Now that ILADS.org and IDSociety.org are *DONE* and out of the picture, where do we go from here?
Mort Zuckerman
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Subject: Now that ILADS.org and IDSociety.org are *DONE* and out of
the picture, where do we go from here?
Date: May 25, 2010 6:49 PM
Where do we go from here?
http://www.actionlyme.org/index.htm
"The treatment of lyme disease can be antibiotics in order to
eliminate the symptoms. If this is not given much attention from a
professional then the treatment will vary depend on the complications.
Serious problem resulting to this disease can be difficult to treat."
http://whatisthetrend.net/more-information-about-lyme-disease-2010959.html
Now that it is well-known and accepted science that Pam3Cys, the
LYMErix and HIV vaccines and the failed lipoprotein vaccine trials
for
http://www.actionlyme.org/FUNGAL_VACCINES.htm
Tuberculosis cause immunosuppression via the mechanisms described in
the Pam3Cys PPT presentation:
http://www.lymecryme.com/rich_text_21.html
and with the revelation that Epstein-Barr virus also has TLR2 agonist
ligands,
http://www.ncbi.nlm.nih.gov/pubmed?term=ebv[All%20Fields]%20AND%20tlr2[All%20Fields]&cmd=DetailsSearch
people with Chronic Lyme may wonder,
"Where do we go from here?"
If it is true that the National Institute of Neurological Disorders
and
http://www.actionlyme.org/MARTIN_NINDS_MS_CHRONIC_LYME.htm
Stroke's, Roland Martin was treating Lyme-MS as Lyme and MS (with both
ceftriaxone and MS meds), and that this is truly the evidence-based
medicine:
http://www.ncbi.nlm.nih.gov/pubmed/16783164
A) IDSA's Treatment Failure reports
The Biology of Parasitic Spirochetes:
http://catalog.library.ksu.edu.sa/digital/130214.html
Allen Steere on treatment failure after multiple courses of
antibiotics:
http://www.annals.org/cgi/content/full/121/8/560
http://content.nejm.org/cgi/content/full/330/4/229
http://www.ncbi.nlm.nih.gov/pubmed/8769624
Congenital Lyme post-treatment of the mother, Allen Steere:
http://www.ncbi.nlm.nih.gov/pubmed?term=4003991[uid]&cmd=DetailsSearch
”Persistence of Borrelia burgdorferi Following Antibiotic Treatment in
Mice”
http://aac.asm.org/cgi/content/abstract/AAC.01050-07v1
B) Ben Luft's recent claim
“These results extended previous studies with ceftriaxone, indicating
that antibiotic treatment is unable to clear persisting spirochetes,
which remain viable and infectious, but are nondividing or slowly
dividing.”
http://www.ncbi.nlm.nih.gov/pubmed/19995919
C) CDC says "Bb is intracellular"
“Cytopathic effects were not observed following infection of these
cell lines with B. burgdorferi, and internalized spirochetes were
found to be viable. Invasion of neural cells by B. burgdorferi
provides a putative mechanism for the organism to avoid the host's
immune response while potentially causing functional damage to neural
cells during infection of the CNS.”
http://www.ncbi.nlm.nih.gov/pubmed?term=17045505[uid]&cmd=DetailsSearch
D) Mark Klempner in 1992 reported that "Bb is intracellular and
thereby resistant to ceftriaxone,"
http://www.ncbi.nlm.nih.gov/pubmed/1634816
E) Brian Fallon discovered that indeed, Lyme is Relapsing Fever and
the longer term treatment past the 30-days-of-Mark-Klempner’s-Standard-
of-Care results in remission, but then relapse (making Lyme
FUNCTIONALLY identical to Relapsing Fever in addition to it being
Taxonomically the same disease):
http://www.ncbi.nlm.nih.gov/pubmed/17928580
F) and now that Gary Wormser and Mark Klempner have re-admitted that
Bb antigens like OspA cause anti-brain/anti-nerve antibodies, patients
may wonder,
http://www.nature.com/nm/journal/v5/n12/abs/nm1299_1346.html
http://www.ncbi.nlm.nih.gov/pubmed/20227484
"Where do we stand?"
"How should I be treated?"
