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
This is a known virus already. Even if you can’t get the virus, you can actually clone it from the sequence. The point is, you don’t need a clinical sample as a positive control.
Tests will not get passed regulators without this requirement.
I’m suggesting that you are the one incapable of reading the information provided to you, or you are just a blatant liar.
Now you are asserting that Lombardi et al. was lying?
Did Lombardi et al. use nested PCR or not?
You are correct that well documented N of 1 trials can be considered a starting point. This is a very different beast from anecdotal evidence however which is what @JohnDoe related. Even then I believe some would argue with some merit that non-scientific observations or studies, which do not provide proof may assist research efforts as well. But a starting point is only that – a place to start not validation at the same level as a clinical trial.
However, to put that in perspective, in his book The Emperor of All Maladies: The History of Cancer oncologist Siddhartha Mukherjee refers to all patients as storytellers from the kingdom of illness. One of the stars of the book is not a patient however, but a pathologist named Sidney Farber. In the summer of 1947, a 2-year-old boy, the child of a Boston shipyard worker, fell sick. Examining a drop of the baby’s blood through the microscope, Farber saw the telltale signs of acute lymphoblastic leukemia, billions of malignant white cells “dividing in frenzy, their chromosomes condensing and uncondensing, like tiny clenched and unclenched fists.†By December, the boy was near death. In the last days of the year, Farber injected his patient with an experimental drug, aminopterin, and within two weeks the child was walking, talking and eating again. It wasn’t a cure, only a remission; but for Farber it was the beginning of a dream of cures, of what one researcher called “a penicillin for cancer.â€
Farber had no proof that essentially poisoning patients would make them better, he took a very great risk as did his patients and their parents, but he clearly felt compelled to try.
So are ME/CFS patients sick enough to merit the risk from an outsider’s viewpoint? Veteran broadcast journalist Llewellyn King describes the ME/CFS patients’ plight thusly, ” To know them is to peer into hell.”
The question then might be whether “poisoning” ME/CFS patients with anti-virals, without scientific evidence that it will work for all patients, is worth the risk to the patient. Doctors generally say no without more clinical evidence and patients say yes for they are living the disease. From what was on the post you linked to, Dr. Snyderman appears to be both and he gambled on the anti-virals.
I jokingly replied to the person that saw a correlation between finding “post hoc fallacies” and Alan Dove’s name using google, teherby implying that finding these two things together does not mean that Alan Dove is the cause of post hoc fallacies, which the poster seemed to imply and you seemed to like.
Please read more carefully in the future.
Thanks for your response profvrr. I guess my positive culture result could have been contamination, but, I didn’t realize that the antibody test was that non specific. So, if I’m hearing you correctly, even if it’s not xmrv specifically that I am mounting an immune response to, it’s still a retro-virus, which means it’s not contamination.
Is that chance based on your personal preference? Do you perhaps mean statistical significance?
Phase IIb results were deemed to be inconclusive for the WPI as a procedural error was discovered before results were finalised. The blood working group choose to move forward. The data on the new assays has been presented at conferences and will no doubt be available for others to use if they wish to follow the scientific method.
The CDC switched assays in the working group after detecting the virus.
You don’t address the fundamental question at hand.
You suggest that Singh must validate her assay using a “known positive” in order to investigate if the “known positive” is truly positive?
Please do answer.
Yet when the WPi switched assays you deemed it “improving their mothodology”.
Please answer this: if the CDC didn’t want to detect those “known positives”, why did they report them? Reporting positives and then “switching assays” doesn’t seem like a smart thing to do when you are covering up evidence….
Please don’t waste our time with “ask the CDC’. Can’t you see it’s wholly illogical that they actually abondened their working assay? It’s far, far more logical that WPI somehow contaminated these samples (as they went through the WPI lab).
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Alan please google the phrase sea sickness, you will not find it on the same page as the word psychosomatic.
Then google the phrase ME and you will find it is listed by the WHO as a neurological disease coded G93.3.
Then when you understand the distinction between chronic fatigue and ME google the word scientist.
The above states that ” These assays could detect at least 5 viral copies of XMRV DNA”. How sensitive do you want? They also state that the positive controls were consistently positive in the same range of 50 and 5 copies.
What I don’t understand:
AFAIK did the Coffin study find live XMRV in one CFS patient. Are there other independently confirmed XMRV blood/serum samples for validating assays? Against what known positive samples did Singh test their assays?
