMErix Damage Coverup (short)
1998, CIA Oilmen & Israelis plan to overthrow
Saddam for the oil.
ActionLyme/Kathleen Dickson predicts all of Bushie's outcomes in Oct 2000
predicts Bush will have us worshipping his bombs (Shock and Awe"), in Oct 2000
during the Gore Debates
This page not changed since early
2008, first created March-May, 2003.
Regarding other failed vaccines of
the OspA type.
10 on Biomarkers for more data related to immune-suppression outcomes of
Lyme and LYMErix vaccinations (Pam3Cys or OspA from fungi)
Previous Chp 15,
PLUM ISLAND SLYME (OspA) AND
CHAPTER 16, FUNGAL VACCINES
First of all, What is
From Chp 3 and
Chp 9, we know that these fungal antigens are
a big problem. At first they're very immunogenic, but then they seem
to make the victim more susceptible through tolerization process and their
downstream mechanisms, as well as the now well-known inhibition of the
auto-kill kinases (activated latent viruses are not stopped from
look like Epstein-Barr transformed or mutated lymphocytes... I wonder if
reactivates latent virus infections in tissues?
I wonder if it's related to
inhibition of the auto-kill kinases in latently, virally-infected
cells that would otherwise undergo auto-kill when the viruses
started replicating again, but don't due to the suppression of such
functions caused by these fungal lipopeptides?
Mycoplasma are known to be
associated with cancer. Perhaps it is due to the fact that they are
associated with activated latent viral infections because we know
for sure viruses are associated with the production of cancer or
HIV vaccine with OspA adjuvant stuck on it?
~OspA stuck on an HIV vaccine:
Back when we knew LYMErix
was not a vaccine because the Dearborn
testing standard was bogus (misses 85% of all cases) and because of all the terrible outcomes
of OspA vaccines, we
looked into the matter of whether or not this idea of trying out a fungal or
a triacyl Pam3Cys lipoprotein had been tried before and what were the
Here is what I found:
LPS binding protein (LBP) is
an acute-phase protein synthesized predominantly in the liver
of the mammalian host. It was first described to bind LPS of
Gram-negative bacteria and transfer it via a CD14-enhanced
mechanism to a receptor complex including TLR-4 and MD-2,
initiating a signal transduction cascade leading to the
release of proinflammatory cytokines. In recent studies, we
found that LBP also mediates cytokine induction caused by
compounds derived from Gram-positive bacteria, including lipoteichoic
acid and peptidoglycan fragments. Lipoproteins and lipopeptides
have repeatedly been shown to act as potent cytokine inducers,
interacting with TLR-2, in synergy with TLR-1 or -6. In this
study, we show that these compounds also interact with LBP and
CD14. We used triacylated lipopeptides, corresponding to
lipoproteins of Borrelia burgdorferi, mycobacteria, and
Escherichia coli, as well as diacylated lipopeptides,
corresponding to, e.g., 2-kDa macrophage activating
lipopeptide of Mycoplasma spp. Activation of Chinese
hamster ovary cells transfected with TLR-2 by both
lipopeptides was enhanced by cotransfection of CD14. Responsiveness
of human mononuclear cells to these compounds was greatly enhanced
in the presence of human LBP. Binding of lipopeptides to LBP
as well as competitive inhibition of this interaction by LPS
was demonstrated in a microplate assay. Furthermore, we were
able to show that LBP transfers lipopeptides to CD14 on human
monocytes using FACS analysis. These results support that LBP
is a pattern recognition receptor transferring a variety of
bacterial ligands including the two major types of lipopeptides
to CD14 present in different receptor complexes.
The 19-kD antigen
and protective immunity in a murine
model of tuberculosis.
Yeremeev VV, Lyadova IV, Nikonenko
BV, Apt AS, Abou-Zeid C, Inwald J, Young
19-kD antigen is a cell wall-associated lipoprotein present in
Mycobacterium tuberculosis and in bacille Calmette-Guérin (BCG) vaccine
strains. Expression of the 19-kD antigen as a recombinant protein in two
saprophytic mycobacteria-M. vaccae and M. smegmatis-resulted in
abrogation of their ability to confer protection against M. tuberculosis
in a murine challenge model, and in their ability to prime a DTH
response to cross-reactive mycobacterial antigens. Induction of an
immune response to the 19-kD antigen by an alternative approach of DNA
vaccination had no effect on subsequent M. tuberculosis challenge. These results are consistent with a model in which the presence of the
19-kD protein has a detrimental effect on the efficacy of vaccination
with live mycobacteria. Targeted inactivation of genes encoding
selected antigens represents a potential route towards development of
improved vaccine candidates."
tuberculosis 19-kilodalton lipoprotein
inhibits Mycobacterium smegmatis-induced
cytokine production by human macrophages
Post FA, Manca C, Neyrolles O, Ryffel
B, Young DB, Kaplan G.
