Chronic Pain and
Disease without Classical HLA-linked
Autoimmune "inflammation" (see the Pac
Man guys)
By Kathleen Dickson on Sunday, November
23, 2014 at 5:44am
Our goal here is to counter the claim by
the CDC, the Lyme crooks, and the
American Psychiatric Association who
falsely claim that you can't have a
"disease" unless you have the classical
HLA-linked hypersensitivity response and
their version of "autoimmunity" with the
too-many-antbodies and a heritable,
genetic, Major Histocompatability (MHC
or HLA) link.
Again, you are not allowed to have a
"disease" unless it is HLA-associated
with too many antibodies. Everything
else, like Lyme, CFIDS, etc, is labeled
psychiatric, or the newer terminology "neuro-immune,"
but "neuro-immune" is code language for
"psychiatric." Currently all the focus
on further abusing people with severe,
multiple infections (Lyme, Fibro, CFIDS)
is to say there is a gene link to
"crazy-in-the-brain."
This
file will be incorporated into the one
working @ Khan Academy of Lyme, section
4.
The reason for this fraud - the abuse of
CFIDS, Fibromyalgia, Lyme, ME, Gulf War
Illness Victims, and the Medical
Kidnapees like Justina Pelletier - has
to do with covering up the mechanisms of
the Autism-From-Vaccines-Pandemic (also
fungal-viral synergy, and now also
called "post-sepsis syndrome" but this
post-sepsis syndrome is by definition, a
state of chronic active herpes and other
infections. And that data can be found
here:
https://www.facebook.com/groups/OccupyUSDOJ/287567894779154/
Mol Neurobiol. 2012 Dec;46(3):614-38.
doi: 10.1007/s12035-012-8320-7. Epub
2012 Aug 17.
Infectious agents and neurodegeneration.
"A growing body of epidemiologic and
experimental data point to chronic
bacterial and viral infections as
possible risk factors for
neurodegenerative diseases, including
Alzheimer's disease, Parkinson's disease
and amyotrophic lateral sclerosis.
Infections of the central nervous
system, especially those characterized
by a chronic progressive course, may
produce multiple damage in infected and
neighbouring cells. The activation of
inflammatory processes and host immune
responses cause chronic damage resulting
in alterations of neuronal function and
viability, but different pathogens can
also directly trigger neurotoxic
pathways. Indeed, viral and microbial
agents have been reported to produce
molecular hallmarks of neurodegeneration,
such as the production and deposit of
misfolded protein aggregates, oxidative
stress, deficient autophagic processes,
synaptopathies and neuronal death. These
effects may act in synergy with other
recognized risk factors, such as aging,
concomitant metabolic diseases and the
host's specific genetic signature. This
review will focus on the contribution
given to neurodegeneration by herpes
simplex type-1, human immunodeficiency
and influenza viruses, and by Chlamydia
pneumoniae."
http://www.ncbi.nlm.nih.gov/pubmed/22899188
YOU WILL SEE MORE OF THE LINES BLURRING
BETWEEN MULTIPLE SCLEROSIS AND CHRONIC
FATIGUE SYNDROME AS WE GO ON HERE...
J Virol. 1999 Oct;73(10):8817-23.
Localization of a passively transferred
human recombinant monoclonal antibody to
herpes simplex virus glycoprotein D to
infected nerve fibers and sensory
neurons in vivo.
"A human recombinant monoclonal antibody
to herpes simplex virus (HSV)
glycoprotein D labeled with the
fluorescent dye Cy5 was administered to
mice infected in the cornea with HSV
type 1 (HSV-1). The distribution of such
antibody in the corneas and trigeminal
ganglia of the mice was then
investigated by confocal microscopy. The
antibody was detected on HSV-infected
nerve fibers in the cornea--identified
by colocalization with HSV antigens and
the neuritic markers neurofilament,
GAP-43, synapsin-1, and CNPase--and on
the perikarya of sensory neurons in the
HSV-1-infected neurons in ipsilateral
trigeminal ganglia. Antibodies have been
shown to be effective against many
neurotropic viruses, often in the
absence of obvious cell damage.
