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Reference:

*Infectious XMLV in Human Cultures from
Mouse Xenografts* - Help ME circle, 9 July
2011 - Co-Cure: http://bit.ly/ncSEon


~jvr


````

http://bit.ly/nCVJUH


[]


When Science Journals are
Scarier than Science Fiction


By Kent Heckenlively, Esq.


My choice for the scariest reading of the year was
recently published in the journal Cancer Biology and
Therapy and has the unwieldly title of *Frequent
Detection of Infectious Xenotropic Leukemia Virus
(XMLV) in Human Cultures Established from Mouse
Xenografts* (http://bit.ly/oONQ5N).

For those of you who may be confused by the idea of
a "xenograft" I'll provide you with the definition given
by the U. S. Public Health Service:

*Any procedure that involves the transplantation,
implantation, or infusion into a human recipient of
either

(a) live cells, tissues, or organs from a non-human
animal source or

(b) human body fluids, cells, tissues or organs that
have had ex vivio contact with live non-human animal
cells, tissues, or organs.*

This covers vaccines as well as other surgical
procedures in which human tissue is manipulated prior
to transplantation.


In the scientific community mouse xenografting is
often used to manipulate cancer cells for research
purposes, among other things.

With research that has linked XMRV (which is a
xenotropic murine leukemia virus) to prostate cancer,
chronic fatigue syndrome/ME, and to a lesser extent
autism, scientists from Johns Hopkins University and
the University of Texas Southwestern Medical Center
as well as a few other institutions thought it made
sense to investigate the frequency of XMLVs in human
cell lines *established from mouse xenografts and to
search for the evidence of horizontal spread to other
cell lines.*

In layman's terms the question they were asking was,
*when we do xenografting with mouse biological
products how often do we get XMLVs popping up in
our samples?*

The answer they found is that six out of twenty three
(26%) mouse DNA free xenografts *were strongly
positive for MLV and their sequences had greater than
99% homology to known MLV strains.*

These samples were obtained from seven independent
laboratories.

Further on the authors wrote:

*Of the 78 non-xenograft derived cell lines maintained
in the xenograft culture containing facilities, 13 (17%)
were positive for MLV, including XMRV, a virus strain
first identified in human tissues.* (My daughter with
autism has tested positive for XMRV.) In scientific
terms this is an absolute train wreck.

This means that every surgical patient receiving any
biological product which used mouse tissue in any way
has a one in four chance of being exposed to an
XMLV.

And that also means that any biological sample which
is maintained in a facility containing xenograft cultures
has a 17% chance of becoming infected.

On the question of vaccines, let's just say that only
10% of the nearly 40 vaccines children are expected
to receive prior to the age of five contain mouse
biological products. This translates into roughly a
100% chance that our current generation of children
will be exposed to an XMLV through a vaccination.

Are you scared yet?

It gets worse.

From the article is the following passage:

*In one case XMRV virus infection to a non-xenograft
colorectal carcinoma cell line RKO was demonstrated
from an XMRV containing prostate xenograft derived
cell line 221 Rv1 even though the two cell lines had
been maintained in the same culture facility for only a
few days.*

The translation for a non-medical person is this:

XMRV is highly infectious and spreads easily.

How about this for scary?

*Provirus integration into the genome is not random,
and occurs preferentially at transcription start sites,
CpG islands, DNase-hypersensitive sites and gene
dense regions, suggesting that provirus integration
may influence transcription in the host cell.*

For those of you keeping score at home, the CpG
islands are responsible for methylation. Is any of this
starting to sound familiar? And the transcription start
sites of genes? Pretty damned important.

I know there are those who question the role of
viruses in conditions like autism and state correctly
that a well-functioning immune system will deal with
any such pathogens.

I agree.

The problem is that we don't know the immune status
of people in the population. For example, the
discovery of XMRV itself was preceded by the finding
that men with the most aggressive forms of prostate
cancer had a deficiency in their RNasel gene, lowering
the amount of an anti-viral defense enzyme their body
produced.

How widely is that RNasel mutation spread throughout
the population? Do you know the RNasel status of
your genes? Of your children? And that's just what
we know about.

And can toxic chemicals and heavy metals interfere
with your body's immune system response to
pathogens, regardless of your genetic make-up?

You betcha.

The closest example I can make is that of what
happened to the native population in the Americas
when Europeans crossed the ocean.

A natural barrier was breached and the native
population had no immunity to our pathogens. Some
experts speculate that the diesases Europeans brough
to the New World killed 90% of the native population.

While we have shared the Earth with mice and other
creatures from the dawn of history, we haven't been
culturing their cells, then injecting those cells into our
bloodstream.

We have breached a natural barrier and we need to
ask the question of what consequences have been
wrought from this decision.

In the conclusion the authors write:

*Thus laboratories handling or culturing human
xenografts should monitor for the presence of MLV,
and should consider monitoring personnel for viral
antigens or antibodies to them.

Laboratories working with xenograft cultures should
have full knowledge and understanding of the
potential biological and biohazardous risks and should
not distribute or publish their findings without full
disclosure of the virus status of their
xenograft-derived materials.*

I've heard some commentators lament what it will
take for the medical authorities to deal with this issue
seriously.

They've noted with the despair the finding of XMRV in
men with prostate cancer, those with chronic fatigue
syndrome/ME and children with autism and how it has
failed to provoke action.

They've said to me:

"These people have no problem screwing over the old
men, those with CFS/ME, and even the children."

With this recent finding regarding the dangers of
XMLV and XMRV transmission in labs, the question
becomes,

*Will these same medical authorities screw the very
people who work for them?*




Kent Heckenlively is a Contributing Editor to Age of
Autism









~~~~

Blood Test for Chronic Fatigue Syndrome (CFS)

~~~~~~~~~~~~~~~~~~~~~
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>>>> 7 April 2011 <<<

Editorship : j.van.roijen@chello.nl
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http://bit.ly/gq5Y39




CHRONIX BIOMEDICAL
Routine Laboratory Blood Tests for Cancer


News and Resources


Press Releases



CHRONIX BIOMEDICAL AND HEMISPHERX
BIOPHARMA JOINTLY FILE PATENT
APPLICATION FOR A BLOOD TEST FOR
CHRONIC FATIGUE SYNDROME (CFS)




—CHRONIX TECHNOLOGY FOCUSES ON
CHANGES TO CFS PATIENTS’ DNA—



— HEMISPHERX AND CHRONIX PLAN
STUDIES TO VALIDATE TECHNOLOGY
AS A POTENTIAL DIAGNOSTIC TEST
FOR CFS —





San Jose, CA March 3, 2011 – Chronix Biomedical
("Chronix") announced today that it filed a
provisional United States patent application jointly
with Hemispherx Biopharma, Inc. (NYSE Amex:HEB)
("Hemispherx") on a blood test for Chronic Fatigue
Syndrome (“CFS”).

Patients with CFS exhibit a wide range of disabling
symptoms including the inability to overcome fatigue
by rest, swollen lymph nodes and cognitive
deficiencies.

CFS is estimated to affect approximately 4 million
Americans, according to the Centers for Disease
Control and Prevention (CDC). The disorder has a
negative economic impact in the United States
estimated at more than $9 billion annually.



The Chronix experimental approach analyzes
fragments of DNA often released into the
bloodstream during the process of apoptosis or
programmed cell death.

Chronix is using its proprietary technology and
advanced DNA sequencing platforms to measure
alterations in specific regions of the chromosome,
which can be detected as distinctive “signatures” in
cell-free blood-borne DNA.

By focusing on these signatures, Chronix’s
technology can detect the presence of
disease-damaged cells in simple blood samples
without needing to biopsy diseased cells or tissues.



“Our technology - based on DNA released into the
bloodstream by dying and damaged cells - taps into
the dynamic information provided by the genomic
alterations unique to each diseased cell.

We capture what is happening to the DNA very early
in and throughout the disease process, in real time,
and patient by patient.

That’s how our approach differs from other tests that
focus on static genomic data or protein biomarkers,”

said Dr. Urnovitz.


The patient-unique signatures captured by the
Chronix technology may prove useful as a companion
diagnostic – a test that is used to help guide
treatment decisions – and to provide information
about the disease process to help pharmaceutical
companies select the most efficacious drug
candidates.



Use of the Chronix diagnostic technology in CFS will
be evaluated in a study being planned by Chronix
and Hemispherx, a leader in CFS pharmaceutical
research.

Dr. William Carter, Hemispherx CEO, commented:

“It is with great enthusiasm that we will be
conducting studies aimed at validating the utility of
the Chronix technology to identify how different
individuals can respond to Hemispherx’s
experimental drug Ampligen®.”


The Chronix Biomedical blood test for Chronic Fatigue
Syndrome is experimental in nature and has not been
evaluated by any regulatory agency. It is currently
limited to investigational use.




About Chronix Biomedical

Chronix Biomedical is pioneering a breakthrough
approach to the diagnosis, monitoring and
management of a broad range of cancers and other
conditions. It has developed proprietary technology
that measures and categorizes DNA sequences
circulating in the blood that are associated with
specific changes in disease and health status. Using
advanced genome analysis methodology, proprietary
data tools and disease-specific databases, Chronix
has demonstrated the utility of its diagnostic and
prognostic approach in a chronic neurologic disease,
in breast and prostate cancer and in multiple
myeloma. It is currently conducting studies in other
cancers. The company initially plans to offer an
Apoptotic Serum DNA testing service to cancer
clinical researchers “For Investigational Use Only” to
track disease recurrence and monitor treatment.
Chronix is headquartered in San Jose, California and
has research facilities in Germany.



About Hemispherx Biopharma


Hemispherx Biopharma, Inc. is an advanced specialty
pharmaceutical company engaged in the manufacture
and clinical development of new drug entities for
treatment of seriously debilitating disorders.
Hemispherx’s flagship products include Alferon N
Injection® (FDA approved for a category of sexually
transmitted diseases) and the experimental
therapeutics Ampligen® and Alferon® LDO.
Ampligen® is an experimental RNA nucleic acid being
developed for globally important debilitating
diseases and disorders of the immune system.
Hemispherx’s platform technology includes
components for potential treatment of various
severely debilitating and life threatening diseases.
Hemispherx has patents comprising its core
intellectual property estate and a fully
commercialized product (Alferon N Injection®). The
Company wholly owns and exclusively operates a
GMP certified manufacturing facility in the United
States for commercial products. For more
information please visit www.hemispherx.net.

Information contained in this news release, other
than historical information, should be considered
forward-looking and is subject to various risk factors
and uncertainties. For instance, the strategies and
operations of Hemispherx involve risk of competition,
changing market conditions, change in laws and
regulations affecting these industries and numerous
other factors discussed in this release and in
Hemispherx’s filings with the Securities and
Exchange Commission. Any referenced
investigational drugs and associated technologies of
Hemispherx or Chronix are experimental in nature
and as such are not designated safe and effective by
a regulatory authority for general use and are legally
available only for investigational use. The
forward-looking statements represent Hemispherx’s
and Chronix’s respective judgments as of the date of
this release. Both Companies disclaim, however, any
intent or obligation to update these forward-looking
statements. The planning, completion, results or
submission of investigations do not imply that any
study product or test will ever be approved or
permitted for commercial distribution for the studied
or other treatment uses.









~~~~

Comment XMRV Mouse DNA contamination -Retrovirology

~~~~~~~~~~~~~~~~~~~~~
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RETROVIROLOGY




Mouse DNA contamination
in human tissue tested for XMRV

Mark J Robinson, Otto W Erlwein, Steve Kaye,
Jonathan Weber, Oya Cingoz, Anup Patel,
Marjorie M Walker, Wun-Jae Kim, Mongkol
Uiprasertkul, John M Coffin and Myra O McClure


Retrovirology 2010, 7:108

doi:10.1186/1742-4690-7-108


````````````````
This study *Mouse DNA contamination in human
tissue tested for XMRV* by Robinson MJ et al, can
be found at: http://bit.ly/h1sz1q


~jvr

````````````````



http://bit.ly/eEqexI




Comments:


Robinson et al
flaws in study design


Gerwyn Morris


(21 January 2011)

PA institute



This article presents a methodological critique of the
study carried out by Robinson et al (1).

In essence this article submits that the work in
question departs so profoundly from the work of
other research groups that the results must be
treated with caution.

In particular these results are at best open to
interpretation and at worst may be the product of
experimentally induced artifacts.


Initially the results of the study by Robinson et al
appear unremarkable. The detection rate by PCR is in
line with that reported by Danielson et al but some
400% lower than that achieved by IHC using XMRV
specific probes (2, 3).

This of course means that any conclusion made by
PCR alone regarding the association of XMRV and
mouse DNA is profoundly unsafe.

One must also point out that Robinson et al did not
find higher rates of XMRV infection in cancerous
versus non cancerous sequences which is a serious
departure from the results of other workers.

In fact it is such a notable departure that an
explanation is needed.


The association between XMRV and mouse DNA in
this study is imperfect whereas in a contaminant
scenario it would not be. The authors theorise that
this may be due to the inability of their PCR assay to
detect XMRV in low copy numbers.


This hypothesis was unfortunately not put to the
test by using IHC which has been shown to be far
more sensitive than PCR.

As PCR is by some considerable margin the least
sensitive method for detecting XMRV in prostate
cancer (2, 3) and chronic fatigue syndrome (4) no
association between the presence of mouse DNA
and XMRV can be safely made.


The authors expressed surprise that their PCR
approach produced gag sequences which did not
contain the 24-nt deletion characteristically present
in the XMRV sequences cloned to date, as they
expected their primers to be specific to VP62 gag.

This raises a number of issues.

Firstly, despite the authors' expectations they
provide no evidence that their primers were specific,
merely that they were capable of detecting XMRV
gag (5, 6).

The only study which has detected XMRV in prostate
cancer using primers set for unique sequences in the
XMRV genome is Schlaberg et al 2009 (2).


It is therefore something of a mystery why
researchers concerned about mouse contamination
did not engage in a literature search to establish
whether the primers used in their experiments were
in fact specific to XMRV sequences which are unique
to the virus.

This is particularly vital as if the Schlaberg primers
did not produce the same results this study would
fall.


Secondly the presence of a recombinant with a
different gag sequence is entirely consistent with the
behaviour of XMRV-related viruses in vivo and is to
expected in tumour tissue (7).

This occurs via the interaction of the nucleic acid of
the exogenous viruses and the endogenous viruses
which permanently occupy mammalian genomes.


Indeed, the clone reported by the authors which
contained a 24 base pair deletion in glycogag would
be a classic example of a viral variant caused by the
recombination of XMRV and an endogenous MLV
virus.

The authors were in a position to clarify the issue
themselves which sadly they did not.

XMRV has unique sequences in the U3 integrase and
SU region.


From the authors report they had access to
sequences or whole clones containing the
information needed to confirm whether these were
recombinants or not. It seems astonishing that they
did not provide this information in the paper.


Finally,the authors by their own admission expected
a primer sequence constructed against a region
between U5 and the 5' end of GAG to be only
capable of amplifying XMRV.

These primers were part of a specific assay
developed by Urisman et al (2006) (5) but do not
compliment any region that is unique to XMRV.

It is possible that these authors misunderstood this
essential point.



It is difficult to fathom therefore why the authors
would conclude that these expected PCR findings
were evidence of mouse contamination when a far
more parsimonious explanation was available.


Indeed, one would argue that the authors (if aware
of recent research conducted by Danielson et al
2010) (8) should have been surprised that primer
sequences that they believed were specific to XMRV
gag would have produced any product at all.

The important point to note is that at this
juncture in the study there were no results
suggestive of any mouse contamination at all.



Next we turn to the section of the study where the
authors test the ability of their PCR assays (IAP and
mtDNA) to detect mouse DNA in mouse cell lines.

The cell lines named are McCoy and RAW264.7
(RAW). It is not clear whether both cell lines were of
mouse origin.

The McCoy cell line used could have been human in
origin. If so, it would have been spiked, as the
authors stated that they amplified mouse DNA from
both cell lines.


If they were both mouse cell lines then other
considerations enter the equation.

McCoy mouse cell lines express a polytropic MLV (9)
and the RAW cell line was initially transformed by
Abelson MLV.

These cell lines have the potential of introducing
other viruses into the experimental environment.


In any event, the presence of mouse DNA in these
cells must be considered as the source of
contamination reported in this experiment.

This seems to be a parsimonious explanation as
there was no evidence of contamination prior to the
use of these cell lines.



Finally, we examine the claim made by the authors
that IAP was a much more sensitive assay than
mtDNA PCR in detecting mouse DNA in transformed
cell lines.

The normal criticism of this statement would centre
on unfounded extrapolation from in vitro to in vivo
conditions. There is however more to consider here.


The environment of transformed and immortalised
cells is one of extremely high levels of oxidative
stress (10). Mitochondrial DNA is much more prone
to oxidative damage (due to its nudity) than genomic
DNA (11).

Indeed studies have demonstrated that such cell
lines are either depleted of mtDNA (12) or that the
mitochondrial genome is highly mutated (13).


Therefore the amount of mtDNA actually recoverable
by PCR in this experiment may well have been
minimal.

Thus before any claims regarding the relative
sensitivity of the two assays were made, the
integrity of the mitochondrial DNA should have been
investigated.


Moreover while the authors demonstrated that their
IAP assay could not amplify human DNA they did not
demonstrate that it could not amplify IAP sequences
in prostate tumour tissue.

This is particularly remiss of them as IAP sequences
have only been detected in PMBCS in cases of
Sjiornes syndrome but occur at a high frequency in
the DNA of people suffering from cancer (14).

The greatest concern however relates to the known
ability of retroviruses to package IAP sequences into
their genomes.

Hence a positive response to a IAP assay
may well just indicate XMRV or PMLV
infection.


The following is a quote from A Dusty Miller
expressing his view about the IAP test in a
communication to people with ME/CFS.


*....However, unpublished results suggest that IAP
sequences might be transferred by retroviruses, so
finding IAP sequences in human samples might
simply reflect IAP transfer by the XMRV and
XMRV-like viruses we are trying to detect....*



In conclusion, the findings of this study are
inconsistent with the reports of other workers.

Given the potential for the accidental introduction of
contaminant DNA into this experiment, the
conclusions cannot be safely generalised.

Similarly the claim that IAP is superior to , or even
as reliable, as mtDNA PCR in vivo is not supported
by the data cited as alternative explanations for the
findings are readily available.





References:


1) MJ Robinson, OW Erlwein, S Kaye, J Weber, O
Cingoz, A Patel, MM Walker , W-J Kim, M
Uiprasertkul, JM Coffin and MO McClure; Mouse DNA
contamination in human tissue tested for XMRV;
Retrovirology 2010,
7:108doi:10.1186/1742-4690-7-108

2) Schlaberg R, Choe DJ, Brown KR, Thaker HM, Singh
IR (2009) XMRV is present in malignant prostatic
epithelium and is associated with prostate cancer,
especially high-grade tumors. Proc Natl Acad Sci USA
106:16351–16356

3) RS Arnold, NV Makarova, AO Osunkoya, S Suppiah,
TA Scott, NA Johnson, SM Bhosle, D Liotta, E Hunter,
FF Marshall, H Ly, RJ Molinaro, JL Blackwell, JA
Petros; XMRV Infection in Patients With Prostate
Cancer: Novel Serologic Assay and Correlation With
PCR and FISH; Urology - April 2010 (Vol. 75, Issue
4, Pages 755-761,
DOI:10.1016/j.urology.2010.01.038)

4) JA Mikovits, Y Huang, MA Pfost, VC Lombardi, DC
Bertolette, KS Hagen and FW Ruscetti; Distribution
of Xenotropic Murine Leukemia Virus-Related Virus
(XMRV) Infection in Chronic Fatigue Syndrome and
Prostate Cancer; AIDS Rev 2010; 12: 149-52

5) Urisman A, Molinaro RJ, Fischer N, Plummer SJ,
Casey G, et al. 2006 Identification of a Novel
Gammaretrovirus in Prostate Tumors of Patients
Homozygous for R462Q RNASEL Variant. PLoS Pathog
2(3): e25. doi:10.1371/journal.ppat.0020025

6) B Dong, S Kim, S Hong, J Das Gupta, K Malathi,
EA Klein, D Ganem, JL DeRisi, SA Chow, and RH
Silverman; An infectious retrovirus susceptible to an
IFN antiviral pathway from human prostate tumors;
PNAS January 30, 2007 vol. 104 no. 5 1655-1660
10.1073/pnas.0610291104

7) H van der Puttena, W Quinta, J van Raaija, ER
Maandaga, IM Verma and A Bernsa; M-MuLV-induced
leukemogenesis: Integration and structure of
recombinant proviruses in tumors; Cell, Volume 24,
Issue 3, 729-739, 1 June 1981 doi:10.1016/0092
8674(81)90099-4

8) BP Danielson, GE Ayala and JT Kimata; Detection
of Xenotropic Murine Leukemia Virus-Related Virus in
Normal and Tumor Tissue of Patients from the
Southern United States with Prostate Cancer Is
Dependent on Specific Polymerase Chain Reaction
Conditions; J Infect Dis. (2010) 202 (10):
1470-1477. doi: 10.1086/656146

9) Fong CK, Yang-Feng TL, Lerner-Tung MB;
Re-examination of the McCoy cell line for
confirmation of its mouse origin: karyotyping,
electron microscopy and reverse transcriptase assay
for endogenous retrovirus; Clin Diagn Virol. 1994
Apr;2(2):95-103.

10) RH Burdon, V Gill and C Rice-Evans; Oxidative
Stress and Tumour Cell Proliferation; Free Radical
Research 1990, Vol. 11, No. 1-3 , Pages 65-76

11) C Richter, J W Park, and B N Ames; Normal
oxidative damage to mitochondrial and nuclear DNA
is extensive; PNAS September 1, 1988 vol. 85 no. 17
6465-6467

12) J-I Hayashi, M Takemitsu and I Nonaka;
Recovery of the missing tumorigenicity in
mitochondrial DNA-less HeLa cells by introduction of
mitochondrial DNA from normal human cells;
Somatic Cell and Molecular Genetics Volume 18,
Number 2, 123-129, DOI: 10.1007/BF0123315

13) M Bakhanashvili, S Grinberg, E Bonda, AJSimon, S
Moshitch-Moshkovitz and G Rahav; p53 in
mitochondria enhances the accuracy of DNA
synthesis; Cell Death and Differentiation (2008) 15,
1865–1874; doi:10.1038/cdd.2008.122

14) W Seifarth, H Skladny, F Krieg-Schneider, A
Reichert, R Hehlmann, and C Leib-Mösch;
Retrovirus-like particles released from the human
breast cancer cell line T47-D display type B- and
C-related endogenous retroviral sequences; J Virol.
1995 October; 69(10): 6408–6416




Competing interests

None declared








~~~~

GcMAF -Promise & Pitfalls -ME/CFS

~~~~~~~~~~~~~~~~~~~~~
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http://bit.ly/hReUuz




Rutts tankespinn og ME-nyheter

Det meste av det siste innen biomedisinsk forskning
pD ME



GcMAF – The promise and the pitfalls


By Rutt


21.01.11




*Gcmaf is one of the most promising, if not the
most promising drug for ME/CFS this side of
ampligen and far cheaper than ampligen.


Dr. Cheney, Dr. Kenny de Meirleir and others are
running small-scale studies with this compound
which was found by its proprietor, Dr. Yamamoto to
eradicate HIV.


Dr. De Meirleir recently announced that the combo of
gcmaf and nexavir (an immune modulator) converted
a patient from XMRV sero-positive to -negative.

I have been in contact with multiple patients,
including one XMRV-pos whom has improved
significantly from this natural compound which
stimulates macrophage activity.



The questions that remain are:

1) which source out of the three (Yamamoto, Dr De
Meirleir, BGLI in the Netherlands) has the most
potency and contains 100% human derived material
– this question can only be answered by a truly
independent lab.


2) what is the true role of VDR status in predicting
treatment outcome and which lab has the accurate
results (currently redlabs Belgium seems to produce
conflicting results with Amy Yasko’s lab)


3) what role will the FDA play? Currently shipments
of BGLI gcmaf are being held up at customs, yet
patients are biting the bullet and ordering in hopes
their shipment will slip through the cracks. As if
patients haven’t been skewered financially enough.



In my own opinion, this drug holds so much promise
not only in terms of results but in terms of method
of action.

It triggers innate immunity so it is unlikely to lead to
viral resistance, superbugs, or the viral biofilms that
were announced in sciencedaily this morning.

Bacterial biofilms developed theoretically due to
rampant antibiotic use. Life will find a way, and
therapeutically we have a choice to try to beat the
bug into submission with WMDs like ARVs or bolster
our own immunity.


However, the caveat is, Ampligen theoretically was
supposed to stimulate our immunity to enable us to
win the war, and patients inevitably always relapsed
once they stopped the drug.


With that said, perhaps a combination of both routes
can cover the gamut, which may be why some
high-profile XMRV researchers are discussing testing
terrain therapies such as peptide T, gcmaf, nexavir,
and even stem cells in combination with HAART.


With XMRV, it is far more likely than with HIV, that
reservoirs are a primary issue because it is
slow-replicating.

Therapies such as interleukins have been used to
draw HIV out of latency with varying success.

XMRV researchers will likely need to consider the
problem of drawing virus out of latency (ie stem cells
since stem cell division equals viral replication) as
well as cutting the provirus (the viral DNA integrated
into our human DNA) with methods that mimic
restriction enzyme systems which remove foreign
viral DNA from our own DNA.

Leave the provirus in there and it may trigger
oncogenes, which may be why XMRV has been found
in prostate and breast cancer.


A somewhat overlooked risk with gcmaf is that XMRV
and HIV have been found in macrophages, so taking
a macrophage-stimulator is in theory a bit like giving
your crippled bodyguard steroids to take on the guy
that did the crippling. A logical fallacy if you will, but
results speak louder than funny-looking bodyguards.

Another thing is macrophages have been found in the
temporal lobes, so triggering latent retroviruses in
the brain may be a recipe for disaster.


In the end, gcmaf is but one way to attack the virus.
I just hope we get to find out what it can really do
before the powers that be decide to intervene
because its an unpatentable substance that happens
to achieve what billions of dollars of research into
HIV drugs has failed to achieve.*





~~~~

XMRV presentation -Dr. Mikovits & Annette Whittemore -Part 2

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>>>> 21 January 2011 <<<<
Editorship : j.van.roijen@chello.nl
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http://bit.ly/h8r59k


Lannie in the Lymelight

Actively pursuing a new title. Soon to read:
"The girl who healed herself of CFS and Lyme"



Wednesday, January 19, 2011


PART 2:


1/17/11


XMRV presentation by
Dr. Judy Mikovits and
Annette Whittemore


For Part 1 CLICK HERE: http://bit.ly/g6tqzB






And now back to the story of XMRV.
What do we know about XMRV?




slide 1: see below



What we know about XMRV is that it integrates into
human tissue, demonstrating that it is a human
infection.

We can confirm it is NOT an endogenous virus to
humans. It is in fact a new human retrovirus.

However, how it got into humans is still unclear at
this time. We know that XMRV expression is
stimulated by androgens(hormones), cortisol and
inflammation.

And we know that it is an envelope gene that is
highly related to xenotropic, polytropic and SSFV
MLVs. This relation, or similarity, that the XMRV
envelope has is important.

We know in the animal world that Xenotropic,
polytroips and SSFV MLVs cause neuroimmune
disease and lead to tumors.

There is information available to us in these animal
models that allow for us to make very short leaps to
humans. It is common place in science to utilize
these similarities in animal models.

These do not usually point hysterically to animal
contamination, but are considered a starting point
or, as both Whittemore and Mikovits called it, *a
bridge* for researchers.



We also know a bit more related to biomarkers
common to those with XMRV.


slide 2: see below


I’m afraid I can’t remember what ATL stands for, but
basically it’s representing a category of people with
XMRV and comparing them to uninfected.

You’ll notice extreme increase in Cytokine and
Chemokine Production.


There is also proof that XMRV infected patients have
fewer T-cell white blood cells.



slide 3: see below


There are further immune cell abnormalities for those
with XMRV.


slide 4: see below


As we’ve heard before, XMRV infected patients have
reduced Natural Killer cells. What does this actually
mean?

The CD56, the cell that manages the killing off of
bad things is significantly reduced. Therefore we
can’t fight off infection as well as a healthy
counterpart.

The CD19, which creates B cells is severely reduced.
The CD19 is related to our production of immature
CD20, which has a direct correlation with tumors.

Mikovits did note some reported success published in
regards to Rituxan, a chimeric monoclonal antibody
against the protein CD20, which is primarily found on
the surface of B cells.

Rituximab is used in the treatment of many
lymphomas, leukemias and transplant rejection. It
has also been used off label for numerous
autoimmune disorders such as Rheumatoid Arthritis,
Multiple Sclerosis and Lupus to name just a few.

The last note is very important, XMRV infected
patients have clonal populations of gd T-cells. This is
important, as look at the next slide…


slide 5: see below



This slide depicts 20 CFS patients, all XMRV+(less 3
not tested), all Clonal TCRg positive (less 5 not
tested), and these are all of the types of
Lymphoma/cancer they have (the 3 suspicious means
they’re showing signs of early stage).


Until the team of Lombardi, Mikovits, et al, no one
had a tool to detect XMRV. This is an image of how
they perform the lab work to find XMRV results.


slide 6: see below


The top half shows the original process performed for
the Science, 2009 published research.

Mikovits spoke of step 1 was Plasma. Step 2 was
Serology. Step 3 was to culture with the XMRV
prostate cancer cell lines and then let grow for 21-42
days, varying awaiting activation.
Then Step 4, a western blot of the cultured sample.

She noted that the lab can only handle 10 samples
through each stage at a time, as this process is so
labor intensive, hence the delay in results.


The bottom half with images under *Current* is the
process they’re using and planning to have available
at VIP Dx by June 2011.

This is a new assay that cultures in 4-18 days. You
can see it is active, or ready when it turns green
(see white squares with blue and green dots).


In discussing tests, another very important take
away was that if you test positive you are positive.

If you test negative, they are not able to confirm it
is absolutely negative. Until there is further
understanding of the XMRV lifecycle, they can not
confirm this.

One last note, she mentioned that serology AND
culture were so very important to have run.

As a patient, I remember filling out the form for VIP
Dx. It is cheaper to only run serology, but that is not
recommended.

Mikovits noted *especially the sickest, get negative
antibody response, but positive culture.*

I’ll cover treatment later, but she also noted that
once some of these especially sick patients went on
antiretrovirals they were able to create an antibody
response.

Prior to, their systems were just too weak. Creating
an antibody response would cause the patient to
then also report positive on serology.


slide 7: see below


You *never see these in healthy people!* exclaimed
Mikovits. She stressed how the positives and
negatives are SO CLEAR.

You can see in this slide above, sample 1197 is
clearly negative. Yet the rest are so clearly positive.

She showed an interesting example here. I
unfortunately wasn’t quick enough with my camera to
nab the initial slide.

We first saw an initial antibody test where sample
1118 was negative. Then this slide was shown, after
more extensive culture testing, 1118 is clearly
positive.

This is where she stressed that 1118, like many,
many not specifically have XMRV, but most definitely
has an MRV.

Going back to my comment from Part 1, of the
Phylogenic Tree. There are multiple sequences these
patients can fall under. Some can even be positive
for more than one.


So where are we seeing XMRV? The disease
association seems limitless. It’s showing up in every
corner of the neuroimmune world.


slide 8: see below


One private practice shared it’s associations with
Mikovits and the WPI team. This practice started
testing its neuroimmune patients and soon found
they were treating XMRV positive patients with CFS,
Fibromyalgia, Chronic Lyme Disease, Multiple
Sclerosis, Parkinson’s Disease, ALS, the list goes on.

I think it is safe to say this is a private practice for
adults, therefore we’re not seeing the children with
autism in this example as we did with the family
profiles from Part 1 discussion.

Finally, it was noted that XMRV research has
concentrated around ME/CFS to date, but larger
studies on the presence of XMRV in these other
neuroimmune diseases are coming.


As a Chronic Lyme Disease patient, I found it very
interesting that much of this conversation seemed to
go back to Lyme again and again. During the
presentation and the Q&A session.

In the presentation they referenced a study where 65
Chronic Lyme Disease patients were tested for
XMRV, and 100% came back positive.

