Update, Epstein-Barr associated with MS... IDSA Guidelines Panel- Data on Pam3Cys Submission
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Mort Zuckerman
Oct 4, 2008, 8:10:08 PM10/4/08
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Subject: Update, Epstein-Barr associated with MS... IDSA Guidelines
Panel- Data on Pam3Cys Submission
Date: Oct 4, 2008 8:06 PM
Here is more evidence of the criminal negligence committed by
IDSA/ALDF in blowing off the LYMErix vaccine injurees and
chronic Lyme victims, knowing full-well, that there was an
entire division of the NINDS dedicated to finding the link
between Lyme and MS, knowing the MS version of Lyme was
"seronegative" (means not a genetically linked hypersensitivity
reaction to OspA. That division was run by the German Roland
Martin.
In 1989 and 1992 the US Army's (Ft Detrick plus the National
Cancer Institute) Paul Duray informed IDSA and the world that
the B cells of chronic Lyme victims looked mutated like
Epstein-Barr mutated cells.
IDSA/ALDF later claimed that the only kind of "Lyme disease"
there was, was the knee-kind, as that served their Kaiser-Permanente
partner in the ALDF at New York Medical College, instead of
following up on this real science from a real expert pathologist.
(you can see this data on my homepage and
http://www.actionlyme.org/PAM3CYS_IMMUNE_SUPPRESSION.htm )
The result was the inhibition of progress in HIV, cancer, MS and ALS
research for the ~20 years since. Now we find:
http://www.ncbi.nlm.nih.gov/pubmed/18703007?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Lancet Neurol. 2008 Sep;7(9):852-8.Click here to read Links
Comment in:
Lancet Neurol. 2008 Sep;7(9):766-7.
B cells and multiple sclerosis.
Franciotta D, Salvetti M, Lolli F, Serafini B, Aloisi F.
Laboratory of Neuroimmunology, IRCCS Neurological Institute C
Mondino, via Mondino
2, 27100, Pavia, Italy. diego.fr...@mondino.it
Clonal expansion of B cells and the production of oligoclonal IgG
in the brain
and cerebrospinal fluid (CSF) of patients with multiple sclerosis (MS)
have long
been interpreted as circumstantial evidence of the immune-mediated
pathogenesis
of the disease and suggest a possible infectious cause. Extensive work
on intrathecally
produced antibodies has not yet clarified whether they are
pathogenetically relevant.
Irrespective of antibody specificity, however, the processes of
antibody synthesis
in the CNS of patients with MS are becoming increasingly clear.
Likewise, targeting
B cells might be therapeutically relevant in MS and other autoimmune
diseases that
are deemed to be driven predominantly by T cells. Accumulating
evidence indicates
that in MS, similar to rheumatoid arthritis, B cells aggregate into
lymphoid-like
structures in the target organ. The process of aggregation is mediated
through the
expression of lymphoid-homing chemokines. In the brain of a patient
with MS, ectopic
B-cell follicles preferentially adjoin the pial membrane within the
subarachnoid
space. Recent findings indicate that substantial numbers of B cells
that are infected
with Epstein-Barr virus (EBV) accumulate in these intrameningeal
follicles and in
white matter lesions and are probably the target of a cytotoxic immune
response.
These findings, which await confirmation, could be an explanation for
the continuous
B-cell and T-cell activation in MS, but leave open concerns about the
possible pathogenicity
of autoantibodies. Going beyond the antimyelin-antibody dogma, the
above data warrant
further work on various B-cell-related mechanisms, including
investigation of B-cell
effector and regulatory functions, definition of the consistency of
CNS colonisation
by Epstein-Barr virus-infected B cells, and understanding of the
mechanisms that
underlie the formation and persistence of tertiary lymphoid tissues in
patients
with MS and other chronic autoimmune diseases (ectopic follicle
syndromes). This
work will stimulate new and unconventional ways of reasoning about MS
pathogenesis.
That's a damned lot of damages to be redeemed from the cabal.
