The Fire Smolders

Here are more abstracts about XMRV from Belgium which strongly suggest that it is more than a contaminant:

Restricted infection of xenotropic murine leukemia virus-related virus in human lymphoid tissue
Marta Curriu, Jorge Carrillo, Marta Massanella, Elisabet Garcia, Bonaventura Clotet, Julian Blanco, Cecilia Cabrera
http://www.retrovirology.com/content/8/S1/A208

Heme oxygenase-1 activation inhibits XMRV pathogenesis and carcinogenesis in prostate cancer cells
Subhash Dhawan
http://www.retrovirology.com/content/8/S1/A218

A prototype RT-PCR assay for detection of XMRV in multiple human sample types
Ning Tang, Andrea Frank, Robert Kowal, Gregor Leckie, John Hackett Jr, Graham Simmons, Michael Busch and Klara Abravaya
http://www.retrovirology.com/content/8/S1/A220

Dr. De Meirleir’s presentation was listed in the Poster Section of the agenda and was called “Serological evidence of XMRV in CFS and blood donors in Belgium”. I don’t believe it’s available online, but certainly look forward to his report.

The take home message from this conference and the recent publications from the point of view of what does it all mean to a patient? If you have prostate cancer, you may be allowed to have it, but if you have CFS, you aren’t. But there are a few fighting for us, Mikovits, Russcetti, Lombardi, Hanson, Snyderman, Bell and co-authors.

If you look at the conflicting papers of which Graham Simmons is a co-author, assuming that you believe that Knox et al is worthy of consideration in light of the various potential conflicts of interest of its authors, the combined findings suggest that blood isn’t the best place to look for XMRV by PCR. The Tang et al paper referenced above is co-authored by more people who work for Abbott. The author’s of the paper looking for XMRV in blood donors (#3 last blog) also work for Abbott; they concluded the positives were due to cross-reactivity with HTLV sequences.

Simmons and Busch work for Blood Systems Research Institute, an institute dedicated to transfusion safety, primarily funded by NIH grants according to their website, apparently a for profit organization; they are also part of the Blood XMRV Scientific Research Working Group, whose abstract (#4 last blog) states they found enough going on with Phase II to keep going, even though it was inconclusive. More evidence that something’s going on, but we don’t know how to look for it yet. The clinical evidence and the first paper above, suggest that lymphoid tissue would be a good place to look. Gut is another likely reservoir, not too difficult to get tissue. The Tang paper looked at paraffin embedded tissue. There’s lots of that to go around, some small intestine of mine in paraffin at the hospital down the street.

#6, 7 and 8 in the last blog represent the kind of work we need to be seeing, to begin to figure out the nuts and bolts. Fascinating how they are going about producing a mouse that expresses XPR1 receptors in prostate tissue. Exploring receptor physiology, and tissue tropism.

Pointing out the connections between various authors and potential conflicts is not coming from some kind of inside information. Everything I’ve noted is readily available on the internet. I don’t claim to know exactly what’s at the bottom of it. Only that it doesn’t add up, the Knox paper being especially suspect, and the people involved suspect by association. The work isn’t going as well or as quickly as it should be, as we need it to, and there seem to be certain entities and individuals coming up with studies which seem designed to fail. There are an awful lot of people parroting negative studies without looking at the totality of the evidence. People attached to HHV-6 as The Cause come up a lot. People attached to it not being a retrovirus. Different individuals have different stakes I’m sure. There’s too much at stake not to bring out the worst in human nature.

If anybody feels the need to write in the comments that I am biased, don’t bother. I am biased. I believe that ME/CFS and related neuroimmune disorders are caused by retroviruses, of which XMRV is likely only one. The other organisms that turn up with regularity are opportunists and copathogens. There are patients that are both culture and serology positive. Contaminant and cross-reacting antibodies with HTLV? My working hypothesis is that we are infected with simple retroviruses that jumped from mice, probably naturally, but then assisted tremendously by the use of animal cells and gene manipulation in tissue culture and nude mice, for various purposes including vaccine production. That starting point for considering my illness has gotten me very far from where I was when I didn’t have that understanding.

At the bottom of this blog are links and excerpts from the NIH online project reporter that are of interest to us. Sandra Ruscetti giving us clues as to why VIP Dx is getting different serology results than those using tests derived from infected monkeys.

Also Ila Singh’s contention that it is present not only in prostate cancer tumors, but in 6% of controls. And she didn’t wonder why she couldn’t find it in anybody’s blood in her new study, including controls? And that didn’t bother her because? It makes me shake my head in disbelief every time I think of it. Scientists like Singh, Knox and Coffin telling people they don’t have the right to treatment based on such flimsy evidence and faulty logic? It’s disgusting.

Maribeth Eiden is an expert in GALV, the only other gammaretrovirus found in a primate. “In addition to being a horizontally transmitted infectious agent, xmrv is a threat to the human genome.”

A clinical trial of IV saline for POTS found its way into my inbox today: http://clinicaltrials.gov/ct2/show/NCT01000350?term=NCT01000350&rank=1. It’s fascinating that doctors in an academic setting taking care of a condition that used to be very rare, but now isn’t, haven’t noticed that it occurs mostly in ME/CFS patients, and seem unaware of XMRV as even a possibility. In any case this approach has had some success anecdotally for keeping ME/CFS patients on their feet, but isn’t practical for most, and like everything, it doesn’t help everyone, including me. It helps Ali a little, but, in general, not enough for the stick, and she doesn’t have enough veins for daily access, nor does she tolerate indwelling lines or FB’s of any kind.

The infusions so far seem very helpful to Ali: more energy, less reactive. I had an adverse reaction to the first one, generalized over-activation, sleep disruption, PVC’s, GI hypermotility, etc. The only thing in the infusion I haven’t had before was Leukovorin, and too much Deplin can cause a similar, though less severe, reaction. It took almost 5 days to resolve and was yet another reminder that sometimes it’s best to leave well enough alone. I did an infusion of glutathione alone about 10 days after the first one and didn’t notice anything. I haven’t been too excited about sticking myself again, since I’m doing amazingly well (knock on wood).

The mild hyperbaric treatments are wonderful for me. I feel great in the chamber, a little slowed after, then really good later on. Ali continues to be sensitive to odors and has stayed away from the chamber because of the new plastic smell. However, the fire burning in Arizona has made the air quality very poor here (in Santa Fe). The horizon is obscured by smoke and there is ash on the ground, though the fire is hundreds of miles away. It burns your eyes, nose and lungs. Yesterday she became short of breath and decided to use the concentrator with a well aired non-rebreather mask at 10L/min. After 20 minutes she felt much better. She repeated that treatment again last night before bed and slept much better than usual, something I notice after each treatment (I’m going in about 3 times/week). Since she tolerates the mask, she can wear it in the chamber and will be protected from any other smells inside the chamber itself. We are both grateful for something so safe that helps in such an immediate way.

Ongoing NIH projects:

Sandra Ruscetti
http://projectreporter.nih.gov/project_info_description.cfm?aid=8157190&icde=8392424
In collaboration with the laboratories of Judy Mikovits and Frank Ruscetti, we were able to use antibodies developed against the envelope protein of SFFV to detect infectious xmrv in the blood cells and plasma of patients suffering from the neuroimmune disease chronic fatigue syndrome (CFS). We were further able to develop a seroconversion assay using cells expressing the SFFV envelope protein to detect antibodies against the virus in the plasma of CFS patients. We now plan to apply our knowledge of the pathogenesis of mouse retroviruses that cause cancer and neurological disease in rodents to study the molecular basis for similar diseases associated with xmrv. We are in the process of developing rodent models for determining the biological effects of xmrv in vivo, which if successful will provide a small animal model for preclinical testing of potential anti-xmrv drugs. In addition, we are testing both in vitro and in vivo the biological effects of the envelope protein of xmrv, which like its related SFFV counterpart may be responsible for the pathogenicity of xmrv.

Ila Singh
http://projectreporter.nih.gov/project_info_description.cfm?aid=8040941&icde=8392424
Narrative: xmrv is a new retrovirus that was recently identified from human prostate cancers. This study will attempt to understand the replication of this virus in vitro and its association with cancer. We will explore mechanisms of oncogenesis in cells, in tumors, as well as in animal models, and carry out epidemiological studies to estimate prevalence of viral infection in the general population.

Maribeth Eiden
http://projectreporter.nih.gov/project_info_description.cfm?aid=8158079&icde=8392424
Our lab is recognized for our research on a similar gammaretrovirus isolated from nonhuman primates, gibbon ape leukemia virus (GALV). GALV is the only gammaretrovirus other than xmrv found in primates. In collaboration with Frank Ruscetti at the NCI, Bill Switzer at the CDC and Suzan Winfield and Jessica Siegal-Willcot at the National Zoo, we are investigating the source animal for xmrv, and screening gibbon apes in US zoos for the presence of GALV and xmrv. We have obtained samples from the CDC and the Biological Research Steering Committee that provide us with materials permitting us to determine that many gibbon apes at various zoos have been infected with an xmrv-like virus. We have determined the cell tropism of xmrv using an engineered biologically active xmrv virus with a GFP reporter gene and are identifying cellular factors that restrict xmrv infection of receptor bearing cells. These factors that can restrict xmrv infection will be used as a means of developing xmrv antiviral drugs. In addition to being a horizontally transmitted infectious agent, xmrv is a threat to the human genome. We are in the process of isolating rat germ line cells and exposing these cells to engineered biologically active xmrv virus with a GFP reporter. Sperm obtained from these cells are being assessed. Positive results of sperm expressing GFP indicate that xmrv can be transmitted from infected individuals horizontally (i.e., to offspring as a mendelian trait) as well as vertically through the more traditionally route of viral infection. We used cysteine scanning mutagenesis (SCAM) methods to assess the topology of the GALV receptor and intend to identify extracellular domains of the xmrv receptor using similar methods. These studies will lead to the identification of the xmrv-binding domain. Finally the spread of most retroviruses is mediated not by direct virus infection but by cell-cell transmission from an infected cell to an uninfected cell. We have developed a model system to assess blocks to cell-cell virus transmission using spinning-disc confocal microscopy to visualized individual budding of fluorescently labeled virus particles into adjacent cells in three dimensional space over time.

Frank Maldarelli
http://projectreporter.nih.gov/project_info_description.cfm?aid=8157762&icde=8392424
We have established useful collaborations with Drs. W. Marston Linehan and Peter Pinto (Urologic Oncology Branch, CCR) to study samples from patients with prostate cancer, and with Drs. Frank Ruscetti and Kathryn Jones (Laboratory of Experimental Immunology, CCR) and Dr. Judy Mikovits (Whittemore Peterson Institute) to study patients with severe CFS. As immune deficiency may contribute to infection by xmrv, we have also established collaborations with NIAID to obtain samples from study individuals with immune deficiency, including HIV-infected patients and patients with both HIV infection and prostate cancer. In addition, we are collaborating with Dr. Vinay Pathak (HIV Drug Resistance Program, CCR) in a study of xmrv pathogenesis and prostate cancer as part of a Bench to Bedside Award to Dr. Pathak. Reports of xmrv infection in individuals with chronic fatigue and in otherwise healthy individuals raised concerns regarding new health risks. Within a year of these reports, we have optimized a series of detection and analytical assays with excellent performance characteristics. In the next year, we will apply these approaches to shed new light on the potential role of mouse-related viruses in human disease.

Arthur Horowitz
http://projectreporter.nih.gov/project_info_description.cfm?aid=8157670&icde=8392424
In a related and collaborative project, we have joined Dr, Frank Ruscetti in his studies of the link between prostate cancer and xmrv, a recently-identified retrovirus associated with prostate cancer. Together, we are testing the hypothesis that inflammatory cells serve as a viral reservoir or infection route. We are characterizing the susceptibility of prostate-infiltrating myeloid cells (macrophages and dendritic cells) to xmrv infection. A long-term goal is to identify murine models to study the link between xmrv pathogenesis and prostate carcinogenesis.

Susan Swedo
http://projectreporter.nih.gov/project_info_description.cfm?aid=8158154&icde=8392424
D. Vargas et al (Johns Hopkins) demonstrated that individuals with autism and a history of neurodevelopmental regression had evidence of chronic brain neuroinflammation, as exemplified by activation of microglia and astroglia and the abnormal production of inflammatory cytokine and growth factors assayed in both tissue samples and CSF. The authors remarked that chronic microglia activation appeared to be responsible for a sustained neuroinflammatory response that facilitated the production of a number of neurotoxic mediators. Alternatively, neuroglial activation could occur in response to a secondary neurotoxic factor(s) and thus represent the result, rather than the cause, of the injury. Neuroglial activation requires the nuclear translocation of the pro-inflammatory transcription factor NF-kappaB. A small pilot study of minocycline, an antibiotic with known effects on NF-kappaB was undertaken in an effort to determine if the drug might have an effect on autistic behaviors or change patterns of distribution for the CSF or serum cytokines or chemokines. At the doses used in the pilot investigation, no clinically meaningful improvements were seen in behavior nor in the pattern of distribution of the CSF or serum cytokines or chemokines. Thus, no further investigations are planned for minocycline, but the search for novel therapeutic agents continues through the phenotyping study, where longitudinal assessments provide the opportunity to identify biomarkers of neuroinflammation in serial CSF and serum samples and to correlate the results of the assays with clinical symptomatology.

Christine Kozak
http://projectreporter.nih.gov/project_info_description.cfm?aid=8156820&icde=8392424
We are also interested in determining the extent to which virus resistance is mediated by polymorphisms of the cell surface receptor. We seek to analyze the XPR1 receptor for the xenotropic/polytropic gammaretroviruses and for xmrv, a xenotropic virus-like virus isolated from humans with prostate cancer or chronic fatigue syndrome.

Some interesting abstracts from the conference in Belgium about HTLV:

HERV’s and MS
http://www.retrovirology.com/content/8/S1/A210

Stem cells for HTLV
http://www.retrovirology.com/content/8/S1/A32
http://www.retrovirology.com/content/8/S1/A33

Raltegravir inhibitis HTLV
http://www.retrovirology.com/content/8/S1/A34

AZT/IFN for ATL
http://www.retrovirology.com/content/8/S1/A37
http://www.retrovirology.com/content/8/S1/A53

Arsenic trioxyde for ATLL
http://www.retrovirology.com/content/8/S1/A59

Ascorbic acid and HTLV
http://www.retrovirology.com/content/8/S1/A61

Risk of vertical transmission of HTLV correlates with maternal proviral load.
http://www.retrovirology.com/content/8/S1/A72

γδ T cell immunotherapy for HTLV ???
http://www.retrovirology.com/content/8/S1/A109

Estradiol and HTLV
http://www.retrovirology.com/content/8/S1/A196

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21 thoughts on “The Fire Smolders

  1. >Thanks for another good blog. Dr. Ila Singh's behavior is puzzling. After being entirely sure none of her CFS test subjects had XMRV, she told CFSCentral.com that she was "not entirely sure" why she couldn't detect the ~5% background level, and maybe it was because of "different sample types" and "different assays". A Freudian slip perhaps.

    The abstracts on HTLV you posted reminded me of these two studies which I think you will find interesting if you are not familiar with them already:

    Fucoidan therapy decreases the proviral load in patients with human T-lymphotropic virus type-1-associated neurological disease. http://www.ncbi.nlm.nih.gov/pubmed/21311112

    Valproate activates bovine leukemia virus gene
    expression, triggers apoptosis, and induces
    leukemia/lymphoma regression in vivo (animal model for HTLV-induced leukemia).
    http://www.pnas.org/content/102/29/10309.full.pdf

  2. >I feel i've witnessed the ugly side of our patient community as this XMRV investigation has progressed and feel that the blame for this can partially be attributed to you for the unprofessional way you have spoken.

    As far as i'm concerned there has been way to many insinuations, accusations and unsubstantiated claims coming from you. The conspirational tone of your recent blog posts is uncalled for and it's unfair to question the motivation of some researchers who are coming to different conclusions. If you are right then the evidence will talk for itself.

    The Blood Working Group and Lipkin studies provide an opporunity to see who is correct. I hope that whatever the result, everybody involved will accept it and move on accordingly. Please don't undermine confidence in this process if it goes against your position, it will only harm us in the long run!

    Furthermore, the WPI can hardly claim to be victims of other teams who have conflicts of interest when they themselves have sold a clinical test on the back of the original Lombardi et al study. Maybe the test should be withdrawn until your hypothesis has been proven correct.

    I know i'll probably get flamed for what i've said but maybe some of you should consider the position i've taken. I am one of you (had ME/CFS since mid 90's) and have no agenda other than i want to get better and get my life back.

  3. >I think that if you get flamed it will likely be for behaving like a coward and hiding behind an 'anonymous' posting. Why is it that you don't want to reveal your identity and always feel the need to stay anonymous. Because people will attack you when it proofs you had it wrong all the time?

    It's so easy to put someone down, make fun of them and insult them behind the safety of the anonymous mask. Why dont you be a man or a woman and post under your real name so we know who we are dealing with. But maybe you're just too scared for repercussion and not enough man to face that. Sad, really.

    @Jamie I really am amazed that you're able to tolerate these anonymous ramblings. If it was my blog I would have disabled that feature right from the start. I'm all for openess and 'no holding back'. It seems that some people only dare to be open and opinionated if they can hide behind a 'anonymous' protection. It irritates the hell out of me. :-)

  4. >"If you are right then the evidence will talk for itself."

    I'm afraid that's the problem. The evidence has not been speaking for itself for a long time. Instead limelight grabbers and press agencies have been deciding outcomes all the while ignoring piles of legitimate scrutiny.

    How can Coffin claim a contamination theory in certainty when a) the contamination selects M.E patients en masse ignoring HCs and b) those supposedly contaminated samples go to a false replication lab and come back negative. Those are just my two layman examples as well.

    Sometimes you have to shake a few trees and see what falls down.

    "The Blood Working Group and Lipkin studies provide an opportunity to see who is correct. I hope that whatever the result, everybody involved will accept it and move on accordingly.

    That just sounds like blind faith to me. If it's done right and it's not shown over days and weeks that the methodology has been poorly replicated, then people will accept it. I'm afraid the days of accepting what somebody says or does purely because of a qualification are over.

  5. >I find your analysis and the links you provide invaluable, and your reports about your own course of treatment and progress very heartening. Thank you for your frequent posts and for your tenacity.

  6. >Thank you for providing us with this invaluable information. Regarding the second citation "Heme oxygenase-1 activation inhibits XMRV pathogenesis and carcinogenesis in prostate cancer cells" by Subhash Dhawan, it may be time to revisit the Hydrogen sulfide hypothesis: http://aboutmecfs.org.violet.arvixe.com/RsRch/H2S.pdf
    and
    http://webcache.googleusercontent.com/search?q=cache:3axVgg956QkJ:www.prohealth.com/me-cfs/blog/boardDetail.cfm%3Fid%3D1314423+marian+dix+lemle&cd=12&hl=en&ct=clnk&gl=us&client=safari&source=www.google.com.

    I think we will find that the relationship between H2S and heme oxgenase may provide some direction to our research.

  7. >thank you for hashing out the results of the conferences for us – i am so confused due to me/cfs that i find myself asking "what the heck did i just read?" often enough to need someone to lay it all out. the suggestion not to allow anonymous comments is a very good one. it is apparent that the person who makes such an effort to follow and criticize you is ashamed of their actions. that is why they remain anonymous – not up to criticism themselves. as for myself, if xmrv is it, great, but if it isn't i know something is. i've come to have great respect for the people trying to get to the bottom of this disease after watching a doctor cut down by politics and a great researcher lost to us. i am speaking of dr jay goldstein, my first attending to this illness. the medical community is fast losing any claim to respect or deference just because they have the title of dr.

  8. >Random things that crop up for me today:

    It was clear pretty early on that HGRVs migrate quickly to tissues and are not easily detectable in the blood. The macaque study indicated this in flashing neon.

    So WHY on earth has the focus been so relentless on finding it in the blood? I know, because high-throughput serum analysis is the quick, inexpensive, easy standard by which to
    find pathogens. But that would be like trying to find giardia by a blood test. You don't do that. You check the place where it lives. WTF is up that no one is INSISTING that we change the focus and start looking for it in tissues? Why isn't WPI doing this? Why isn't the NIH or CDC? It seems of utmost importance.

    I'm glad to see that one study that indicates the lymph tissue is a good place to look. I appreciate that biopsy is a much more invasive process but there would be a line around the block of from the patient community, I would think, for such a study.

    Another thought is regarding Ila Singh again. She has a patent on XMRV. Like anyone else, she does not want to ruin her promising career with the career-killer "CFS". There is likely pressure to distance herself and her research from it, from whatever financial interests the patent or her research funding are associated with. This is the way of "science" now.

    It is quite possible that her continued research in prostate cancer will prove useful for other diseases down the pike, and it seems likely she will continue research in XMRV (and friends) since she does hold a patent. Call me crazy.

    Finally, as I was slowly waking up this morning I had a random question pop into my head: does anybody know, when they did the autopsy on Sophia Mirza and found an infection in her brain/CNS if anyone identified the pathogen?
    I feel funny speaking like this of a real person, who died so tragically and unnecessarily, but I have not seen reference to
    whether or not a pathogen was identified, or just "evidence of infection." This seems really important, and causes me to wonder what Singh cam up with in the autopsy study and how or why it is that is being held up.

    Thanks, Jamie for continuing this excellent, ongoing convo. Everyone is entitled to their opinion. The requirement to be "professional" by the way, does not apply to a personal blog. Courtesy, however, anonymous angry persons, is always appreciated.

  9. >When you actually purchase the chamber, ask to get a used one, because it will take a while for this to offgas and the mask is not sufficient to protect one from MCS reactions to the urethane coating while enclosed in the chamber for an hour.

    It is possible that whatever infectious triggers, switch on HERVs. That could explain the variety in sick people.

    All disease, in the CFS/lyme/ME wastebasket is not caused by a family of mouse retroviruses, though. Even if there turn out to be some mouse retroviruses involved in some cases, there has to be more. You can't explain slow onset and sudden onset with the same pathogen…even with variations in the immune system. A mosquito with dengue bites you, it isn't like some people smolder along carrying the dengue and come down with it after a slow decline years later…

  10. >By the way, I've been meaning to add for a long time that having read your blog, I had to conclude that actos was almost as beneficial as anything else you've done. There is a distinct improvement since you began actos, so that is interesting. It seemed to lift you to a whole new level.

  11. >Oh, i think it has brought the worst out in human nature all right. let's see,the people involved in the knox study are 'suspect' and scientists are designing studies to fail. Can any XMRV supporters say this is worse than the criticisms in the comment above?

    Neal

  12. >The first three abstracts have ABSOLUTELY NOTHING to do with your statement:

    "Here are more abstracts about XMRV from Belgium which strongly suggest that it is more than a contaminant"

    Those do not address anything about whether XMRV is or is not a contaminant.

    "Also Ila Singh's contention that it is present not only in prostate cancer tumors, but in 6% of controls. And she didn't wonder why she couldn't find it in anybody's blood in her new study, including controls? And that didn't bother her because? It makes me shake my head in disbelief every time I think of it. Scientists like Singh, Knox and Coffin telling people they don't have the right to treatment based on such flimsy evidence and faulty logic? It's disgusting."

    You're kidding me right? So now what you're saying is that prostate cancer and CFS is the same? Let me get this straight: Your saying through implication that just because you can find a signal in PC (that did not look at blood) and not in CFS (that did look at blood) they should question every negative result? Right. So if I eat an apple and then eat an orange, I guess I should question why the orange does not taste like an apple?

    "If anybody feels the need to write in the comments that I am biased, don't bother. I am biased."

    Not only are you biased but I seriously question your experience and intelligence as a medical doctor doing literature research. Your conclusions and vague conspiracy theories from disparate sources are so far out there it boggles the mind. I am SOOO happy you are NOT doing research.

    Not only are you doing a HUGE diservice to science in general, but you are also giving CFS patients, who have suffered enough, false hope and more anger.

    You should be ashamed.

  13. >Sorry i forgot to add that anti-retroviral drugs can cause health problems and shouldn't be recommended for ME/CFS as (of yet) no evidence exists that they would help. Anecdotal evidence doesn't count. Some people might find it disgusting to push these drugs rather than withold them.

    Neal

  14. >The ascorbic acid article was interesting.

    My experience is that if I am getting a modest amount of exposure to toxic mold or other environmental biotoxins, Vitamin C IV's are very helpful at letting me tolerate that last bit. At a high level of exposure, the IV's do nothing.

    The theory here is that the Vitamin C serves to help to "erase" the oxidative stress created by the biotoxins.

    I don't see a mechanism posited in the paper cited here, and so am not sure if the control of oxidative stress is what's helping to keep the virus in check. If it is, that would be consistent with our general theory — that by decreasing exposure to oxidative-stress producing biotoxins, various sorts of pathogens (including retroviruses) can be better kept under control.

    I've found Vitamin C IV's to be far more helpful than glutathione or anything else administered IV (provided that I'm in a reasonably clean environment…..nothing helps with too much exposure).

    But people with ME/CFS have to be careful. If the dose of Vitamin C is too high, it will convert to hydrogen peroxide in the cells, thereby killing pathogens such as Lyme. This could be a good thing, but (as with most treatments) it can be very bad for people who are especially ill with this disease.

    My impression is that anything higher than 15g will convert to hydrogen peroxide. Starting much more conservatively than this to gauge the extent of die-off issues seems a good idea.

    Best,

    Lisa Petrison

  15. >Neal, thanks for signing your name.

    Unfortunately, there is no question that some studies were designed to fail.

    You can't not replicate and call it a replication; you can't use cohorts of people who do not have the disease; you can't draw conclusions unsupported by the body of the paper.

    … and expect to avoid reasonable questions about whether you designed your study to fail.

    Surely you agree? Please read the studies!

  16. >Jill,

    HIV smolders for a long time before igniting. In many cases, it may turn on and off at low level for a long time, before really mucking up the works irreversibly. It reared it's ugly head in my history, in hindsight, several times before my first real crash. A full crash probably requires a constellation of things. Virus(es), genetics, injury.

    Jamie

  17. >Do you mean "XMRV" smolders?

    We'll still have to see how this all plays out…btw tho in the early days of HIV, people smuggled in Compound Q and infused it in groups in their homes…people thought it was working…but it wasn't. Early anecdotal reports can be very confusing, and inaccurate…

    Seroconversion with HIV is usually marked by a very nasty flu…you don't even see that common event in "ME/CFS" cases. To me, and I know who will argue with me, there are lots of pathogens around that can muck up lives in varying degrees, going on a spectrum of "ME/CFS/Lyme" with various endpoints that look similar…there is no "this disease" nor "one retrovirus"…the picture doesn't fit. But whether there are mouse retroviruses implicated in disease in interesting ways and have been smoldering in some of us for long periods of time, either doing no harm, or needing other viruses/pathogens to activate, or perhaps activating HERVs or permanently upregulating or downregulating important genes, all that is very interesting but probably a very broad deep picture that will take decades to decipher. If it is even the case.

  18. >I dare any scientist to take a group of Vipdx XMRV positive patients with moderate to severe ME to test certain Arvs shown to inhibit XMRV vs CBT and GET and see which treatment gets better results using the same measurements for improvement. Any takers.
    Keith

  19. >Thank you for your courage and your common sense, Dr. Deckoff-Jones. Apparently this has brought out the full contingent of HGRV-deniers to post anonymous comments criticizing you. I hope you ignore them. They are irrelevant. Those of us who are the real stakeholders here, those of us who are suffering and dying while the pseudo-scientists with their rigged studies play with our lives, are grateful to you for speaking the truth.

    Your honesty and courage give me hope. There may be a way for the real scientists such as Dr. Mikovits to discover the real workings of M.E. and help sufferers after all.

    Thank you for your continuing work, Dr. Deckoff-Jones.

    Patricia Carter
    XMRV+, 24 years M.E.

  20. >"XMRV does not cause CFS" said "You're kidding me right? So now what you're saying is that prostate cancer and CFS is the same? Let me get this straight: Your saying through implication that just because you can find a signal in PC (that did not look at blood) and not in CFS (that did look at blood) they should question every negative result?"

    I think it's the fact that in one study she found it in controls, and in the other study she did not find it in controls. If your first study tells you it is present at a low level in controls, and your second study can't find it at all, then maybe your second study test is not good enough at finding it.

  21. >Plz watch this is you think Jamie was wrong in accusations of those scientist reporting Contamination.

    Its about A Cancer Scientist who has been harrassed by his peers and Federal agencies to destroy him to take his patents!

    Documentary …. Burzynski The Movie on vimeo

    Burzynski: Cancer Is Serious Business http://vimeo.com/24821365
    Jamie keep doing what your doing…Love your blog very much and keep Fighting for us!
    Long live WPI :)
    GaryK

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