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Subject: CDC not a reliable source of information on vaccines
(scientific proofs)

Date: Sep 15, 2008 3:30 PM

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

TWELVE ITEMS OF PUBLISHED SCIENTIFIC EVIDENCE:
(and there is more in the book, CRYME DISEASE)

- - - - - - -

1)  The PNAC document, page 60:
http://www.actionlyme.org/PNAC.pdf

What could "race-specific bioweapons" be?

Is that like the known fact that CCR5 mutations increase
susceptibility to congenital
HIV
occurs 5 times more often in blacks than Caucasians and Asians?
http://www.actionlyme.org/The_Fauci_Files.htm

2) Encephalitis complicating smallpox vaccination.
Arch Neurol. 2003 Jul;60(7):925-8.

Miravalle A, Roos KL.

Department of Neurology, Indiana University School of Medicine, and
Indiana University
Hospital, Indianapolis, USA.

”A smallpox vaccination program has been initiated. The vaccine is a
live virus
that was used in the last century. Postvaccinal encephalitis is a
complication of
this vaccine. The clinical presentation, course, neuroimaging
findings, and spinal
fluid abnormalities are similar to a disorder that physicians are
familiar with,
acute disseminated encephalomyelitis. This complication can be
prevented with the
administration of antivaccinia gamma globulin at the time of
vaccination. Antivaccinia
gamma globulin is not efficacious once this complication occurs.
Intravenous methylprednisolone
is the recommended therapy, although intravenous immunoglobulin and
plasmapheresis
should be investigated in the treatment of postvaccinal encephalitis.”

- - - -
Notice the action is to give people antibodies.  That means the
attenuated virus
was not attenuated enough.  Similarly, children with HIV immune
suppression are
treated to this:

3) Measles, mumps, and rubella--vaccine use and strategies for
elimination of measles,
rubella, and congenital rubella syndrome and control of mumps:
recommendations of
the Advisory Committee on Immunization Practices (ACIP).

Watson JC, Hadler SC, Dykewicz CA, Reef S, Phillips L.  MMWR Recomm
Rep. 1998 May
22;47(RR-8):1-57.

These revised recommendations of the Advisory Committee on
Immunization Practices
(ACIP) on measles, mumps, and rubella prevention supersede
recommendations published
in 1989 and 1990. This statement summarizes the goals and current
strategies for
measles, rubella, and congenital rubella syndrome (CRS) elimination
and for mumps
reduction in the United States. Changes from previous recommendations
include: Emphasis
on the use of combined MMR vaccine for most indications; A change in
the recommended
age for routine vaccination to 12-15 months for the first dose of MMR,
and to 4-6
years for the second dose of MMR; A recommendation that all states
take immediate
steps to implement a two dose MMR requirement for school entry and any
additional
measures needed to ensure that all school-aged children are vaccinated
with two
doses of MMR by 2001; A clarification of the role of serologic
screening to determine
immunity; A change in the criteria for determining acceptable evidence
of rubella
immunity; A recommendation that all persons who work in health-care
facilities have
acceptable evidence of measles and rubella immunity; Changes in the
recommended
interval between administration of immune globulin and measles
vaccination; and
Updated information on adverse events and contraindications,
particularly for persons
with severe HIV infection, persons with a history of egg allergy or
gelatin allergy,
persons with a history of thrombocytopenia, and persons receiving
steroid therapy."

- - - - -

That means the vaccines could fail, and we know they fail, and we know
Rubella results
in Autism, since that was the reason for vaccination in the first
place.  Children
are NOT routinely screened for their immune status, and these two
governments, the
USA and the UK. NEVER address this issue publicly, they keep answering
the non-question:
It is NOT the Thimerasol, it is VACCINE FAILURE.  And outbreak
strains.