Kathleen M. Dickson
http://www.actionlyme.org
emcsw...@nasw.org, zerh...@od.nih.gov, Spin...@yahoogroups.com,
kshe...@calea.org, fit...@gmail.com, patrick.f...@usdoj.gov,
model...@sbcglobal.net, jdr...@nejm.org, let...@courant.com,
Jgerb...@cdc.gov, michae...@po.state.ct.us,
con...@po.state.ct.us, executiv...@nytimes.com, managing-
edi...@nytimes.com, news...@nytimes.com, the-...@nytimes.com,
biz...@nytimes.com, for...@nytimes.com, me...@nytimes.com,
nati...@nytimes.com, dv...@cdc.gov, brigidc...@optonline.net,
tr...@hotmail.com, illino...@aol.com, jle...@courant.com,
tinaj...@yahoo.com, jhorn...@fff.org, thomas...@usdoj.gov,
thoma...@po.state.ct.us, kur...@washpost.com,
georg...@washpost.com, p...@allegorypress.com,
commissi...@po.state.ct.us, FalN...@aol.com,
brans...@comcast.net, vts...@comcast.net, o...@po.state.ct.us,
freet...@charter.net, scott....@po.state.ct.us,
govern...@po.state.ct.us, attorney...@po.state.ct.us,
randall...@usdoj.gov
Cc: fra...@ucia.gov, dr-ahma...@president.ir,
eugener...@washpost.com, hor...@courant.com,
bmi...@newstimes.com, tr...@hotmail.com, rast...@aol.com,
billc...@gmail.com, amcg...@rms-law.com, rjmu...@aol.com,
paulcrai...@yahoo.com, sidney_b...@yahoo.com,
criminal...@usdoj.gov, karla.d...@usdoj.gov,
christophe...@usdoj.gov, harol...@yale.edu,
richar...@yale.edu, james.p...@yale.edu
Subject: Update, Epstein-Barr associated with MS... IDSA Guidelines
Panel- Data on Pam3Cys Submission
Date: Oct 4, 2008 8:06 PM
Here is more evidence of the criminal negligence committed by
IDSA/ALDF in blowing off the LYMErix vaccine injurees and
chronic Lyme victims, knowing full-well, that there was an
entire division of the NINDS dedicated to finding the link
between Lyme and MS, knowing the MS version of Lyme was
"seronegative" (means not a genetically linked hypersensitivity
reaction to OspA. That division was run by the German Roland
Martin.
In 1989 and 1992 the US Army's (Ft Detrick plus the National
Cancer Institute) Paul Duray informed IDSA and the world that
the B cells of chronic Lyme victims looked mutated like
Epstein-Barr mutated cells.
IDSA/ALDF later claimed that the only kind of "Lyme disease"
there was, was the knee-kind, as that served their Kaiser-Permanente
partner in the ALDF at New York Medical College, instead of
following up on this real science from a real expert pathologist.
(you can see this data on my homepage and
http://www.actionlyme.org/PAM3CYS_IMMUNE_SUPPRESSION.htm )
The result was the inhibition of progress in HIV, cancer, MS and ALS
research for the ~20 years since. Now we find:
http://www.ncbi.nlm.nih.gov/pubmed/18703007?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Lancet Neurol. 2008 Sep;7(9):852-8.Click here to read Links
Comment in:
Lancet Neurol. 2008 Sep;7(9):766-7.
B cells and multiple sclerosis.
Franciotta D, Salvetti M, Lolli F, Serafini B, Aloisi F.
Laboratory of Neuroimmunology, IRCCS Neurological Institute C
Mondino, via Mondino
2, 27100, Pavia, Italy. diego.fr...@mondino.it
Clonal expansion of B cells and the production of oligoclonal IgG
in the brain
and cerebrospinal fluid (CSF) of patients with multiple sclerosis (MS)
have long
been interpreted as circumstantial evidence of the immune-mediated
pathogenesis
of the disease and suggest a possible infectious cause. Extensive work
on intrathecally
produced antibodies has not yet clarified whether they are
pathogenetically relevant.
Irrespective of antibody specificity, however, the processes of
antibody synthesis
in the CNS of patients with MS are becoming increasingly clear.
Likewise, targeting
B cells might be therapeutically relevant in MS and other autoimmune
diseases that
are deemed to be driven predominantly by T cells. Accumulating
evidence indicates
that in MS, similar to rheumatoid arthritis, B cells aggregate into
lymphoid-like
structures in the target organ. The process of aggregation is mediated
through the
expression of lymphoid-homing chemokines. In the brain of a patient
with MS, ectopic
B-cell follicles preferentially adjoin the pial membrane within the
subarachnoid
space. Recent findings indicate that substantial numbers of B cells
that are infected
with Epstein-Barr virus (EBV) accumulate in these intrameningeal
follicles and in
white matter lesions and are probably the target of a cytotoxic immune
response.
These findings, which await confirmation, could be an explanation for
the continuous
B-cell and T-cell activation in MS, but leave open concerns about the
possible pathogenicity
of autoantibodies. Going beyond the antimyelin-antibody dogma, the
above data warrant
further work on various B-cell-related mechanisms, including
investigation of B-cell
effector and regulatory functions, definition of the consistency of
CNS colonisation
by Epstein-Barr virus-infected B cells, and understanding of the
mechanisms that
underlie the formation and persistence of tertiary lymphoid tissues in
patients
with MS and other chronic autoimmune diseases (ectopic follicle
syndromes). This
work will stimulate new and unconventional ways of reasoning about MS
pathogenesis.
That's a damned lot of damages to be redeemed from the cabal.
Kathleen M. Dickson
http://www.actionlyme.org
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