Vaccination of mice with
Mycobacterium vaccae or M. smegmatis induces some protection against M.
tuberculosis challenge. The 19-kDa lipoprotein of M. tuberculosis,
expressed in M. vaccae or M. smegmatis (M. smeg19kDa), abrogates this
protective immunity. To investigate the mechanism of this suppression
of immunity, human monocyte-derived macrophages (MDM) were infected
with M. smeg19kDa. Infection resulted in reduced production of tumor
necrosis factor alpha (TNF-alpha) (P < 0.01), interleukin-12 (IL-12) (P
< 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared to infection
with M. smegmatis vector (M. smegV). Infection with M. smeg19kDa and
with M. smegV had no differential effect on expression of costimulatory
molecules on MDM, nor did it affect the proliferation of presensitized T
cells cocultured with infected MDM. When MDM were infected with M.
smegmatis expressing mutated forms of the 19-kDa lipoprotein, including
non-O-glycosylated (M. smeg19NOG), nonsecreted (M. smeg19NS), and
nonacylated (M. smeg19NA) variants, the reduced production of TNF-alpha
or IL-12 was not observed. When the purified 19-kDa lipoprotein was
added directly to cultures of infected monocytes, there was little
effect on either induction of cytokine production or its inhibition.
Thus, the immunosuppressive effect is dependent on glycosylated and
acylated 19-kDa lipoprotein present in the phagosome containing the
mycobacterium. These results suggest that the diminished protection
against challenge with M. tuberculosis seen in mice vaccinated with M.
smegmatis expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha
and IL-12 production, possibly leading to reduced induction of T-cell
Infect Immun. 2003
tuberculosis recombinant 27-kilodalton
lipoprotein induces a strong Th1-type
immune response deleterious to
Hovav AH, Mullerad J, Davidovitch
L, Fishman Y, Bigi F, Cataldi A,
Department of Clinical Microbiology,
Faculty of Medicine, The Hebrew
University, Jerusalem, Israel.
Th1 immune response is essential in
the protection against mycobacterial
intracellular pathogens. Lipoproteins
trigger both humoral and cellular
immune responses and may be candidate
protective antigens. We studied in
BALB/c mice the immunogenicity and the
protection offered by the recombinant
27-kDa Mycobacterium tuberculosis
lipoprotein and the corresponding DNA
vaccine. Immunization with the 27-kDa
antigen resulted in high titers of
immunoglobulin G1 (IgG1) and IgG2a
with a typical Th1 profile and a
strong delayed hypersensitivity
response. A strong proliferation
response was observed in splenocytes,
and significant nitric oxide
production and gamma interferon
secretion but not interleukin 10
secretion were measured. Based on
these criteria, the 27-kDa antigen
induced a typical Th1-type immune
response thought to be necessary for
protection. Surprisingly, in
27-kDa-vaccinated mice (protein or DNA
vaccines) challenged by M.
tuberculosis H37Rv or BCG strains,
there was a significant increase in
the numbers of CFU in the spleen
compared to that for control groups. Furthermore, the protection
provided by BCG or other mycobacterial
antigens was completely abolished once
the 27-kDa antigen was added to the
vaccine preparations. This study
indicates that the 27-kDa antigen has
an adverse effect on the protection
afforded by recognized vaccines.
We are currently studying how the
27-kDa antigen modulates the mouse
Induction of Pro- and
Anti-Inflammatory Cytokines by Borrelia burgdorferi Lipoproteins in
Monocytes Is Mediated by CD14
We looked into the matter
of whether or not the Lyme criminals had actually published anything
that really proved they had a vaccine. We found numerous reports that
showed this vaccine failed in animal studies.
methods of the invention provide a powerful and selective approach for
modulating the innate immune response pathways in animals without giving
rise to the toxicities often associated with the native bacterial
components that normally stimulate those pathways."
single ligation of TLRs induces responses such as TNF production,
repeated ligation will lead to a loss of response, i.e., the
cells become tolerant." http://www.jimmunol.org/cgi/content/full/173/4/2736
"Borrelia burgdorferi-Induced Tolerance as a Model of Persistence via
Immunosuppression" - "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."