- - - -
4)
The CDC is not a reliable internet source of information on vaccines,
because as
you can see from their 1992 patents with SmithKline in Europe,
http://www.actionlyme.org/CDCS_PARTICIPATION_IN_LYME_CRIMES.htm
they are aware of "HLA-restricted and HLA-non-restricted antibodies,"
meaning they know that the new, 1994 Dearborn, or Steere's
hypersensitivity
reaction diagnostic standard for Lyme is bogus.  See page 3 of the
RICO complaint,
the graphics.
http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm

It is also true that the FDA has rules on the validation of an
analytical method,
and that there is no such thing as "receiver operating characteristic"
as a criterion in validations:
http://www.relapsingfever.org/index.htm

5)
It is also true that the NIH and National Cancer Institute and US Army
scientist,
Paul Duray
http://www.actionlyme.org/Duray.htm
in 1992 questioned the source of the "Epstein-Barr transformed-like"
cells
in chronic Lyme victims, at the Cold Spring Harbor Crooks Conference,
http://www.actionlyme.org/COLDSPRINGHARBOR.htm
where they said very different things than what Mark Klempner is now
saying about
Chronic Neurologic "Lyme Disease."
http://www.actionlyme.org/MKLEMPNER.htm

6)
It is also true that mycoplasma are associated with cancer, which are
usually caused
by viruses (immune suppression by mycoplasmal antigens, resulting in
activation
of latent viruses of all kinds)...

(Yale happens to be looking into this right now.)

You know how they say in the New York Times, that
    September 7, 2008
    Unboxed

    When Academia Puts Profit Ahead of Wonder
    By JANET RAE-DUPREE
    “It is the policy and objective of the Congress to use the patent
system to
promote the utilization of inventions arising from federally supported
research
or development” and “to promote collaboration between commercial
concerns and nonprofit
organizations, including universities.”

    — The Bayh-Dole Act, a k a the University Small Business Patent
Procedures Act

    THE law of unintended consequences is perhaps less a “law” than a
simple statement
of fact: We cannot accurately predict all the results of our actions.
We may do
something with the best of intentions, and sometimes even accomplish
the good toward
which we aim. Yet, at the same time, we are all too often surprised by
results that
didn’t occur to us beforehand....

Well, that can't be said about the mad dash for a Lyme vaccine.  Yale,
et al,
have never in 30 years said anything about how they are going to cure
us or even
treat the symptoms of chronic Lyme, but worse, in 1992, at the Cold
Spring Harbor
conference, it was revealed to them by probably the US' top
pathologist, Paul
Duray, what exactly chronic Lyme was (immune suppression or
dysregulation), and
why it was called the New Great Imitator (why it resulted in ALS,
Lupus, MS, stroke,
cancer, etc.):

"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 Crooks' Conference, published in Steve Schutzer's
Lyme
Disease: Molecular and Immunologic Approaches.

- - -

"These look like Epstein-Barr transformed or mutated lymphocytes... I
wonder
if Bb infection reactivates latent virus infections in tissues? "-
Paul Duray.

- - - - - - -

7) OspA- like molecules turning off the immune system, Part I:

Downregulation of the antigen-presenting HLAs mean no antibodies will
be produced):

        The Journal of Immunology, 2004, 173: 2660-2668.
        Copyright © 2004 by The American Association of Immunologists
        Mycobacterium tuberculosis LprG (Rv1411c): A Novel TLR-2
Ligand That Inhibits
Human Macrophage Class II MHC Antigen Processing1

         "Signaling 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."
http://www.jimmunol.org/cgi/content/full/173/4/2660

8)
OspA- like molecules turning off the immune system, Part II:

The inhibitory effect of Mycoplasma fermentans on tumour necrosis
factor (TNF)-alpha-induced
apoptosis resides in the membrane lipoproteins.

        Gerlic M, Horowitz J, Farkash S, Horowitz S.

        Department of Microbiology and Immunology, Faculty of Health
Sciences, Soroka
    University Medical Center, Ben-Gurion University of the Negev,
Beer-Sheva, Israel,
    84105.

        Mycoplasma have been shown to be involved in the alteration of
several eukaryotic
    cell functions, such as cytokine production, gene expression and
more. We have
previously
    reported that infection of human myelomonocytic U937 cell line
with live Mycoplasma
    fermentans (M. fermentans) inhibited tumour necrosis factor (TNF-
alpha)-induced
    apoptosis. Mycoplasmal membrane lipoproteins are considered to be
the most potent
    initiators of inflammatory reactions in mycoplasmal infections.
The aim of this
    study was to clarify whether the inhibitory effect on TNFalpha-
induced apoptosis
    is exerted by M. fermentans lipoproteins (LPMf). A significant
reduction in
TNFalpha-induced apoptosis was demonstrated by stimulation of U937
cells with M.
fermentans total proteins, LPMf or MALP-2 (M. fermentans synthetic
lipopeptide),
[LIKE OspA] but not with M. fermentans hydrophilic protein preparation
(AqMf).
***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.***  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.***

9) Borrelia burgdorferi-induced tolerance as a model of persistence
via immunosuppression.
    Diterich I, Rauter C, Kirschning CJ, Hartung T.

    Biochemical Pharmacology, Faculty of Biology, University of
Konstanz, Konstanz,
Germany.

    If left untreated, infection with Borrelia burgdorferi sensu lato
may lead to
chronic Lyme borreliosis. It is still unknown how this pathogen
manages to persist
in the host in the presence of competent immune cells. It was recently
reported
that Borrelia suppresses the host's immune response, thus perhaps
preventing
the elimination of the pathogen (I. Diterich, L. Härter, D. Hassler,
A. Wendel,
and T. Hartung, Infect. Immun. 69:687-694, 2001). Here, we further
characterize
Borrelia-induced immunomodulation in order to develop a model of this
anergy. We
observed that the different Borrelia preparations that we tested,
i.e., live, heat-inactivated,
and sonicated Borrelia, could desensitize human blood monocytes, as
shown by attenuated
cytokine release upon restimulation with any of the different
preparations. Next,
we investigated whether these Borrelia-specific stimuli render
monocytes tolerant,
i.e. hyporesponsive, towards another Toll-like receptor 2 (TLR2)
agonist, such as
lipoteichoic acid from gram-positive bacteria, or towards the TLR4
agonist lipopolysaccharide.
Cross-tolerance towards all tested stimuli was induced. Furthermore,
using primary
bone marrow cells from TLR2-deficient mice and from mice with a
nonfunctional TLR4
(strain C3H/HeJ), we demonstrated that the TLR2 was required for
tolerance induction
by Borrelia, and using neutralizing antibodies, we identified
interleukin-10 as
the key mediator involved. Although peripheral blood mononuclear cells
tolerized
by Borrelia exhibited reduced TLR2 and TLR4 mRNA levels, the
expression of the respective
proteins on monocytes was not decreased, ruling out the possibility
that tolerance
to Borrelia is attributed to a reduced TLR2 expression. In summary, we
characterized
tolerance induced by B. burgdorferi, describing a model of
desensitization which
might mirror the immunosuppression recently attributed to the
persistence of Borrelia
in immunocompetent hosts.

------------

10, 11, 12)

http://www.actionlyme.org/FUNGAL_VACCINES.htm
    A)   http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&...
    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
DB.

        "The 19-kD antigen is a cell wall-associated lipoprotein
present in
Mycobacterium tuberculosis and in bacille Calmette-Guérin (BCG)
vaccine strains.
Expression of the 19-kD antigen as a recombinant protein in two
saprophytic mycobacteria-M.
vaccae and M. smegmatis-resulted in abrogation of their ability to
confer protection
against M. tuberculosis in a murine challenge model, and in their
ability to prime
a DTH response to cross-reactive mycobacterial antigens. Induction of
an immune
response to the 19-kD antigen by an alternative approach of DNA
vaccination had
no effect on subsequent M. tuberculosis challenge. These results are
consistent
with a model in which the presence of the 19-kD protein has a
detrimental effect
on the efficacy of vaccination with live mycobacteria. Targeted
inactivation of
genes encoding selected antigens represents a potential route towards
development
of improved vaccine candidates."

     B) http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&...

    Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits
Mycobacterium
smegmatis-induced cytokine production by human macrophages in vitro.

    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 activation."

    C) http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubme...

      Infect Immun. 2003 Jun;71(6):3146-54. Related Articles, Links

        The Mycobacterium tuberculosis recombinant 27-kilodalton
lipoprotein induces
a strong Th1-type immune response deleterious to protection.

        Hovav AH, Mullerad J, Davidovitch L, Fishman Y, Bigi F,
Cataldi A, Bercovier
H.

        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 immune
response.

============

How much more proof does anyone need?
Either these clowns are clueless or they're lying.

Kathleen M. Dickson
http://www.actionlyme.org