Somebody mentioned “blatant liar,” which seems to fit the bill here sadly. HIV was isolated and fully sequenced before any ARVs were tested for activity in vitro, let alone approved for prescription.
The behavior of Gob987 mirrors the bullying pseudoscientific soothsayers of AIDS denial, whose self-appointed job is to hand-wave away the research findings they don’t like (see the interminable AIDS denial threads on Tara Smith’s Aetiology blog from a few years ago).
I think something that might be being misunderstood is that there are numerous potential avenues for contamination, not just one and done. Some of the potential avenues are the reagents which I believe have been shown to contain mouse DNA, XMRV from the 22rv1 cell line, primers previously thought to be XMRV-specific actually not being XMRV-specific, mouse DNA entering the experiment through some other avenues(s), etc. There are many different potential avenues for contamination so it’s not contradictory to cite different potential sources of contamination.
Yes this is quite significant. The Singh study was about looking for correlation not proving causation so why conclude with the line about people with ME not taking ARVs? A little over the top and dramatic one might say. More of a marketing line it seems drawn up by vested interested groups.
Unless it was the whole purpose of the study to stall HGRV studies get patents in place and try to steal the glory if the government eventually allow the most credible hypothesis of a Human retrovirus being the cause of ME.
All one has to do is bury XMRV association then refind and rename it. This seems the name of the game now. “Its not XMRV but it could be another HGRV”. Quite a ploy if you choose your own definition of XMRV and claim it is a clone. Then you are not looking for a HGRV. Very wordy and a built it get out clause for the future.
I am assuming Singh is actively advocating for ARV treatment in her positive cancer patients?
On that subject why didn’t she try a blood assay on those cancer patients she found positive with tissue sample then use it for people with ME/CFS if she validated it on the cancer patients. Instead she used a “Novel” method. How telling!
How unscientific. How non replication!!
How!!
I’ve asked this several times but I get never tired… 😉
Can you provide us with a single example of a proper replication study in the field of retrovirology? You know, where the scientists really replicated each and every aspect of the finding that they were trying to validate?
She tested the known positive samples of the WPI and found them to be negative. Now the WPI will have to calibrate their assays to these known negative samples. Only when the WPI has really calibrated their assays against the now known negative Singh samples, we can trust their future results.
See how silly this line of reasoning seems when you are on the other end of it?
And for known positives, is it positive to check for viral budding with EMs? There has to be a way to establish true known positives.
To a synthetic clone, not the wild-type virus. Where is the evidence, ie. validation, that these assays can detect at that level when looking for the virus. What quantiy of blood are we looking in. What if the virus is at an even lower level as previous studies have shown. They are working at the end of PCR sensitivity.
Yes, you are incorrect. All 14 patients tested positive by WPI, but not all 14 patients were used in the original Science study. This is a minor error in the paper but is purely semantic: nothing on God’s earth can change the fact that those 14 patients were designated as positive for XMRV by Judy Mikovits….
You remind of a defense attorney grasping at straws, trying to establish a reasonable doubt. If you are suggesting that the virus its present but at levels below PCR sensitivity in this study (and others), then you should be able to back that up with evidence that Lombardi et al used even more sensitive yet still 100% reliable methods. I think the basic problem is your apparent belief that the WPI results were 100% accurate, ie, an scientific established fact. ‘Tis not the case.
What does a 0/0 study prove? If a 0/0 study is more credible than positive studies that consistently show 70-80% in ME patients and 3-7% in healthy controls should we stop all science now?
Because contamination could happen does not me it did. How will a HGRV model ever be provable if we abide by such a premise?
Should we stop the argument of the definition of XMRV and look for a HGRV in ME then prove or disprove that it is the same one that WPI, CC, NCI and Alter found?
Its seems those who cant find XMRV keep shifting from “its not there” to “its contamination” to its recombination to its not the same virus being found etc etc.
Those who can find it just keep finding it in the same % in PWME and healthy controls.
Surely not finding something means nothing if the assay is not validated and two groups are not really looking for the same thing defined in the same way. It tells us nothing. It can never be seen as credible science.
Why are so many scientists so afraid of a true replication study it is so obvious it is the best way to go.
This paper states that “certain Taq preparations contain very small amounts of mouse DNA that can cause false-positive reactions when used in highly sensitive assays for XMRV”. They state in this paper that they didn’t actually find contaminating infective XMRV virus in the reagents, but just mouse DNA.
