Since the first association of the retrovirus XMRV with chronic fatigue syndrome in 2009 in the US, subsequent studies have failed to detect evidence of infection in patients from the US, Europe, and China. These studies were potentially compromised by a number of factors, such as differences in patient characterization, geographic locations, clinical samples used, and methods used to detect the virus. These and other potentially confounding conditions have been addressed in the most comprehensive study to date on the association of XMRV with CFS.
In the introduction to their paper, published in the Journal of Virology, the authors note other problems with many of the studies of XMRV in CFS patients:
- Too small control populations
- Patient and control samples collected at different times
- Investigators generally not blinded to sample identity
- PCR assays that rely on conservation of viral sequence mainly used
- Limits of detection, reproducibility, and precision of assays unknown
- Controls for each step that would identify analysis not done
- Insufficient numbers of negative controls included
- No study included positive samples from the original 2009 patient cohort of Lombardi et al.
To address these issues, the authors collected blood from 105 CFS patients and 200 healthy volunteers in the Salt Lake City area. One hundred of the patients fulfilled both the CDC-Fukuda and the Canadian consensus criteria for diagnosis of ME/CFS. The patients were selected from a clinic that specializes in the diagnosis and management of CFS and fibromyalgia.
New blood samples were also collected (by a third party) from 14 patients from the original study by Lombardi et al. The samples were blinded for subsequent study. Detection of viral nucleic acids was done using four different PCR assays. Anti-XMRV antibodies in patient sera were detected by ELISA. Finally, virus growth from clinical specimens was attempted in cell culture. The authors used the multiple experimental approaches reported by Lombardi and colleagues.
Let’s go through the results of each assay separately.
PCR for viral nucleic acids. Four different quantitative PCR assays were developed that detect different regions of the viral genome. The assay for pol sequences has been used by several groups and is the most specific PCR assay for XMRV. Three other PCR assays were also used that target the LTR, gag and env regions of XMRV DNA. These assays could detect at least 5 viral copies of XMRV DNA. The precision and reproducibility of the PCR assays, as well as their specificity for XMRV, were also demonstrated. DNA prepared from white blood cells of 100 CFS patients and 200 controls were negative for XMRV. For every 96 PCR reactions, 12 water controls were included; these were always negative for XMRV DNA.
XMRV antibodies in human sera. To detect XMRV antibodies in human serum, a portion of the viral envelope protein, called SU, was expressed in cells and purified from the cell culture medium. The SU protein was attached to plastic supports, and human serum was added. Any anti-XMRV antibodies in human sera will attach to the SU protein and can subsequently be detected by a colorimetric assay (we have discussed this type of assay previously). This assay revealed no differences in the amount of bound human antibodies for sera from CFS patients or healthy controls. Some of the patient sera were also used in western blot analysis. Recombinant XMRV SU protein was fractionated by gel electrophoresis. The protein on the gel is then transferred to a membrane which is mixed with human serum. If there are anti-XMRV antibodies in the human serum, they will react with the SU protein on the membrane, and can be detected by a colorimetric assay. When rabbit anti-XMRV serum was used in this assay, the SU protein was readily detected. None of the human sera analyzed by this method were found to contain antibodies that detect SU protein.
Infectious XMRV in human plasma. It has been suggested that the most sensitive method for detecting XMRV in patients is to inoculate cultured cells with clinical material and look for evidence of XMRV replication. The XMRV-susceptible cell line LNCaP was therefore infected with 0.1 ml of plasma from 31 patients and 34 healthy volunteers; negative and positive controls were also included. Viral replication was measured by western blot analysis and quantitative PCR. No viral protein or DNA was detected in any culture after incubation for up to 6 weeks.
Analysis of previously XMRV-positive samples. Blood was drawn from twenty-five patients who had tested positive for XMRV as reported by Lombardi et al. These samples were all found to be negative for XMRV DNA and antibodies by the PCR and ELISA assays described above. In addition, no infectious XMRV could be cultured from these 25 samples.