Observations from experimental HSV
infections suggest that antibodies could
act in part by interfering with virus
expression in the ganglia and/or with
axonal spread. The present results
provide morphological evidence of the
localization of antiviral antibodies at
anatomical sites relevant to such
putative antibody-mediated protective
actions and suggest that viral
glycoproteins are accessible to
antibodies on infected nerve fibers and
sensory neurons."
http://www.ncbi.nlm.nih.gov/pubmed/10482637
Right now I am working from this and
finding the other herpes, like zoster
and simplex more often associated with
chronic nerve pain; not sure what that
means... whether this is about lack of
investigation or we are sporting more
than just CMV, EBV, and HHV-6, which
most Lyme victims have said they have
elevated antibodies to (perhaps not the
cut-off for acute stage, but still):
http://www.ncbi.nlm.nih.gov/pubmed/?term=how+do+herpes+viruses+act+on+nerve
New from the NIH: Talks about treatment
for chronic active herpes viruses as the
cause of Multiple Sclerosis:
PLoS One. 2014 Aug 22;9(8):e105434. doi:
10.1371/journal.pone.0105434.
eCollection 2014.
A complex role of herpes viruses
in the disease process of multiple
sclerosis.
Wuest SC1,
Mexhitaj I1, Chai NR1, Romm E1, Scheffel
J2, Xu B3, Lane K3, Wu T4, Bielekova B1.
Author information
1Neuroimmunological Diseases Unit,
Neuroimmunology Branch, National
Institute of Neurological Disorders and
Stroke, National Institutes of Health,
Bethesda, Maryland, United States of
America.
2Molecular Immunology Section,
Laboratory of Molecular Immunogenetics,
National Institute of Arthritis and
Musculoskeletal and Skin Diseases,
National Institutes of Health, Bethesda,
Maryland, United States of America.
3Imaging Probe Development Center,
National Heart, Lung, and Blood
Institute, National Institutes of
Health, Bethesda, Maryland, United
States of America.
4Clinical Neurosciences Program,
National Institute of Neurological
Disorders and Stroke, National
Institutes of Health, Bethesda,
Maryland, United States of America.
"Multiple sclerosis (MS) is a chronic
inflammatory disorder of the central
nervous system (CNS). Neither the
antigenic target(s) nor the cell
population(s) responsible for CNS tissue
destruction in MS have been fully
defined. The objective of this study was
to simultaneously determine the antigen
(Ag)-specificity and phenotype of
un-manipulated intrathecal CD4+ and CD8+
T cells of patients with
relapsing-remitting and progressive MS
compared to subjects with other
inflammatory neurological diseases. We
applied a novel Ag-recognition assay
based on co-cultures of freshly obtained
cerebrospinal fluid T cells and
autologous dendritic cells pre-loaded
with complex candidate Ag's. We observed
comparably low T cell responses to
complex auto-Ag's including human
myelin, brain homogenate, and cell
lysates of apoptotically modified
oligodendroglial and neuronal cells in
all cohorts and both compartments.
Conversely, we detected a strong
intrathecal enrichment of Epstein-Barr
virus- and human herpes virus 6-specific
(but not cytomegalovirus-specific)
reactivities of the Th1-phenotype
throughout all patients. Qualitatively,
the intrathecal enrichment of herpes
virus reactivities was more pronounced
in MS patients. This enrichment was
completely reversed by long-term
treatment with the IL-2 modulating
antibody daclizumab, which strongly
inhibits MS disease activity. Finally,
we observed a striking discrepancy
between diminished intrathecal T cell
proliferation and enhanced cytokine
production of herpes virus-specific T
cells among progressive MS patients,
consistent with the phenotype of
terminally differentiated cells. The
data suggest that intrathecal
administration of novel therapeutic
agents targeting immune cells outside of
the proliferation cycle may be necessary
to effectively eliminate intrathecal
inflammation in progressive MS."
http://www.ncbi.nlm.nih.gov/pubmed/25148387
.
J Virol. 2014 Nov 1;88(21):12740-51. doi:
10.1128/JVI.02106-14. Epub 2014 Aug 20.
Gammaherpesvirus Latency
Differentially Impacts the Generation of
Primary versus Secondary Memory CD8+ T
Cells during Subsequent Infection.
"IMPORTANCE:
"CD8(+) T cells are critical for the
clearance of intracellular pathogens,
including viruses, certain bacteria, and
tumors. However, current models for
memory CD8(+) T cell differentiation are
derived from pathogen-free laboratory
mice challenged with a single pathogen
or vaccine vector. Unlike laboratory
animals, all humans are infected with
multiple acute and chronic pathogens,
including the highly prevalent
herpesviruses Epstein-Barr virus (EBV),
cytomegalovirus (CMV), herpes simplex
viruses (HSV), and varicella-zoster
virus (VZV). The purpose of these
studies was to determine the effect of
gammaherpesvirus latency on T cell
number and differentiation during
subsequent heterologous viral
infections. We observed that ongoing
gammaherpesvirus latency affects the
number and phenotype of primary versus
secondary memory CD8(+) T cells during
acute infection. These results suggest
that unlike pathogen-free laboratory
mice, infection or immunization of
latently infected humans may result in
the generation of T cells with limited
potential for long-term protection."
http://www.ncbi.nlm.nih.gov/pubmed/25142586
^^^ As you can see, the disease paradigm
is shifting to the more rational - stuff
we learned from the OspA vaccines
outcomes :) Also TOO MANY VACCINES,
anyone?