tuberculosis LprG (Rv1411c): A Novel TLR-2 Ligand That Inhibits Human
Macrophage Class II MHC Antigen Processing1
through TLR-2 by lipoproteins may represent a double-edged
sword for host responses to chronic intracellular pathogens
such as M. tuberculosis. Short-term signaling through TLR-2
activates macrophages and initiates acute inflammation that
may help control initial infection. In contrast, prolonged
TLR-2 signaling in macrophages results in down-regulation of
certain critical immune functions, such as MHC-II Ag
processing. M. tuberculosis infects, survives, and
persists in macrophages. The ability of M. tuberculosis to
survive acute inflammation positions the bacilli to take
advantage, through secretion of lipoproteins such as LprG and
LpqH, of this
down-regulation of macrophage immune function."
The Journal of Immunology, 2004, 173: 2660-2668.
Copyright © 2004 by
The American Association of Immunologists
FROM THE 2003 ACTIONLYME.com WEBSITE:
1) OspA vaccination was not demonstrated to
protect monkeys from infection:
The outer surface
protein A (OspA) vaccine against Lyme
disease: efficacy in the rhesus monkey.
Philipp MT, Lobet Y, Bohm RP Jr,
Roberts ED, Dennis VA, Gu Y, Lowrie RC
Jr, Desmons P, Duray PH, England JD,
Hauser P, Piesman J, Xu K.
Vaccine. 1997 Dec;15(17-18):1872-87.
2) rOspA vaccination did not
protection in rabbits against
host-adapted and cultivated Borrelia
burgdorferi following infection-derived
immunity or immunization with outer
membrane vesicles or outer surface
Shang ES, Champion CI, Wu XY, Skare
JT, Blanco DR, Miller JN, Lovett MA.
Department of Microbiology and
Immunology, Department of Medicine,
School of Medicine, University of
California, Los Angeles, California
of the antibody responses to outer
membrane proteins, including DbpA, OspA,
and OspC, suggests that the remarkable
protection exhibited by the
infection-immune rabbits is due to
antibodies directed at antigens unique
to or markedly up-regulated in
host-adapted B. burgdorferi."
3) OspA was not shown to protect mice,
and why, by Russell Johnson:
tick-borne spirochete challenge induced
by Borrelia burgdorferi strains that
differ in expression of outer surface
Kurtti TJ, Munderloh UG, Hughes CA,
Engstrom SM, Johnson RC.
Infect Immun. 1996 Oct;64(10):4148-53
There was no reduction of strain 297
spirochetes in ticks that fed on four
hamsters immunized with M297, but the
hamsters were protected.
The journal publications of Russell
MEDLINE: "Johnson RC [au] and
4) rOspA vaccination
results in escape mutants or variants
spirochetes which INCREASE at a greater
rate than normal.
variant Borrelia burgdorferi isolates
from mice immunized with outer surface
protein A or B.
Fikrig E, Tao H, Barthold SW, Flavell
Experiments in vitro in which complement is added demonstrate the
antibodies to rOspA
alone do not kill the spirochetes:
burgdorferi escape mutants that survive
in the presence of antiserum to the OspA
vaccine are killed when complement is
Sole M, Bantar C, Indest K, Gu Y,
Ramamoorthy R, Coughlin R, Philipp MT.
5) Yale did not
demonstrate that there were not spirochetes in the ticks after vaccination and
then feeding ticks on animal blood, then assaying for spirochetes:
Elimination of Borrelia
burgdorferi from vector ticks feeding on OspA-immunized mice.
Fikrig E, Telford SR 3rd, Barthold SW, Kantor FS, Spielman A, Flavell RA.
Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5418-21.
As we Lyme warriors cannot engage any earthly assistance;
As the entire US medical community chooses not to assist sick and
abused people and put a stop to this;
As there is not one MD or group in the entire USA who will take these
criminals to court;
As there is not one lawyer or Department of Justice official who will do the job
they were hired to do and protect us from corporate crime;
As there are no men left among us:
Saint Michael the Archangel,
defend us in battle.
Be our protection against the wickedness and snares of the devil.
May God rebuke him, we humbly pray;
and do Thou, O Prince of the Heavenly Host -
by the Divine Power of God -
cast into hell, satan and all the evil spirits,
who roam throughout the world seeking the ruin of souls.