Presence of mouse DNA. After not finding XMRV using qPCR, serological, and viral culture assays, the authors used the nested PCR assay described by Lo et al. Although positives were observed, they were not consistent between different assays. This led the authors to look for contamination in their PCR reagents. After examination of each component, they found that two different versions of Taq polymerase, the enzyme used in PCR assays, contained trace amounts of mouse DNA.
Given the care with which these numerous assays were developed and conducted, it is possible to conclude with great certainty that the patient samples examined in this study do not contain XMRV DNA or antibodies to the virus. It’s not clear why the 14 patients resampled from the original Lombardi et al. study were negative for XMRV in this new study. The authors suggest one possibility: presence of “trace amounts of mouse DNA in the Taq polymerase enzymes used in these previous studies”. I believe that it is important to determine the source of XMRV in samples that have been previously tested positive for viral nucleic acid or antibodies. Without this information, questions about the involvement of XMRV in CFS will continue to linger in the minds of many non-scientists.
At the end of the manuscript the authors state their conclusion from this study:
Given the lack of evidence for XMRV or XMRV-like viruses in our cohort of CFS patients, as well as the lack of these viruses in a set of patients previously tested positive, we feel that that XMRV is not associated with CFS. We are forced to conclude that prescribing antiretroviral agents to CFS patients is insufficiently justified and potentially dangerous.
They also note that there is “still a wealth of prior data to encourage further research into the involvement of other infectious agents in CFS, and these efforts must continue.”
Clifford H. Shin, Lucinda Bateman, Robert Schlaberg, Ashley M. Bunker, Christopher J. Leonard, Ronald W. Hughen, Alan R. Light, Kathleen C. Light, & Ila R. Singh1* (2011). Absence of XMRV and other MLV-related viruses in patients with Chronic Fatigue Syndrome. Journal of Virology : 10.1128/JVI.00693-11
Um, isn’t that what controls are for? The controls all seemed to work as they should. Try another one?
Wow I didn’t realize a placebo effect could last 2 years and work well enough that some have returned to work and are actually able to get out of bed. You know it’s easy to tell people what they should and shouldn’t do when you haven’t experienced this sickness yourself . Or witnessed your family member suffering. People have been in their beds for years unable to deal with light or sounds just for starters. Now why is it ok for perfectly healthy partners of the HIV infected to receive ARVS to prevent the illness. We don’t have a life anyway so there is no risk. We are already mostly dead.
Anti-HIV Drugs Slash Risk of Virus Transmission by 92 Percent
http://www.thebody.com/content/art56911.html
A newly published study’s results provide perhaps the strongest evidence to date that the drugs used to treat HIV also prevent its spread. In a trial involving heterosexual couples where one partner was HIV-infected and the other was not, AIDS drugs reduced the risk of viral transmission to the uninfected partner by 92 percent.
A synthetic clone does not prove an assay is capable of detecting wild-type virus.
What do you mean who. This study did not prove the assays are capable of detecting positives and was shown incapable of detecting a clinically positive sample.
I have nothing to say on the PACE trial because I know very little about it. I don’t generally opine on subjects I know little about. But from what little I do know, it does not seem to have anything to do with the Singh study, XMRV, or virology. Therefore, I don’t understand why you are asking the question?
I am all in favor of patients and patient advocates learning as much as possible about their conditions and following the various lines of research. More knowledge is almost always better, and no one is generally more motivated than the patient him/herself and family. However, I also frequently see patients, especially in a condition like CFS/ME, who jump to and then cling to conclusions that are simply not validated. The internet is a wonderful information tool, but it also often leads people to believe that they know more than they actually do. You can almost always find a study, a paper, a blog that supports and reinforces your belief no matter what. BTW, this is true on almost any issue in any field, not just science and medicine.
hi lawrence! thank you for your comments! i happen to be one of those “trialling” arv’s (along with long term high dose av’s in combo – for nearly 5 years!)…under the strictest of care by knowledgable id docs. i was extremely ill (bedbound/housebound) – and for many years – though not what i consider desperate. i educated myself (i was a good candidate – being very “viral”)…trusted my docs expertise – and made a calculated decision to try! (both in an effort to help myself…and to help others down the road with my “anecdotal” contributions in the quest for helpful treatments.)
im mystified at the recent admonitions to avoid arvs (particularly by medical professionals in the me/cfs community). dont “they” realize that many seasoned me/cfs specialists (in the US), have been “experimenting” with them for quite some time – regardless of xmrv? (doesnt anyone “talk” to anyone else anymore? wheres the collaboration…the sharing of data?)
The PACE trial has nothing to do with this study, absolutely nothing. CBT or GET are no cure for ME/CFS; studies have to be very “creative” to demonstrate a positive effect even for patients selected on the Oxford criteria.
A testimonial is nothing more or less than an anecdote. Yes, I have read testimonials that some patients got better on anti-retrovirals, but you can find “patients” promoting just about anything (as treatment or even cure): antibiotics, raw food, lightning process, religion, reiki, and in my country there is a self-proclaimed patient-organization that, I kid ye not, promotes cranio-sacral therapy and dolphin therapy for ME/CFS. So yes, you cannot discount the placebo effect in testimonials
Well Roy your reply just about says it all about the subject of ME. You don’t know what the PACE trial is??? Wow!!
Then you say:
“I also frequently see patients, especially in a condition like CFS/ME, who jump to and then cling to conclusions that are simply not validated”
So forgive me if you have stated this already but what is your interest in the ME issue?
You are in favour of patients learning as much as they can but are you in favour of the scientific method through replication? Yes or no?
Are you in favour of patients expecting the science they wish to learn about to be watertight.
Do you believe that CBT and GET are useful methods for treating ME/CFS and if so is the weight of scientific eveidence in that favour due to published papers on it.
What effect would GET have on a person with ME especially as you seem to be letting go of the idea of a HGRV XMRV being associated with ME?
Should someone who has tested positive engage in GET with the current evidence base from PACE and the WPI and others XMRV studies including the Ila Singh one?
Answer how you like.
If you’re suggesting that constant mutation in the wild-type virus means any synthetic clone may be invalid, “outdated” so to speak when tested, then wouldn’t that call in question the ability of any group to detect wild-type virus consistently? And has WPI or anyone else yet shown that the same assay shows positive for wild-type virus but negative for a synthetic clone?
I have no idea whether or not CBT and GET are useful methods for treating ME. Your logic on this issue boils down to: The PACE trials were supposedly comprehensive and well-designed. But they were in fact flawed. The Singh studies are similarly described as comprehensive and well-designed. Therefore, they must be flawed too. Wow.
I don’t doubt that you know a fair amount about CFS/ME, perhaps even personal experience. But that’s not the same thing as an MD or a PhD in virology, which is the issue at hand here. As I said previously, belief perseverance is even more prevalent these internet days, because you can always find someone to agree with your original premise.
Who are the regulators? The regulators? Who are you referring to by saying regulators? Get the question? Should I write it in a different language?
This study shows that the qPCR assay is capable of detecting at least 5 copies of the proviral sequence. If that assay doesn’t detect anything in the blood then that blood doesn’t have integrated provirus.
Since when is XMRV = HGRV? I haven’t seen any studies on HGRV. For that matter, I haven’t seen any studies on XMRV and ME, just XMRV and CFS. 😛
I observe that there are a lot more negative studies than positive ones. Conclusion: it is becoming more and more unlikely that there is a link between XMRV and ME/CFS. Is XMRV even pathogenic?
I want scientists to find a cause and/or treatment and/or cure. The more lines of research (or susupects) (bacterial, viral, retroviral) the better in my opinion. I am not emotionally attached to XMRV.
You are a piece of work. You put words in my mouth on HIV in 1983 and then you are astonished about my (!?) statement. You must have fun on your own making up entire discussions.
Furthermore, the calibration to a ‘wild type’ sample in no way means that you can detect another ‘wild type’ sample. These other ‘wild type’ samples can just as easily mutate from the ‘wild type’ sample you have calibrated your assay to.
I like how you ask about my interests and then state that people are waking up and asking about my purpose in the debate.
You didn’t answer the question.
Obviously I agree with you over PACE when it comes to it being genuine science Johan. So please tell me what the purpose of PACE was and whether it will be easy for the government to force it on us in the UK and other places whilst they claim a lack of evidence for viral or Retroviral infection.
Please also explain how all the other 0/0 studies have such heavy involvement form the psychiatric brigade and their paymasters. is it just a coincidence?
Also why is every biomedical approach to ME always shot down continuously by the people who have a firm grip on the destiny of ME Patients? it doesn’t matter whether it is claimed to be a connection a cause or a biomarker. Why is that!
Actually I disagree with you when you say that PACE has nothing to do with this study. It will have disastrous consequences when PACE is pushed on virally infected patients as a “cure” or treatment for a “non existent Retrovirus” in ME when people are forced into regression and disease progression if they are carrying a HGRV.
Anyone here who thinks XMRV is a proven contaminate would you be happy for your child to receive the blood of someone tested positive God forbid they should ever need a blood transfusion?
Well hopefully the UK gov will stick to the lifelong ban on the blood of people with ME being donated that they brought out soon after the Alter validation study.
The only problem is if people are infected without knowing it just like in the case of HIV they may very well be passing it around.
Bearing in mind all those circumstances should there be a number of high quality replication studies or should we just forget about XMRV and move on to something else?
Perhaps we could go back to 1983 and forget about HIV and let history judge whether we were Retrovirus denialists.
It would be awesome if Ila Singh and/or Judy Mikovits could be invited to one of the next TWIVs.
Roy says:
“I have no idea whether or not CBT and GET are useful methods for treating ME.”
Well that just about says it all.
The Singh study is not flawed because the PACE study is flawed that is a non scientific summary. The Singh study is flawed and offers no prove of contamination in positive studies because it is not a replication study and used unvalidated methods and unvalidated assay and a synthetic clone.
XMRV is in the general population it at least a small percentage as an infectious agent according even to the CDC, so anyone that studies 300 samples and cant find it even in 1% has just proven that there assay, methods, wahtever you want to call it DO NOT WORK!
It can makes as many claims as it likes but it is proof of nothing. That is a scientific fact. If you cant grasp that there is no such thing as science.
Ok Roy I am a patient, so what is you interest in ME.
Since you ask:
I am no patient but I am a family member of someone with ME/CFS. When this person told me a retrovirus was implicated with ME/CFS I started following the news and it seemed pretty solid, but pretty soon the bullshit meter exploded (at least, in my eyes). This family member with ME/CFS is also skeptical of the XMRV connection, I might add, although she remains hopeful. As for my scientific background, I recently graduated cum laude and was offered a position as a graduate student but declined. Virology is not in my field of knowledge, I must admit. Scientific methodology is, by the way.
There is zero evidence for contamination in your eyes, but I bet you cannot provide us with a single (independent) experiment that would provide us with evidence, which renders your definition of evidence rather meaningless.
You could call me an ex-scientist. That means if you put me in a lab now and I had to run my own experiments I’d be challenged. However, my ability to read data and understand studies is as good or better than ever. I’m also someone who was once was incorrectly diagnosed with “catch-all” CFS years ago (it was actually food allergies), and although my condition was brief compared to the vast majority of real CFS patients, I know what it is like to lie awake at night praying for someone to find a clear and treatable causative agent. So I genuinely feel badly for the CFS community in general, since the XMRV “theory” if you will made a lot of sense and looked very promising. And I will certainly agree that the jury is still out on XMRV, but the tide appears to be moving strongly against it now in my opinion. I do find the almost knee-jerk response by the pro-XMRV crowd to any negative study, such as this one, to be troubling, because the goal should be truth and objectivity, not “us vs. them”. Good luck to you.