They are implying that previous positive study results must have been false positives due to the mouse DNA in the reagents, not actual XMRV infection.
If we take this as truth that this is the source of “contamination” as they suggest, how then can you explain the electron micrographs showing actual budding C-type gamma-retrovirus in the Lombardi paper? Singh states herself that the “contaminated” reagents don’t include infectious virus. So how can non infectious mouse DNA turn into infectious XMRV in an electron micrograph?
something doesn’t add up here…
Gob is not really suggesting PCR sensitivity is the problem, but specificity: the strains of XMRV in patient samples are undetectable by assays calibrated to VP62 because they are different to this strain and other known strains of XMRV. At least, that is the current ad hoc hypothesis to explain away the mounting negative studies.
Of course, there are several problems with this line of reasoning and Gob’s proposed way of solving this in unprecedented in the history of science. Oh, and it is circular (which is why it is unprecedented, but now I am starting to reason in circles).
Of course, if “live” XMRV is so different from VP62 and other known strains, people who claim to be able to find these strains must publicize these strains or the proper methodology to find these strains. Only then other scientists can calibrate their asssays accordingly.
Of course, it’s much easier to hang back in your chair and shout that everybody else is doing it wrong without providing solid (i.e. non-circular) alternative methodology…
Guest what is your personal hypothesis for your 10 years of ME/CFS if its not a HGRV? Don’t you want to see fellow patients the ones you call trolls push for credible science instead of cover up and deception such as we have faced for numerous decades now.
XMRV/MLV is still the leading hypothesis, is yet to be disproved and has been shown to be present in the same figures in numerous labs consistently.
Do you oppose this as a patient and do you want to see it put to bed without being disproved?
There isn’t a single study that has disproved the association shown by Lombardi et al and Alter. Or perhaps you prefer the explanations offered up by the Science Media Centre etc.
Why would a long suffering patient oppose the sentiments of Gob987 and the obvious anomalies he keeps reminding people of.
Also, they state in this paper “We discovered that both recombinant Taq polymerase (Invitrogen) and the Platinum Taq polymerase (Invitrogen) tested positive for IAP sequences.”
They imply that these reagents were used in previous studies that found correlation between XMRV and CFS patients.
“Since we were unable to find any evidence of XMRV using our sensitive qPCR assays, serological methods or viral growth assays, we decided to test our samples using the PCR assay first used in the original study that found XMRV in CFS (12). Another study utilized a modified, nested version of this assay to discover the presence of polytropic murine leukemia virus-like sequences in CFS (11). Using this assay, we found approximately 5% of our samples to be positive for products of the expected size, regardless of whether they were patients or healthy volunteers.” (11 and 12 refer to Lo and Lombardi papers respectively)
However, if these reagents were the source of positive results in the Lo and Lombardi papers wouldn’t we expect to see a more even distribution of positive results between patients and controls? How can contaminated reagents selectively contaminate patients and not controls? This needs to be explained as well.
There are no (peer reviewed) studies that consistenly show XMRV in 70-80% of ME/CFS patients.
How will a HGRV model be ever be disprovable in your eyes? How can contamination be ever provable by an independent scientific experiment in your eyes?
Can you provide us with a single proper replication study in the field of retrovirology to convince us that this is the usual way that science progresses?
“There isn’t a single study that has disproved the association shown by Lombardi et al and Alter.” Oh? What do you call this one?
Why is it so complicated? Why is this disease underfunded? How can you explain documented epidemics in the 1980’s, though deemed “hysterical” by epidemiologists at the CDC.
How is it that ME/CFS patients have the same cytokine signature that suggest a chronic viral infection, and low natural killer cell number and function, yet 30 years down the road, we still don’t know why?
Why many patients have abnormal RNASE-L ? Why do we have chronic viral infectious like EBV, CMV, HHV-6, parvovirus, Lyme ( this one is not a virus) and enterovirus?
Why researchers stay well away from researching us and why governments only want to fund psychiatric studies like childhood adversity and CFS (CDC)
Why can’t dr Mikovits publish her papers in her drawers?
Why is there families, blood or non blood related “catching” ME/CFS? and why is it passed from generation to the other?
And lastly, how long will patients have to wait for answers? And will all of us be willing to wait, isolated in a dark and quiet bedroom? Is that a life?
Probably what Gob987 means is that only 2 out of the 14 came from the original Science paper, but if the rest were declared XMRV+ by WPI, even if they are not coming from the Science paper patient cohort, still is material information to take into account as 14, and not 2…
This should be the final nail in a coffin that has been sufficiently closed for some time now in any case. Sadly, however, this has taken on a distinct flavor reminiscent of the anti-vaccine movement. The CFS-XMRV LINK conversation should have ended months ago, much less any whisper of causality.
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kellylatta: I’m having trouble parsing some of your posts, because you seem to be referring to “antivirals” when the context suggests you mean “anti-retrovirals.” It’s an important distinction; for instance, researchers such as Montoya at Stanford have been and are actively trialling long-term therapy with valganciclovir and other antivirals, but there are no trials yet of anti-retrovirals in ME/CFS patients, just these one-off anecdotal situations.
I think it’s a little over-dramatic to call administering legitimate drugs “poisoning” patients. Are we suffering enough now to be willing to accept fairly serious risks of side effects? Hell yes, many of us are. But both antiretrovirals and antivirals have been proposed based on plausible theories of the disease, not as some sort of crazy Hail Mary pass. XMRV wasn’t implausible on the face of it – a retrovirus could cause the immune dysfunctions and the neurological problems seen in ME/CFS – and there may yet still be some other retrovirus in the mix that we haven’t properly identified. B-cell depletion with Rituximab is showing some early promise too; that could be because it’s eliminating B-cells that are infected with something, or it could be because it’s interrupting some other immune or autoimmune process. (Now there’s a trial I’d like to get in on. But I don’t live in Norway.)
It’s a sad fact that the pocket lint that ME/CFS gets in the way of research funding does not go a long way toward supporting many large-scale well-designed, well-controlled trials. I live in a tiny backwater devoid of major medical centers called “Los Angeles,” and there ain’t nothing going on here. Not that I begrudge HIV a single penny of its $3 billion a year in research funding … but speaking as a formerly productive member of society, I think a little more than $6 million a year is called for to properly investigate a disease that debilitates and disables so many.
Only your line of reasoing is silly in this example. If you are able to detect something why would you adjust your assay to a calibration that then makes something undetectable.
Thats like seeing a star through a telescope and then changing the focus so that you cant see it anymore then claiming your assay has equal weight to one that proves the star was never there.
Its called a failure to detect. Its not proof that lombardi didnt detect. Next time you cant find your car keys send a five year old in to the room to look for them. If he dont find them does that prove then arent there?
Why should it have ended months ago? That’s a pretty strong statement to make. What do you base it on? Are you yourself a researcher, a doctor, or a patient who deals with this disease? When is the proper time to stop investigating a promising lead into a devastating illness – when you get tired of hearing about it?
Never mind the screeching of those who can’t evaluate or accept new, negative data. I can assure you that they’re not representative of all patients’ attitudes, and they’re not representative of the attitudes of respected, legitimate biomedical researchers who have worked hard trying to run down the XMRV leads as thoroughly as possible. The National Institutes of Health don’t seem to agree with you either, having funded the Lipkin study and even expanded its scope. None of these efforts have been undertaken merely to placate hysterical, irrational patients who are clinging to a crazy fringe theory. All this research is a promising sign that, at long last, the public health agencies are starting to act with proper regard for the seriousness of the disease – which, by the way, includes not only a duty to try to help current patients, but also to attempt to protect the public health against new cases.
Yup, there are some patients who *are* hysterical and irrational. I feel sorry for them, even though the screeching hurts my ears too. But this group doesn’t actually have the power to do anything *but* screech. Those of you who are still walking around with your careers and your lives intact practically have superpowers compared to us. Consider not only your power to point your browser somewhere else if you are irritated, but also the fact that your own continued freedom from this disease is not assured until the cause is found, before you favor us with your opinion about how silly this whole effort has been.
This still doesn’t mean that the 14 samples are negative. The only conclusion that can be drawn is “failure to detect” as so many negative papers actually carry that exact title.
Infact not detecting it in two samples could be put down to chance or discrepancies in the two Singh tests or handling etc. But not finding it in 14 patients consistently tested positive at different times is actually further weight of an incapable Singh assay.
So Ila Singh is a 5 year old child compared to Lombardi, who finished his PhD all of five whole years ago?
Now you are being silly. Like it or not, the Singh study was very thorough and well-designed, and used multiple methods for detection. They found nothing. Yet you happily dismiss it as the equivalent of sending a child to do an adult’s job. It’s very clear that people like you consider the WPI results to be 100% accurate beyond any and all doubt, and therefore any study like this one that does not support those WPI findings must by definition be flawed.
Perhaps it would have been proved as contamination by Alter when he was forced to do further studies and infact proved there was no contamination in his study.
RRM you know your argument is flawed. You have to disprove a finding the emphasis is on you to disprove it using the EXACT METHODS namely a replication study. A method claimed to be similar can only validate original findings it cannot scientifically disprove it.
A replication study which does not validate the original findings can claim to disprove the original findings .
Why are you trying to reinvent the scientific method?
I don’t suppose any of the scientists providing negative studies would go looking for a treasure chest blindly with their own instructions when they had the very map showing where the treasure was claimed to be buried in the first bloody place.
Why do they pretend to claim the upper hand in the scientific method.
By your reasoning RRM would there have ever been one scientific discovery ever or will there ever be one in the future.
All observers please adhere to the principles of the scientific method if you want to disprove a hypothesis. Its the best method there is and has worked for thousands of years.
I’m a patient, and I’ve suffered plenty, and I want good science to prevail here, not “science that gives us the answers that we have already decided we like best.”
There really ARE other good, plausible theories for the causation of ME/CFS. It’s not a matter of XMRV and only XMRV or else we’re back in the loony bin. I don’t think we’ve gotten *quite* to the bottom of XMRV yet, but I give Ila Singh’s work a great deal of credibility and weight, and I believe Singh, the Lights, and Lucinda Bateman when they say “We basically did everything we could think of to come up with a positive result,†– the words of Alan Light as reported today by Amy Dockser Marcus in the WSJ blog.
I don’t think “Gob987,” who I have known by other names and who has been singing this same tune for a long long time in other fora, is contributing much of anything to this discussion. I think he/she is parroting a line of groupthink that has been cooked up over the course of today to fight off this latest challenge to the XMRV hypothesis, and repeating it over and over again in a very obnoxious way, like a three-year-old who really isn’t sure you heard what she said the first fifty times she said it.
The question I have for *you* is: Why is defending the XMRV theory of CFS causation more important than finding out the truth?
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It was not well designed it wasn’t a replication study. Until a replication study proves WPI, Alter, CC, and NIC wrong it is a sound scientific hypothesis.
“Well designed” means nothing. I could design a table very well it doesn’t make it a chair. I suspect you are new to the concept of the scientific method. That’s also why you believe only one lab has found XMRV/MLV.
Well you can send an adult to look for the keys in my above example and if he don’t find them it still amounts to a failure to find not proof of non existence.
Again none of the negative studies disprove the XMRV association found in various labs.
For your information I did not invent the scientific method it has been tried and tested for thousands of years.
I am just reminding people that failure to replicate will never validate a negative study. That is a scientific fact. It proves nothing either way. Claiming it does reeks of desperation.
The PACE study claims to be well designed but does it prove anything? I am assuming you are well groomed in the issue of ME and know what the PACE study is.
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I am defending the scientific method which demands replication. You are jumping to the assumption that the theory of XMRV/MLV causation is not the truth without even letting the science continue.
That is a dangerous path to go down especially with a disease that has been controlled by vested interest groups for decades.
I want science to prove whatever the cause is and that means using the tried and tested replication mehtod as the best means of proving or disproving the science.
Dont we deserve this?
Please explain what “other good, plausible theories for the causation of ME/CFS” are and why they havent been proven after decades.
In order for you above theories to be proven do you think that would even be possible if the same contamination theories are used against them without adhering to replication and the scientific method. What will you do when your chosen theory is consistnetly subject to theories and not replication science, will you just say “oh well that seems to be settled now”?
I have already invited you, in my initial analogy of finding keys to send in a group of adults to find your keys in a room. Like I said if they dont find them is that proof of the keys being non existent especially if a number of other people can find them?
I tried to spell out the scientific method to you and the difffernce between absence and non detection in the most simplified way. However, it seems I didnt make it simple enough and in this instance it appears I should have explained it to you as if you were the five year old in my original example.
My sincerest apologies for assuming you had the intelligence of an adult.
This is not a reply to profvvr..i just didnt know how to post it as a seperate post.
Hey wait a minute something has just struck me…..
In the 8 years that the CIA was looking for Usama Bin Laden it is obvious he didnt exist, its not that they couldnt find him.
Before that all sitings and reports of him were just contamination. Lots of people couldnt find him so it must be true he didnt exist.