Because Lyme Borreliosis is the "New Great Imitator," Syphilis is the
"Great Imitator" and OspA vaccination was the "Greatest Imitator," and
because we know the major clues to the crimes were the publications
of
1) NCI’s and the US Army’s Paul Duray "Immature, badly cloned, Epstein-
Barr-like immortalized B cells,"
http://www.ncbi.nlm.nih.gov/pubmed/2814170
http://www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770
And:
Interaction of Borrelia burgdorferi sensu lato with Epstein-Barr virus
in lymphoblastoid cells.
http://www.ncbi.nlm.nih.gov/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."
2) Justin Radolf [TLR2 agonism (with OspA) described how OspA-like
molecules are responsible for the downregulation of HLA molecules (or
that after a time, no antibodies are produced):
http://www.jimmunol.org/cgi/content/full/167/2/910
3) and the Korean Chemists who revealed that LYMErix was the same as
HIV vaccine antigens gp120/41 (Pam3Cys)
http://journal.kcsnet.or.kr/main/j_search/j_download.htm?code=B961118
how do we deal with all the diseases that we have, since it clearly
looks like we have a form of OspA-induced Acquired Immune Deficiency
and incompetent B cells?
We're not talking only about activated Epstein-Barr, cytomegalovirus
and the other herpes viruses, and we’re not only talking about
incompetent B cells, we are also talking about, in many Lyme cases,
the tick-borne co-infections like the Ehrlichias and Babesia for which
still, today, there are no accurate blood tests.
We can't ask ILADS.org because they have not stayed current with the
science and, of course, the recommendations of IDSociety.org are out
of the question, given that because they a) lied about the outcomes of
their OspA vaccines, b) falsified the testing for Lyme (Dearborn) in
order to falsify their vaccines outcomes, and c)) never reported to
the NIH or especially NIAID - the division headed by Edward
McSweegan’s boss, Anthony Fauci. – that they could not even read their
Western Blots in OspA vaccinated people:
LYMErix results (76% "safe and effective"):
http://content.nejm.org/cgi/content/abstract/339/4/209
ImmuLyme results (92% "safe and effective"):
http://content.nejm.org/cgi/content/abstract/339/4/216
But the same “researchers” said, ”We couldn’t actually read our
Western Blots in this OspA vaccines trials”:
http://jcm.asm.org/cgi/reprint/35/1/233?view=long&pmid=8968914
http://www.journals.uchicago.edu/doi/pdf/10.1086/313920
We lost all those years in discovery in the mechanisms of all major
chronic diseases and cancer through the years of 1995 to 2008 from
when the likes of Yale, Mayo Clinic's Dave Persing (later went to
Corixa), and Allen Steere decided to lie about the outcomes of
LYMErix, and Gary Wormser and Lenny Sigal decided to lie about the
outcome of ImmuLyme.
The EVIDENCE (Roland Martin of thr NIH) says we should treat Chronic
Lyme as a chronic spirochetal infection (the treatment of Q fever and
tuberculosis with antibiotics could take years and this is well-known)
and as some version of some Imitators(s), be it the MS version, the
Lupus Version, or whatever.
We do not know how one treats badly cloned B cells. It could be, in
the end, some sort of leukophoresis or stem cell transfer of new B
cells:
Toll-like receptor [2] agonists [like Lyme and LYMErix]
synergistically increase proliferation and activation of B cells by
Epstein-Barr virus.
http://www.ncbi.nlm.nih.gov/pubmed/20089650
“B cells as under-appreciated mediators of non-auto-immune
inflammatory disease.”
http://www.ncbi.nlm.nih.gov/pubmed/20382544
”B lymphocytes play roles in many auto-immune diseases characterized
by unresolved inflammation, and B cell ablation is proving to be a
relatively safe, effective treatment for such diseases. B cells
function, in part, as important sources of regulatory cytokines in
auto-immune disease, but B cell cytokines also play roles in other non-
auto-immune inflammatory diseases. B cell ablation may therefore
benefit inflammatory disease patients in addition to its demonstrated
efficacy in auto-immune disease. Current ablation drugs clear both
pro- and anti-inflammatory B cell subsets, which may unexpectedly
exacerbate some pathologies. This possibility argues that a more
thorough understanding of B cell function in human inflammatory
disease is required to safely harness the clinical promise of B cell
ablation. Type 2 diabetes (T2D) and periodontal disease (PD) are two
inflammatory diseases characterized by little autoimmunity. These
diseases are linked by coincident presentation and alterations in toll-
like receptor (TLR)-dependent B cell cytokine production, which may
identify B cell ablation as a new therapy for co-affected individuals.