A lot of replies, but fewer CFS patients seems to be replying now than previously. From what I’ve read elsewhere, it seems that most have already moved on from XMRV as a likely cause of their illness.
Actually she looked for everything
PCR- On line 356 she says she used the PCR assay used in the first study to search for XMRV in the Utah patients. She repeated that statement at least twice more in the paper
Culture – She worked with Dr. Ruscetti to used an improved culture test that lasted for 6 weeks. Later she noted the increased risk of contamination from using culture.
She also used the Lo/Alter version of the test and except for some sequences later determined to be due to contamination, failed to find the MLV sequences they had.
On line 421 she says “We also also analyzed the WPI samples using tests utilized in the two studies that found XMRV or XMRV-like viruses in CFS, a PCR assay for gag sequences both in single round (12) and nested formats and a test for viral growth in cultured cells (12)”
On lines 436/438 she repeats those statements – stating we used the gag assays and culture tests used in the original study….
#11 refers to the Lo/Alter study and #12 refers to the WPI study.
She really looked hard – she looked 9 different ways for XMRV in those 14 WPI positive patients; 4 qPCR tests developed by Dr. Singh, two antibody tests, a Ruscetti culture test, nested PCR (gag) (Lombardi) and nested PCR (Lo/Alter).
I think you’re clinging to straws here with the cohort. The most pertinent point was not whether the previously positive WPI patients were in the Lombardi cohort but whether they were positive for XMRV or not. The WPI provided Dr. Singh with patients who had REPEATEDLY tested positive for XMRV at their lab. They had probably been tested more than the Lombardi patients.
Put it this way; if you were the WPI and you wanted to ensure that Dr. Singh would find XMRV – you would give her you ‘top’ XMRV positive patients (whether they came from the first study or not) and that’s what they gave her.
As to the cycling conditions – that’s for someone else to answer 🙂
Roy this is a misnomer:
“I do find the almost knee-jerk response by the pro-XMRV crowd to any negative study, such as this one, to be troubling, because the goal should be truth and objectivity, not “us vs. them”.
All we want is objectivity in XMRV studies and we want in in MRI for lesions and we want it in Pet scans, we want it immune profile testing and gut issues etc etc .
BUT WE DONT GET IT!!
It is explicity stated in all the ME/CFS guidelines not to test patients for such issues. So you are preaching to the choir when you talk to us about what objectivity should be.
A study that is well designed not to replicate a study which finds a clue to how ill we are does not qualify to be called objective. It can claim NOTHING objectively in comparison to another study that used different methods.
The Singh study does not use the same methods as the Lombardi or the Alter study so you cannot even reach an objective conclusion. Anyone that claims otherwise is making a false claim. Also anyone who claims we have knee jerk reactions to 0/0 papers doesn’t understand how well we scrutinise such papers before we comment on them.
There is no such thing as a Pro XMRV crowd there is a crowd who have followed the ME debate for years and know exactly where to look for the holes in certain claims and demand objectivity.
Why do you think it took you so long to get diagnosed with food allergies instead of CFS……You had a number of “Objective” tests didn’t you?
No good if they were using the wrong bloody tests is it. Don’t matter how well they were designed or how objective they were.
One last thing: would you want the blood of an XMRV positive patient for a child in your family if they ever needed it. I didn’t get an answer from you before. It is a pure coincidence that MLVs as found by Alter and WPI cause neuro immune disease and cancer in their original hosts, isn’t it?
No need to worry its now been shown to infect humans? Even the CDC claim xmrv it is infectious. The question is who has got the best assay to test for it in the blood of people with neuro immune disease.
Ah well lets just forget it after all its only a harmless contaminate right? Isla Singh proved that didn’t she?
Danielson et al showed that an assay calibrated to VP62 clone could not detect known positives.
Yes, you cannot rely on a clone.
Correct, but by using clinically positive samples you are not limiting yourself to only the clone.
That is samples not sample.
I am amazed that you don’t know who. Wow!
The study provides no data on detection levels in a clinically positive samples. If the assay does not detected anything, then there is still no proof it is not there.
Incorrect. Proof would be needed to show they had been found positive in a published study, at least that is the party line espoused by those who believe in contamination. However, this is moot if the assays have not been validated, which they have not. Here is an example. An unvalidated assay for other viruses is highly likely to be negative early in the assay development stage even if patients have tested positive repeatedly elsewhere if the assay is unvalidated.
The WPI want people to follow the scientific method, that is all. Singh did not replicate, nor use clinically positive samples to calibrate her assays. It is therefore unknown if those in the study were or were not infected.
Well unfortunately many others in your “camp” do not want objectivity, otherwise they would not be making statements like “Even if someone proves to me that WPI was absolutely incorrect in the conclusions published in SCIENCE, I will still support the Whittemore Peterson Institute. They are the only real hope I have had in 25 years, and I believe they are doing their best to help us”. I found this when I happened across another forum a few hours ago, one which you seem to already know about. I can understand and appreciate the desperation this person feels at this stage. However, I assume you will agree that this is not the expression of an objective open mind. Again, good luck and good-bye.
Unvalidated assays cannot be used to support the claim that the virus is not related to ME/CFS.
Then you have heard wrong. This is about evidence and currently it still strongly supports HGRVs being associated with ME/CFS.
The data was not provided, so why take the sample?
Polytopic, modified polytropic and xenotropic sequences are HGRVs.
Lombardi found polytopic and xenotropic, Lo found polytropic and modified polytopic.
Skepticism is not the scientific method. The data is the all important thing and no evidence exists to support the belief in contamination. No hypothesis has been constructed that can account for all the observations. That is why the association is holding strong.
Shin et al did not “look for everything.”
You admit in another post that you cannot comment on the PCR conditions. Therefore you will not understand how the details of the study disprove your comment.
Dr Ruscetti may have helped, but that does not mean anyone listened. Furthermore, his name is not on the paper.
Contamination is always accounted for by testing for it. That it may happen is not evidence that it has taken place.
Again, the assays mentioned in Shin et al are not the same as those in Lombardi or Lo et al. There is no mention of reverse transcription PCR (RT-PCR).
Perhaps you should read the original paper before you make claims not supported by the data.
Looking hard has no scientific validity whatsoever.
All assays used were novel.
The scientific method removes all need for camps. Apply it and the answers will present themselves. Don’t apply it and prepare for a very long number of years until someone decides they are a scientist.
Maybe I don’t understand some things, but here goes:
WPI got a whole viral sequence and a budding micrograph from a patient’s blood. I should think that right there, under the slide, you have a cell whose DNA could be sequenced to show XMRV in it.
Why wasn’t this done? Why didn’t PNAS insist on it being done? If WPI didn’t have sufficient funds, why in all this time hasn’t NIH or NCI stepped up and done it? Or is really not so simple a thing to do?
Cort is it so ironic that you don’t understand how this adds more weight to Singhs assay being incapable.
If WPI 14 patients repeatedly tested positive at different times it shows how contamination at WPI is not a credible scenario. Only if the same samples where hit and miss for being positive at WPI would Singh be able to take the upper hand in this particular argument.
She also cant detect population levels of XMRV with her blood assay when she can detect 22% in her tissue samples for prostate cancer.
Even the CDC admit that XMRV is in the human population as an infectious agent so any blood assay unable to detect it even in a single % of 300 people for example is flawed.
Its back to the drawing board for all the 0/0 studies designers I am afraid.
By the way Cort when you came to mecfsforums with others under a false name trying to get hold of WPI positives for a study that didnt have ethics committee approval (IRB) did you succeed in getting any names before you were outed?
It is being applied. However, when it produces answers which you don’t like, you will just claim it is “unvalidated”.
You don’t know about this topic, so don’t state categorically that “government bodies want to solve this problem,… there is zero evidence or motive.” Your statements are just flat out false. Read urbantravel’s reply to you.
Flex, despite my previous good-bye, I can’t let one or your last statements go by. “If WPI 14 patients repeatedly tested positive at different times it shows how contamination at WPI is not a credible scenario.” Not at all, if the contamination is constant over time, then the results will be consistently false positive over time as well. In fact, if the virus is actually as transient in the blood as many have claimed, and/or present in extremely low levels only, then one in fact would be far more likely to be hit or miss for positives, not consistently positive. Sorry, but I think your argument on this point is completely backward.
Well I have a question. Just a few days ago this was still about contamination as the 5 or 6th thing that they have come up with to explain XMRV. So if it’s about contamination then why didn’t the 14 positives from WPI come up as showing that? Instead we are back to the 0/0 study that could not even find a positive. Wouldn’t the contaminant have shown up. Or maybe XMRV would have if Singh had used the original assay she used to find it in prostate cancer. Instead she designed a new one that has not been validated to find anything. So it seems.
There is a report from a ME/CFS patient (not me) from a forum who announced he tested positive for XMRV via stomach biopsy, at Red Labs (Brussels)
Wow, it is statements like these that do untold damage to the reputation of CFS patients in the research world. You have no interest in medicine or science but you then go on to make claims of the abuses of science to patients and how bad this disease compared to others… whaattt??? Sure the research CFS has been a mess but you are not helping at all.
I am here to vouch for the majority of CFS patients out their; we are not crazy! What you are seeing is the loud vocal minority. The majority of CFS patients no longer believe XMRV plays any role what so ever in CFS. The majority of CFS patients do not spend time on CFS forums posting ridiculous comments on any story about XMRV or CFS. The majority of CFS patients are sane people that just want more research done on our disease. This is coming from someone who tested positive for XMRV from WPI’s lab over a year ago.
The online forums for CFS patients are filled with crazies hell bent on a belief they hold so dear, that XMRV causes CFS, that no amount of information will change their belief.
To those reading this post or seeing the crazy statements from patients in the comment section. Please do not judge millions of patients (CDC estimated over a million in the US alone) from the statements of a small vocal minority of a few thousand extreme CFS patients.
The basic problem here is people with CFS have very few places to turn for help for there real physical disease. There are only a handful of specialist in the US for millions of patients. When people are left to there own devices for a disease that has derailed their life some are willing to accept any hypnosis or treatment that sounds plausible to them out of desperation.
It seems like you don’t know either! WOW!
It has not, the assays were unvalidated.
Unless the negative person is now positive.
Do you know what the scientific method is?
It is a ridiculous question you are asking and right over your head why.
A replication study will satisfy people, but it will need replication itself if the data produced is considerably different. Is that sinking in? Replication is in the data not a few words carelessly tossed around.
@e0eddb636ed2ccc32d389f3684bf35f4:disqus Patients do cling to unscientific beliefs. From your comments I get the impression that you have made an ultimate decision that it is XMRV/HGRV/MLV.
This is a virology study, why do you keep on mentioning psychological ones? And why cling to ME? All studies (psychological and biomedical) mention CFS, de Canadian Consensus Criteria are for ME/CFS. Where is the publication mentioning a link between ME and XMRV?
@Gob987:disqus Can you point me to a study/publication on HGRV? Are XMLV, MLV, … human retroviruses, as in causing a disease. Think we are not there yet, not even for prostate cancer.