More science on Vit C for chronic EBV:
http://www.ncbi.nlm.nih.gov/pubmed/24793092
Oh, look yet another genius
paradigm-shifter (the original
connection to Burkitt's Lymphoma was
between EBV and Malaria - immune
suppressor with TLR2-agonists, but he
shifts it over to HIV to make it
independent brilliance):
Semin Cancer Biol. 2014 Jun;26:99-115.
doi: 10.1016/j.semcancer.2014.04.004.
Epub 2014 Apr 18.
Co-infections, inflammation and
oncogenesis: future directions for EBV
research.
Rickinson
AB.
School of Cancer Sciences, University of
Birmingham, Birmingham, UK. Electronic
address: A.B.RICKINSON@bham.ac.uk.
"Abstract
"Epstein-Barr virus (EBV) is
aetiologically linked to a wide range of
human tumours. Some arise as accidents
of the virus' lifestyle in its natural
niche, the B lymphoid system; these
include B-lymphoproliferative disease of
the immunocompromised, Hodgkin Lymphoma,
Burkitt Lymphoma and particular forms of
diffuse large B cell lymphoma.
Interestingly, HIV infection increases
the incidence of each of these B cell
malignancies, though by different
degrees and for different reasons. Other
EBV-associated tumours arise through
rare viral entry into unnatural target
tissues; these include all cases of
nasal T/NK cell lymphoma and of
undifferentiated nasopharyngeal
carcinoma plus a small but significant
subset of gastric carcinomas, a tumour
type more generally associated with
chronic Helicobacter pylori infection.
Understanding EBV's involvement in the
pathogenesis of these different
malignancies is an important long-term
goal. This article focuses on two
overlapping, but relatively neglected,
areas of research that could contribute
to that goal. The first addresses the
mechanisms whereby coincident infections
with other pathogens increase the risk
of EBV-positive malignancies, and takes
as its paradigm the actions of
holoendemic malaria and HIV infections
as co-factors in Burkitt lymphomagenesis.
The second widens the argument to
include both infectious and
non-infectious sources of chronic
inflammation in the pathogenesis of EBV-positive
tumours such as T/NK cell lymphoma,
nasopharyngeal carcinoma and gastric
carcinoma."
http://www.ncbi.nlm.nih.gov/pubmed/24751797
Indian J Hematol Blood Transfus. 2014
Mar;30(1):26-8. doi:
10.1007/s12288-012-0207-2. Epub 2012 Oct
25.
Epstein-barr virus infection
masquerading as acute leukemia: a report
of two cases and review of literature.
Chhabra P1,
Law AD1, Sharma U2, Suri V1, Sachdeva
MS3, Kumari S1, Varma S1, Malhotra P1.
"Epstein-Barr virus (EBV) is the first
herpes virus to be completely sequenced.
It is implicated in diseases from the
benign infectious mononucleosis to
malignant nasopharyngeal carcinoma,
Burkitt's lymphoma and primary CNS
lymphoma in AIDS patients. It has also
been found to be associated with some
miscellaneous diseases like chronic
fatigue syndrome, multiple sclerosis
etc. however causality still remains an
issue of debate. As the virus mainly
targets the lymphomonuclear cells and
the reticuloendothelial system of the
body, it's various manifestations are
often mistaken as leukemic malignancies.
We report two such cases of young adults
who had been diagnosed as having acute
leukemia on the basis of atypical cells
in the peripheral blood. One patient
later turned out to be a classical
infectious mononucleosis and second
patient had EBV associated
hemophagocytic lymphohistiocytosis
syndrome."
http://www.ncbi.nlm.nih.gov/pubmed/24554817
Chronic Lyme ^^^ is identical to CLL in
symptoms with the extrme fatigue, so you
have to look out for that proliferation
- CLD being really about Chronic Active
EBV/Similar Herpesviruses.
This we already saw and
was on my
website, reverse correlation with
EBV antibodies and chronic fatigue
syndrome, which fits our paradigm, as we
have said before:
PLoS One. 2014 Jan 15;9(1):e85387. doi:
10.1371/journal.pone.0085387.
eCollection 2014.
Deficient EBV-specific B- and
T-cell response in patients with chronic
fatigue syndrome.
Loebel M1,
Strohschein K2, Giannini C1, Koelsch U3,
Bauer S1, Doebis C4, Thomas S1,
Unterwalder N3, von Baehr V4, Reinke P5,
Knops M1, Hanitsch LG1, Meisel C6, Volk
HD7, Scheibenbogen C7.
1Institute for Medical Immunology,
Charité University Medicine Berlin,
Campus Virchow, Berlin, Germany.
2Institute for Medical Immunology,
Charité University Medicine Berlin,
Campus Virchow, Berlin, Germany ; Julius
Wolff Institute, Charité University
Medicine Berlin, Campus Virchow, Berlin,
Germany.
3Labor Berlin GmbH, Immunology
Department, Charité University Medicine
Berlin, Campus Virchow, Berlin, Germany.
4Institute for Medical Diagnostics,
Berlin, Germany.
5Berlin-Brandenburg Center for
Regenerative Therapies (BCRT), Charité
University Medicine Berlin, Germany ;
Department Nephrology, Charité
University Medicine Berlin, Germany.
6Institute for Medical Immunology,
Charité University Medicine Berlin,
Campus Virchow, Berlin, Germany ; Labor
Berlin GmbH, Immunology Department,
Charité University Medicine Berlin,
Campus Virchow, Berlin, Germany.
7Institute for Medical Immunology,
Charité University Medicine Berlin,
Campus Virchow, Berlin, Germany ;
Berlin-Brandenburg Center for
Regenerative Therapies (BCRT), Charité
University Medicine Berlin, Germany.
"Epstein-Barr virus (EBV) has long been
discussed as a possible cause or trigger
of Chronic Fatigue Syndrome (CFS). In a
subset of patients the disease starts
with infectious mononucleosis and both
enhanced and diminished EBV-specific
antibody titers have been reported. In
this study, we comprehensively analyzed
the EBV-specific memory B- and T-cell
response in patients with CFS. While we
observed no difference in viral capsid
antigen (VCA)-IgG antibodies, EBV
nuclear antigen (EBNA)-IgG titers were
low or absent in 10% of CFS patients.
Remarkably, when analyzing the EBV-specific
memory B-cell reservoir in vitro a
diminished or absent number of EBNA-1-
and VCA-antibody secreting cells was
found in up to 76% of patients.
Moreover, the ex vivo EBV-induced
secretion of TNF-α and IFN-γ was
significantly lower in patients.
Multicolor flow cytometry revealed that
the frequencies of EBNA-1-specific
triple TNF-α/IFN-γ/IL-2 producing CD4(+)
and CD8(+) T-cell subsets were
significantly diminished whereas no
difference could be detected for HCMV-specific
T-cell responses. When comparing EBV
load in blood immune cells, we found
more frequently EBER-DNA but not BZLF-1
RNA in CFS patients compared to healthy
controls suggesting more frequent latent
replication. Taken together, our
findings give evidence for a deficient
EBV-specific B- and T-cell memory
response in CFS patients and suggest an
impaired ability to control early steps
of EBV reactivation. In addition the
diminished EBV response might be
suitable to develop diagnostic marker in
CFS."
http://www.ncbi.nlm.nih.gov/pubmed/24454857
Here they talk about Lyme as if it is
advance aging - which we have said
before and they also talk about badly
cloned B cells - something we also talk
about all the time but say it does not
go as far in most cases as leukemia (so
they say the same things we say,
verifying independently our
observations):
J Immunol. 2014 Jan 15;192(2):603-11.
doi: 10.4049/jimmunol.1301384. Epub 2013
Dec 11.
Effects of aging, cytomegalovirus
infection, and EBV infection on human B
cell repertoires.
Wang C1, Liu
Y, Xu LT, Jackson KJ, Roskin KM, Pham
TD, Laserson J, Marshall EL, Seo K, Lee
JY, Furman D, Koller D, Dekker CL, Davis
MM, Fire AZ, Boyd SD.
1Department of Pathology, Stanford
University, Stanford, CA 94305;
"Elderly humans show decreased humoral
immunity to pathogens and vaccines, yet
the effects of aging on B cells are not
fully known. Chronic viral infection by
CMV is implicated as a driver of clonal
T cell proliferations in some aging
humans, but whether CMV or EBV infection
contributes to alterations in the B cell
repertoire with age is unclear. We have
used high-throughput DNA sequencing of
IGH gene rearrangements to study the BCR
repertoires over two successive years in
27 individuals ranging in age from 20 to
89 y. Some features of the B cell
repertoire remain stable with age, but
elderly subjects show increased numbers
of B cells with long CDR3 regions, a
trend toward accumulation of more highly
mutated IgM and IgG Ig genes, and
persistent clonal B cell populations in
the blood. Seropositivity for CMV or EBV
infection alters B cell repertoires,
regardless of the individual's age: EBV
infection correlates with the presence
of persistent clonal B cell expansions,
whereas CMV infection correlates with
the proportion of highly mutated Ab
genes. These findings isolate effects of
aging from those of chronic viral
infection on B cell repertoires and
provide a baseline for understanding
human B cell responses to vaccination or
infectious stimuli."
http://www.ncbi.nlm.nih.gov/pubmed/24337376
Harvard agrees with our model (It's not
an autoimmune disease but chronic active
EBV and a B cell disease):
Editorial
Epstein–Barr virus in the
development of multiple sclerosis
March 2008, Vol. 8, No. 3 ,
Pages 331-333
(doi:10.1586/14737175.8.3.331)
Alberto
AscherioHarvard School of Public Health,
Departments of Nutrition and
Epidemiology, 655 Huntington Avenue,
Boston, MA 02115, USA. aascheri@hsph.harvard.eduRead
More: http://informahealthcare.com/doi/abs/10.1586/14737175.8.3.331
http://informahealthcare.com/doi/abs/10.1586/14737175.8.3.331
High % of responders to antiviral drugs
in Chronic Fatigue Syndrome:
J Med Virol. 2013 Dec;85(12):2101-9. doi:
10.1002/jmv.23713. Epub 2013 Aug 19.
Randomized clinical trial to
evaluate the efficacy and safety of
valganciclovir in a subset of patients
with chronic fatigue syndrome.
Montoya JG1,
Kogelnik AM, Bhangoo M, Lunn MR, Flamand
L, Merrihew LE, Watt T, Kubo JT, Paik J,
Desai M.
Author information
1Department of Medicine, Stanford
University School of Medicine, Stanford,
California; Division of Infectious
Diseases and Geographic Medicine,
Stanford University School of Medicine,
Stanford, California.
Abstract
"There is no known treatment for chronic
fatigue syndrome (CFS). Little is known
about its pathogenesis. Human
herpesvirus 6 (HHV-6) and Epstein-Barr
virus (EBV) have been proposed as
infectious triggers. Thirty CFS patients
with elevated IgG antibody titers
against HHV-6 and EBV were randomized
2:1 to receive valganciclovir (VGCV) or
placebo for 6 months in a double-blind,
placebo-controlled trial. Clinical
endpoints aimed at measuring physical
and mental fatigue included the
Multidimensional Fatigue Inventory
(MFI-20) and Fatigue Severity Scale (FSS)
scores, self-reported cognitive
function, and physician-determined
responder status. Biological endpoints
included monocyte and neutrophil counts
and cytokine levels. VGCV patients
experienced a greater improvement by
MFI-20 at 9 months from baseline
compared to placebo patients but this
difference was not statistically
significant. However, statistically
significant differences in trajectories
between groups were observed in MFI-20
mental fatigue subscore (P = 0.039), FSS
score (P = 0.006), and cognitive
function (P = 0.025). VGCV patients
experienced these improvements within
the first 3 months and maintained that
benefit over the remaining 9 months.
Patients in the VGCV arm were 7.4 times
more likely to be classified as
responders (P = 0.029). In the VGCV arm,
monocyte counts decreased (P
http://www.ncbi.nlm.nih.gov/pubmed/23959519
THIS IS ALSO A WELL KNOWN "LYME"
SYMPTOM:
BMJ Case Rep. 2013 Apr 22;2013. pii:
bcr2013009171. doi:
10.1136/bcr-2013-009171.
Epstein-Barr virus-associated
cerebellar ataxia.
Ali K1, Lawthom C.
"Cerebellar ataxia is a common
neurological presentation. It can be
acute, subacute or chronic. Neurological
complications of Epstein-Barr virus (EBV)
are well-recognised with a variety of
presentations. Acute cerebellar ataxia
is a rare, but an established
complication. It has been described as
the sole manifestation of EBV infection
without the systemic features of
infectious mononucleosis. The
pathophysiology is not clear. The course
of the illness may last for a few months
with a benign outcome, though serious
complications can happen. We present a
case of a 38-year-old man who presented
with an acute cerebellar ataxia owing to
EBV infection, along with a review of
the literature."
http://www.ncbi.nlm.nih.gov/pubmed/23608862