This was the most reactive group the WPI has seen.
That is a higher rate than ME/CFS! I thought Annette
Whittemore said it best:

*Every time we hear something new
about XMRV, we find a similar finding
within Lyme. It’s amazing!*


So now what we’ve all been waiting for. Treatments
options!!


slide 9: see below



This first slide was a reminder of the study
performed by Singh, et al in vitro.

Three antiretrovirals showed promise amongst 45
compounds and 28 drugs approved for use in
humans. Those three include Zidovudine(most know
it as AZT), Tenofovir and Raltegravir.

The study showed all two-drug-combinations showed
efficacy against XMRV in vitro.


slide 10: see below


Given those results, Dr. Brewer, an infectious
disease specialist who’s spent much of his career in
HIV but more recently in ME/CFS and XMRV, has used
2 and 3 drug combination antiretroviral treatments
with a CFS/XMRV+ patient sample of 25.

The results have been a mixed bag among the
patients on ARVs anywhere from 1-9 months.

The expected Herxheimer response occurred in some
as would be expected.

Symptom reduction has been reported, however
majority reported feeling *about the same.*

(I think it's very important to remember that these
25 patients have been on the AVRs anywhere from
1-9 months, and most likely on the shorter end of it
considering how young the AVR concept is for
XMRV...

if we think about antivirals, patients have to be on
them for much longer before they start feeling
better) Dr. Mikovits referenced Dr. Deckoff-Jones,
along with Brewer’s patients and a few others.

She has noticed a common theme of patients feeling
better around 6 months, followed by a return of all or
most symptoms. It sounds very similar to what
happens to many on antivirals.

I appreciated that she didn’t stop here however. She
went on to ask herself and her team *how can we
add immune modulating supplements to keep up the
response beyond 6 months?*

That might be the next step we see in antiretroviral
(ARV) discussion.




slide 11: see below



Next, Mikovits covered her *other thoughts* beyond
Singh’s and Brewer’s experiences/findings with ARVs.

She recognized ARVs might be part of the picture,
but they do not address the entirety.
XMRV patients are still dealing with metabolic
abnormalities including oxidative stress, glutathione
depletion and DNA hypomethylation.

The concern is that all three of these are not only
abnormalities in XMRV patients, but they all increase
viral replication.



slide 12: see below



She first discussed how the restoration of
glutathione would reduce stress on XMRV patients
remarkably.

Next, she covered the need to restore and or improve
methylation. She suggested methofolate in B12, and
specifically mentioned supplements called Deplin and
Cerefolin NAC.


When discussing Immune Modulation, Mikovits
introduced a few points that were new to me.

She sees great promise in the newer treatment
options popping up such as GcMAF, Stem Cell
Therapy and Peptide T.

However she is concerned that they may *activate
the inactive reservoir XMRV.* Meaning there could be
some XMRV in our bodies that is still dormant, but
activation of our immune system might bring them
out.

However, she didn’t stop there. She mentioned that
this might actually be a good thing. As ARVs are
more effective in HIV since HIV replicates
considerably more than XMRV, maybe one of these
will get XMRV replicating so the ARV has a job to
do.

Another area that will surely be discussed further.


She addressed Ampligen separately. This drug has
been around and documented more than the previous
three discussed.

Her comment on Ampligen was that it activates the
viruses in about 1/3 of the cases. So there again, it
could be a matter of hitting those with ARVs.

However, a little scary for those in the Ampligen
trials and are unable to take antivirals or
antiretrovirals while on Ampligen.


Net, net, more research needs to be done before she
can make recommendations on treatment as a
researcher.


Finally, what does the future look like for XMRV, and
for its patients?


slide 13: see below


The slide is pretty straight forward. It was not
hovered over for all that long. What I took away from
her discussion was that the question of being able it
isolate a polytropic was most interesting to
Mikovits.

Note this was only my opinion.


The subject I’ve stayed away from, that was
discussed intermittently, was the politics of it all.
Our government’s involvement, or lack thereof.

I’d like to close with a quote from Mikovits, when
asked about the politics and all the second guessing
that has occurred regarding her research today.

Very confidently, and quickly she retorted, *I think
the politics will go away shortly.* Period. All she
said. There was a gasp in the room, and she moved
on as if she had just said *please pass me a glass of
water.*

This leads me to believe there is a research paper on
its way to being published that will close the case on
the contamination theories, the replication theories,
and hopefully the cause/effect query.

Just my take, but she seemed pretty darn
comfortable making that statement…:

*I think the politics will go away shortly.*

All I can say to that is, let's sure hope so!


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**Please note, Lannie is not a scientist, doctor or
treating physician. She is a patient that has taken an
interest in her own health and while doing so is
attempting to share her learnings for the larger
patient community.

These are only her opinions and take-aways. If you
feel a piece of science has been incorrectly reported,
feel free to contact Lannie with a suggested change
– via the comments section or at
lannieinthelymelight@gmail.com – Thanks!





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~jan van roijen - Attention:


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