Further analysis of the role B cells and B cell cytokines play in T2D,
PD and other inflammatory diseases is required to justify testing B
cell depletion therapies on a broader range of patients.” Copyright
2010 Elsevier Ltd. All rights reserved.
The TLR1/2 agonist PAM(3)CSK(4) instructs commitment of human
hematopoietic stem cells to a myeloid cell fate.
http://www.ncbi.nlm.nih.gov/pubmed/19641520
”Toll-like receptors (TLRs) constitute a family of nonpolymorphic
receptors that are devoted to pathogen recognition. In this work, we
have explored the impact of TLR ligands (TLR-L) on human hematopoietic
stem cells (HSCs) and hematopoietic progenitor cells (HPCs). We show
that HSCs and HPCs have a comparable pattern of expression of TLR
transcripts characterized by the predominance of TLR1, -2, -3, -4 and
-6. In long-term cultures of HSCs, HPCs and stromal cells, most TLR-L
profoundly inhibited B-cell development while preserving or enhancing
the production of myeloid cells. In short-term cultures, the TLR1/2
ligand PAM(3)CSK(4) induced a large proportion of HPCs to express
markers of the myelomonocytic lineage. PAM(3)CSK(4) induced only
marginal expression of myeloid lineage markers on HSCs but promoted
their myeloid commitment as revealed by their acquisition of the
phenotype of multi- and bipotential myeloid progenitors and by
upregulation of the transcription factors PU.1, C/EBPalpha and GATA-1.
Our results suggest that TLR agonists can bias the lineage commitment
of human HSCs and shift the differentiation of lineage-committed
progenitors to favor myelopoiesis at the expense of lymphoid B-cell
development.”
Innate immunity in human embryonic stem cells: comparison with adult
human endothelial cells.
http://www.ncbi.nlm.nih.gov/pubmed/20463927
“Treatment of human disease with human embryonic stem cell (hESC)-
derived cells is now close to reality, but little is known of their
responses to physiological and pathological insult. The ability of
cells to respond via activation of Toll like receptors (TLR) is
critical in innate immune sensing in most tissues, but also extends to
more general danger sensing, e.g. of oxidative stress, in
cardiomyocytes. We used biomarker release and gene-array analysis to
compare responses in hESC before and after differentiation, and to
those in primary human endothelial cells. The presence of
cardiomyocytes and endothelial cells was confirmed in differentiated
cultures by immunostaining, FACS-sorting and, for cardiomyocytes,
beating activity. Undifferentiated hESC did not respond with CXCL8
release to Gram positive or Gram negative bacteria, or a range of
PAMPs (pathogen associated molecular patterns) for TLRs 1-9 (apart
from flagellin, an activator of TLR5). Surprisingly, lack of TLR-
dependent responses was maintained over 4 months of differentiation of
hESC, in cultures which included cardiomyocytes and endothelial cells.
In contrast, primary cultures of human aortic endothelial cells (HAEC)
demonstrated responses to a broad range of PAMPs. Expression of
downstream TLR signalling pathways was demonstrated in hESC, and
IL-1beta, TNFalpha and INFgamma, which bypass the TLRs, stimulated
CXCL8 release. NFkappaB pathway expression was also present in hESC
and NFkappaB was able to translocate to the nucleus. Low expression
levels of TLRs were detected in hESC, especially TLRs 1 and 4,
explaining the lack of response of hESC to the main TLR signals. TLR5
levels were similar between differentiated hESC and HAEC, and siRNA
knockdown of TLR5 abolished the response to flagellin. These findings
have potential implications for survival and function of grafted hESC-
derived cells.”
100525; KMDickson
http://www.relapsingfever.org
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci