 |
| Author | Post |
|---|
Dr Trevor Marshall
Foundation Staff
|
Posted: Thu Oct 8th, 2009 23:03 |
|
Stoppress 5 Jan 2010:
Just published in PLoS ONE:
"Failure to Detect the Novel Retrovirus XMRV in Chronic Fatigue Syndrome" (in London)
The authors also note that the US link between prostrate cancer and XMRV was also not found in Europe.
A far more exhaustive and unbiased study than WPI's, has shown that XMRV is not causal for CFS. Those who are falling for the CFS community's mischaracterization of the results clearly need to learn a bit more about how PCR machines work, and how Polymerases work, what AZT does, and stuff like that... Life ain't easy these days. But trust me, this was a carefully done study. Very carefully done...
---------------------------------------------------------------------------------------------------
I just received an email from the Suzanne at the CFIDS Association of America saying that the Whittemore Peterson Institute has made a significant step in the CFS community's search for a viral pathogen behind CFS, and has published some interesting results in the prestigious journal 'Science':
http://tinyurl.com/yczdsdr
IMO The concept that a single pathogen could cause the human metabolism to fail in the myriad of ways necessary to give advanced chronic fatigue is a 19th Century concept - the postulates of Koch, which make no sense in the era of the metagenome.
We published a paper on this very subject (disease causation and Koch) earlier this year in Autoimmunity Reviews:
http://AutoimmunityResearch.org/preprints/AR-Proal-Metagenome.pdf
and another just last month in the Annals of the New York Academy of Sciences:
http://autoimmunityResearch.org/preprints/ProalAnnals2009Preprint.pdf
In particular, I note that the retrovirus is only present in 67% of subjects. Ergo, it is not causal. Additionally, I note it is only present in 4% of the control population. That is strange, as, IMO, a greater proportion of the population is suffering than that. Maybe they selected a young control cohort, wee need to examine that anomaly in detail.
Our position is that the innate immune system of people with chronic disease in general, and CFS in particular, is weakened by the metagenomic microbiota which causes this disease spectrum. It is to be expected that they will be carrying a plethora of species which would have been eliminated by a healthy innate immune system.
However, this retrovirus may well be a precipitating or pre-disposing factor, like EBV can be. For more information about these precipitating mechanisms, please see my recent presentation at the Asian Congress on Autoimmunity via YouTube at:
http://www.youtube.com/user/DrTrevorMarshall
Your comments are welcome. And I do congratulate Suzanne Vernon, PhD, the new(ish) Scientific Director of CFIDS, for having gotten Science to publish the paper. I met Suzanne at the Reno conference, she was the only CFIDS TPTB person there who showed any interest in our work... Maybe we should ask her to collaborate with us on publishing the CFS portion of our study results - at the moment we are succeeding getting the word out for just the Autoimmune diagnoses 
Last edited on Wed Jan 6th, 2010 00:22 by Dr Trevor Marshall
|
Dr Trevor Marshall
Foundation Staff
|
Posted: Fri Oct 9th, 2009 02:57 |
|
How to get the editors of SCIENCE really upset with you:
1. Publish on your website data which is at variance with the peer-reviewed data just published in their journal:"Further work has found that 95% tested positive"
2. "Reach" or exaggerate into stating facts about data you don't have:"However, as with other retroviruses, there is no reason to believe that the virus is not present in all other parts of the world"
You can find these gems in the answers to questions 2 and 17 at the Whittemore Peterson Institute website:
http://wpinstitute.org/xmrv/xmrv_qa.html
|
Dr Trevor Marshall
Foundation Staff
|
Posted: Fri Oct 9th, 2009 15:26 |
|
Here is the article in Science:
http://www.sciencemag.org/cgi/content/abstract/1179052v1
But a far more interesting article describing the XMRV genome itself is at:
http://www.pnas.org/content/104/5/1655.full
and a thorough article about XMRV:
http://www.microbiologybytes.com/blog/2007/03/19/viruses-and-cancer-xmrv-and-prostate-cancer/
And another article about XMRV isolation from Prostrate Cancer cell lines:
http://jvi.asm.org/cgi/content/abstract/83/14/7353
OK, so now onto the bad science:“Just like you cannot have AIDS without HIV, I believe you won’t be able to find a case of chronic-fatigue syndrome without XMRV,” one researcher in the study (Dr Mikovits) said.
http://www.dancewithshadows.com/pillscribe/xmrv-virus-linked-to-chronic-fatigue-says-study/
Oh, really? And all CFS patients also get prostrate cancer? It is sad when scientists lose objectivity, and certainly warns me that their published data might also be suspect, colored by thoughts such as these.
That article, incidentally, is worth reading carefully, with gems such as:XMRV was also spotted in 27% of the prostate cancer samples researchers at the University of Utah and Columbia University Medical Center examined in September. That study also showed that 6% of the benign prostate samples had XMRV.
And here is an article with even more very bad science being advanced to the Press:
http://www.healthzone.ca/health/newsfeatures/research/article/707537--chronic-fatigue-syndrome-linked-with-virus-similar-to-hivJudy Mikovits, the senior study author, says that virtually all of the 101 chronic fatigue sufferers she tested for the study were infected with a retrovirus known as XMRV.
And the chance that the virus was there by accident in chronic fatigue sufferers was "infinitesimally small," especially since it was not found in the vast majority of healthy people also tested by researchers.
"It undoubtedly causes some of the symptoms that are associated with it (chronic fatigue)," says Mikovits, research director of Nevada's Whittemore Peterson Institute for Neuro-immune Diseases.
"Infinitesimally small" is not 33%, or even 5%, Judy... But unlike the AIDS virus, which will eventually attack anyone who contracts it, XMRV likely damages only those people with a genetic or physiological susceptibility to the ailment.
"You can be infected and be well," she says.
Oh, really? Does that line up with "Infinitesimally small"?"As I go through the clinical symptoms...there isn't one that I have found so far that couldn't be explained by infection with this virus."
OK, I have had enough for the morning.
Anyway, this is an important discovery, as it alerts us to another pathway whereby the VDR could be being knocked out. Of particular interest to me was this statement in the 'dancewithshadows' blog:XMRV has also been associated with other diseases like autism, atypical multiple sclerosis and fibromyalgia.
IMO That means we better have a closer look at the XMRV genome, HIV, and the VDR...
|
Aunt Diana
Moderator
|
Posted: Fri Oct 9th, 2009 19:04 |
|
There were two doctors on TV discussing the H1N1 flu shot and whether or not to have it. One doctor (an endocrinologist) who had a lot of CFS patients was dead set against it.
He said that whenever he has a new CFS patient who has recently come down with it, his first question is Have you had a flu shot recently? and invariably the answer is yes....usually two weeks earlier than they started feeling ill.
This certainly fits in with MP belief system. That it is the microbacteria that are injected along with the flu shot that cause the problem. They also discussed autism in relationship to flu shots.
____________________
Lyme 1987, neuro cardio fatigue achiness brain fog depression, anxiety. Pacemaker, D.1,25 32; D <5; 12/07 <6, hydrocodone, lorazapam, benedryl, zantac, colase, Noirs, cover-up or avoid sun, house <30lux. Feb 08 Phase 3. 6/08 D <4, D1,25
|
scooker48
Member in Phase 3
|
Posted: Fri Oct 9th, 2009 20:45 |
|
Dr. Marshall,
I am certain other members will join me in urging you to look at the XMRV, HIV and VDR.
I am very excited about whatever you can figure out. It very well might significantly improve human health.
Sherry
____________________
Necrotizing granulomas biopsy 10/88; Dx 12/04 Sarcoid liver spleen. 2/2/05: VitD 25/VitD125 62. 11/7/09 D25 at 6, Liver function normal 4/08; Wear NoIRs outside. No K creme used. 5/09 Liver and kidneys normal. ACE still high at 113 on 11/7/09.
|
Phillyguy
Guests visiting Phase 1/2/3
| Joined: | Tue Feb 26th, 2008 |
| Location: | |
| Posts: | 48 |
| Status: |
Offline
|
|
Posted: Fri Oct 9th, 2009 21:34 |
|
Also curious about your thoughts on poly I:poly C12U (Ampligen). It looks like it will be available by year end and will be the only drug approved by the FDA with the specific indication of treating CFS. It is a TLR3 agonist which appears to normalize levels of Rnase L, which I read somewhere fights viruses as well as mycoplasma infections. I have read some online accounts of patients that participated in the trial and some of these patients appeared to experience pretty good results. They reported immunopathology for many months prior to feeling better. I doubt they gave any consideration to potentially severe immunopathologic reactions. Interested in your thoughts....
I included this in the link because a lot of people in the CFS world are talking about this treatment in the context of XMVR. I'm not sure why this virus has gotten so much attention since CFS patients often times have elevated levels of HHV6, CMV, EBV, mycoplasmas and just about every other pathogen out there.
Last edited on Fri Oct 9th, 2009 21:43 by Phillyguy
|
laura1814
Member in Phase 3
|
Posted: Sat Oct 10th, 2009 22:27 |
|
I thought the quotations from a researchers in this article were interesting:
http://www.scientificamerican.com/article.cfm?id=chronic-fatigue-syndrome-retrovirus
In talking about the virus in context with a lot of other viruses that may be triggers for CFS, one says: "This new retrovirus may be able, through infecting human cells, [to] induce a transcription of an endogenous virus," like EBV does. "It's possible, downstream, that this will all feed into the same mechanism" of what causes CFS.
This is an indication to me that they are at least open to the possibility that this part of a larger picture.
But then they go on to talk about specific drugs to target the virus, so maybe not.
____________________
CFS, EBV, PCOS, POF, TMJ, hypoglycemia, hyperlipidemia, MP Ph1 1/08, Ph2 4/08, Ph3 1/09; enzymes, & ranitidine PRN, NoIRs, low lux home, limited outings, covered up, 1,25D=37, 25D=9.
|
laura1814
Member in Phase 3
|
Posted: Sat Oct 10th, 2009 22:33 |
|
I don't really understand retroviruses, but is it possible that one reason CFS patients seem to take a long time to get better on the MP is that many of these viruses, in addition to the micriobiota, are active, and it just takes the innate immune system longer to fight them-- perhaps because the microbiota have compromised the innate immune system?
Sorry if that doesn't make much sense, a bit brain foggy today. Can't wait to get my brain back.
____________________
CFS, EBV, PCOS, POF, TMJ, hypoglycemia, hyperlipidemia, MP Ph1 1/08, Ph2 4/08, Ph3 1/09; enzymes, & ranitidine PRN, NoIRs, low lux home, limited outings, covered up, 1,25D=37, 25D=9.
|
Dr Trevor Marshall
Foundation Staff
|
Posted: Sat Oct 10th, 2009 23:14 |
|
Well, I have yet to see persuasive evidence of an endogenous virus mutated into human DNA. A recent comment about embedded viral DNA was made with respect to HIV during a seminar at the Salk Institute, but on questioning the speaker was unable to produce any definitive proof that such an 'endogenous virus'had been isolated .
..Trevor..
|
Dr Trevor Marshall
Foundation Staff
|
Posted: Mon Oct 12th, 2009 17:43 |
|
All I can tell you at this point is that the tat signal from XMRV in the NCBI database is not similar to the tat protein of human HIV, which hijacks the human VDR and causes the immune deficiency AIDS.
It does have similarity to murine leukemia virus and murine HIV, but not to the human pathogens. Which is what I would expect, since XMRV would need to target different receptors in the mouse, where the VDR is far less important.
Which all means that XMRV is nothing like human HIV, at present. Of course, it could always adopt the tat protein of HIV, and then there would be some fireworks...
I will continue to explore the genomes
|
Bane
Member
| Joined: | Sun Jan 27th, 2008 |
| Location: | Norway |
| Posts: | 108 |
| Status: |
Offline
|
|
Posted: Thu Oct 22nd, 2009 18:56 |
|
XMRV: WPI Pioneers Interview - October 2009 (Part 1 of 2)
http://www.youtube.com/watch?v=b3OZdvSDdoA
XMRV: WPI Pioneers Interview - October 2009 (Part 2 of 2)
http://www.youtube.com/watch?v=GCKtoOcM_IM
XMRV is catalyst to ME CFS and neuro immune disease.
http://www.youtube.com/watch?v=6vISWCI-13M
Official: ME CFS patients have retrovirus (XMRV).
http://www.youtube.com/watch?v=gB12ydqeQiU
____________________
Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
|
Dr Trevor Marshall
Foundation Staff
|
Posted: Thu Oct 22nd, 2009 19:37 |
|
The third video is particularly disturbing, with Dr Mikovits reaching way beyond what her study identified, into talk about T cells and B cells, Breast Feeding and even vaccines.
Now, I might bring up those issues if I was being interviewed, but I hope that my answers would be somewhat better presented than Judy's. It is tough to talk about the transmission issue, this was made clear in the "Catching Cancer" discussion last night. I note that they used the 95% figure too, rather than the 67% in the paper.
I have carefully looked through the fulltext, and it is a well-done study. Accurate and rigorous. There is no need to reach beyond that achievement, IMO.
It is sad that the ME/CFS community is getting so excited about this discovery, and then, like the HIV community, they will wait decades for the cure which just doesn't come.
|
Dr Trevor Marshall
Foundation Staff
|
Posted: Thu Oct 22nd, 2009 21:54 |
|
One of the patients of Dr Peterson, the 'Peterson' of the Whittemore-Peterson Institute, spills the beans on a number of issues in his blog:
http://forums.aboutmecfs.org/showthread.php?t=771
Now of course, this patient may have not gotten his facts straight, but I thought the following passage was quite interesting, especially the use of Rnase-L as a selection criteria, and the selection between patients with "CFIDS" and "Chronic Fatigue":
Peterson was very selective with his sample. He picked the patients that he thought were most likely to have the illness, and >90% of them were positive. The other sample sizes from around the country averaged out to something lke 60% positivity, so it's definitely possible 1) that XMRV isn't as ubiquitous as it seems, 2) detection methods aren't refined enough, 3) some of the patients in other sample sizes don't have CFIDS but rather have chronic fatigue.
He said I'm a very good candidate for XMRV because 1) it infects NK cells, 2) I have rnase-L abnormalities, 3) it's reactive with other viruses which I documented stealth infections of, and 4) it has a cortisol receptor, which is why my symptoms wax and wane so much due to stress.
I have no idea what he means about XMRV having a Cortisol receptor, the whole organism is only about 8000 base-pairs long, while the human glucocorticoid receptor is over 150,000 base-pairs long. Has anybody any idea where this concept comes from?
|
Bane
Member
| Joined: | Sun Jan 27th, 2008 |
| Location: | Norway |
| Posts: | 108 |
| Status: |
Offline
|
|
Posted: Thu Oct 22nd, 2009 23:16 |
|
Dr Trevor Marshall wrote:
I have no idea what he means about XMRV having a Cortisol receptor, the whole organism is only about 8000 base-pairs long, while the human glucocorticoid receptor is over 150,000 base-pairs long. Has anybody any idea where this concept comes from?
Could the virus hijack/use the human GCR to its own advantage/growth?
Good Morning America Health
http://www.youtube.com/watch?v=JFBY8UKMVp0
Last edited on Thu Oct 22nd, 2009 23:17 by Bane
____________________
Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
|
Dr Trevor Marshall
Foundation Staff
|
Posted: Fri Oct 23rd, 2009 00:31 |
|
Well, of course it could, but this is a loaded question, as so could the hundreds of other pathogens involved in the Th1 microbiota.
I did have a look at whether the tat protein of XMRV was capable of hijacking the VDR in the same way that HIV tat hijacks the VDR. I found that the HIV tat and XMRV tat were totally different, with very little in common. It is unlikely that XMRV wipes out the VDR the same way as HIV does.
It is a pity that other Researchers/Physicians didn't perform the same experiment (the tat comparison) before pontificating about XMRV being similar to HIV, and certainly before suggesting that HIV therapies might be effective against XMRV
|
eClaire
Member in Phase 2
| Joined: | Mon Sep 25th, 2006 |
| Location: | Virginia USA |
| Posts: | 855 |
| Status: |
Offline
|
|
Posted: Sat Oct 24th, 2009 02:46 |
|
Thank you Dr. Marshall for throwing a bit of water on this house on fire.
Prior to your post, I had already decided to take a wait and see approach to this new "cause" of CFS. If they come out with a test, I will take it as much to prove I don't have the retro virus as to prove that I do.
And if I do and it doesn't hijack the VDR the way AIDS does, but it has a significant impact on the immune system (beyond the help of the MP), and they actually figure out the mechanism and figure out a way to help without harming the patient, then I'll take a serious look.
In the meantime, I'm not working myself into a blather (ahem... to my friends on the MP that I've already blathered to  ).
I do know that I don't want to get anywhere near the sorts of drugs my brother took for AIDS. The side affects were awful. Admittedly not as bad as the IP I've had it on the MP, but he wasn't beating back CWD either. And in the end, it was infection that killed him, as no doubt it is for most AIDS patients.
Claire
Last edited on Sat Oct 24th, 2009 02:48 by eClaire
____________________
38mo on MP; CFS FMS MCS COPD hypermob. IBS/GERD osteopor.; 125D48 25D<4;
NoIRs during most daylight outings & covered up; home w/o NoIRs
Ph1.Dec06 * ModPh2.Jun07 * AbxBrk.Mar-May08 * Ph2.Oct-Nov08 * Ph1.Jan2009
|
Dr Trevor Marshall
Foundation Staff
|
Posted: Sat Oct 24th, 2009 11:31 |
|
in the end, it was infection that killed him
Sorry about your loss. AIDS is such a devastating disease.
No, it wasn't 'infection,' in the end analysis it was lack of understanding of the immune system, of the way the VDR is at the heart of innate immunity, and the way that antibiotics work (or don't work) in-vivo that killed him. Failure to effectively treat the infection killed him. You would think that 70 years after the discovery of antibiotics, Medicine would not be routinely defeated by simple pathogens. It is tragic.
Whenever I talk about how the HIV tat protein takes over VDR or P300/CBP, I get a total cold-shoulder from clinical medicine. Molecular mechanisms are known now, but nobody seems equipped to recognize that, or even willing to think through the implications of that knowledge...
|
Rico
Moderator
| Joined: | Wed May 31st, 2006 |
| Location: | |
| Posts: | 349 |
| Status: |
Offline
|
|
Posted: Sat Oct 24th, 2009 14:17 |
|
Trevor, from what you've observed, are there many in the molecular science/microbiology fields that feel shunned by clinical science as you seem to or are they just as guilty for not doing their homework?
____________________
No diagnosis/some symptoms; wife with Sarc on MP; Olm 40mg q6h| avoid D| 1,25D=63 25D=32 (May 2006) 1,25D=44; 25D=10(Dec 2006)PhaseI(May06) PhaseII(Aug06) PhaseIII(Aug07)
|
Dr Trevor Marshall
Foundation Staff
|
Posted: Sat Oct 24th, 2009 14:36 |
|
Translational medicine has not delivered on its promise primarily because
1. the clinical sciences poorly describe the disease to the biologists, so the wrong stuff gets studied, and then
2. fail to implement any technology coming back to the bedside from the bench research.
For their part, IMO the biologists should not be content to being forced to solely study animal models and cell lines.
At the Cincinnati Nuclear Receptors conference, senior researchers were complaining how tough it was to get their institutional research boards (IRBs) to approve them being given any human samples (blood or tissue) even when those samples would normally be thrown away. They first have to describe what they want to do in great detail. This obviously reduces to zero the possibility that a breakthrough will occur "on a hunch."
|
thelymelight
Guests visiting Phase 1/2/3
| Joined: | Fri Nov 4th, 2005 |
| Location: | Ontario Canada |
| Posts: | 222 |
| Status: |
Offline
|
|
Posted: Sat Oct 24th, 2009 18:16 |
|
I have a few questions related to the cortical receptor and CFS/Lyme..
I was initially dx with CFS/ME in 1990, then chronic Lyme/Babesia in 2003…but I wonder, if I have some major virus going on as well…as I have been disabled with these diseases for 19 years now…despite trying every possible therapy under the sun (no punn intended) for CFS and doing years of abx for Lyme/Babs
I was eventually put on low physiological doses of hydrocortisone (5-10mg a day) in 2005 and noticed I had more stamina, less fatigue and pain (especially around 3 pm each day) less social anxiety, and better brain function etc…
1) When one is taking hydrocortisone, they are instructed to increase their dosage if they should develop a cold or flu or have a lot of stress….as their body is not making enough of this hormone….So if it is immune suppressive, wouldn’t taking more of it actually make patients less able to fight off a cold/flu,instead of helping...this doesn't make sense with what the MP says about supplementing with HC.
My understanding is that the body makes approx 20-40mg of cortisol a day…So if ones hypothalamus have been hit by a virus, or Lyme, or both and they are not making or releasing enough cortisol each day…
2) By what mechanism does taking low doses of hydrocortisone (which is what the body naturally makes) actually suppress the immune system?
3) Does it have some blocking affect on the VDR?..could someone please explain this to me..
My understanding is that too little cortisol in the body is just as detrimental to the immune system as too much cortisol
I apologize if I am posting in the wrong thread for this subject.
Cheers
____________________
Lyme, Babesia,19+ yrs, neuro-psych-cogni|Sept08-125D/30.42; 25D/8.40; Feb09/10.40; Jul09/5.60 Feb08~Olmesartan, Feb09~Ph1. Low lux-some areas of home. MEDS: Cipralex 10mg, Rivotril 1/2 of a 0.5 mg for sleep; iodine spray for thyroid, weaned Hydrocortisone
|
Current time is 08:55 | Page: 1 2 3 4   |
|
|
|
|
