Whether or not the retrovirus XMRV is a human pathogen has been debated since the virus was first described in 2006. The answer is now clear: the results of Blood XMRV Scientific Research Group, along with a partial retraction of the 2009 Science paper describing identification of the retrovirus in patients with chronic fatigue syndrome (CFS) show that detection of XMRV in patient samples is a result of contamination.
The Blood XMRV group obtained new blood samples from 15 individuals previously shown to be positive for XMRV (Lombardi et al., 2009) or MLV (Lo et al., 2010) ; 14 of these were from CFS patients. Fifteen blood samples were also obtained from healthy donors. The samples were coded and sent to 9 laboratories for analysis. These laboratories (Abbott Molecular, Abbott Diagnostics, CDC, FDA/Lo, FDA/Hewlett, Gen-Probe, NCI/DRP, and WPI) conducted validated assays for viral nucleic acid, viral replication, or viral antibodies. Positive control samples were also included that were ‘spiked’ with XMRV, in the form of cell culture fluids from the cell line 22Rv1. Each laboratory was at liberty to choose which assays to carry out.
Two laboratories reported evidence of XMRV in the coded samples. Only WPI identified positive specimens by PCR: two from negative controls, and one from a CFS patient. The FDA/Lo laboratory did not detect any positives by PCR, using the same nested assay that they had previously reported in their published study. The samples tested included 5 specimens that were positive in the Lo et al. study.
Lombardi and colleagues have previously concluded that viral culture is the most sensitive method for detecting XMRV; however the FDA/Hewlett laboratory failed to culture virus from CFS samples. This laboratory did culture virus from positive control specimens, demonstrating the sensitivity of their methods. The FDA/Ruscetti laboratory recovered virus from 3/15 CFS samples but also from 6/15 negative control specimens. WPI did not carry out viral culture assays due to contamination of their cell lines with mycoplasma.
Four laboratories tested the samples for the presence of antibodies that react with XMRV proteins. Only WPI and NCI/Ruscetti detected reactive antibodies, both in CFS specimens and negative controls. There was no statistically significant difference in the rates of positivity between the positive and negative controls, nor in the identity of the positive samples between the two laboratories.
These results demonstrate that XMRV or antibodies to the virus are not present in clinical specimens. Detection of XMRV nucleic acid by WPI is likely a consequence of contamination. The positive serology reported by WPI and NCI/Ruscetti laboratories remained unexplained, but are most likely the result of the presence of cross-reactive epitopes. The authors of the study conclude that ‘routine blood screening for XMRV/P-MLV is not warranted at this time’.
One of the authors on Lombardi et al., Robert Silverman, decided to reexamine some of the DNA preparations from CFS patients that were originally used to detect XMRV DNA by PCR. He found that all the positive specimens from CFS patients were contaminated with XMRV plasmid DNA. Therefore the authors of the original study have retracted Figure 1 (single-round PCR detection of XMRV in CFS PBMC DNA); table S1, XMRV sequences, and figure S2, phylogenetic analysis of XMRV sequences.
A puzzling aspect of Silverman’s results is that XMRV plasmid DNA was detected only in samples from CFS patients, not healthy controls. This pattern would not be expected if the specimens were properly blinded, that is, coded so that the investigators did not know which were controls and which were from CFS patients. The authors offer no explanation of these findings.
The paper reporting contamination of samples with XMRV is entitled ‘Partial Retraction‘. It’s not clear to me why the entire paper has not been retracted. After removing the PCR and nucleic acid sequencing results, there is no evidence indicating the presence of XMRV in the patient samples. The remaining experiments show detection of a retrovirus by cell culture experiments, and the presence of viral proteins or antibodies to the virus in clinical specimens. None of these findings prove that what is being studied is XMRV. The title of the original paper ‘Detection of an infectious retrovirus’, XMRV, in blood cells of patients with chronic fatigue syndrome‘, is unsupported.
In an accompanying article on the XMRV story entitled ‘False Positive‘, Judy Mikovits of WPI notes that “Anyone who says this is a lab contaminant has drawn the wrong conclusion and has done a disservice to the public”. She goes on to imply that a gammaretrovirus is likely involved in CFS. On the contrary, pursuing the CFS-gammaretrovirus hypothesis is a disservice to those with CFS, and detracts from efforts to solve the disease. There are no data to support such an association, and to suggest that a lab contaminant, XMRV, has pointed the way to a bona fide etiologic agent seems implausible.
XMRV does not cause CFS. The virus arose in mice between 1993-96, and its detection in patient samples is clearly a result of contamination. Reaching these conclusions has required a long and often contentious journey that has highlighted the best and worst aspects of scientific research. There are many lessons to be learned from XMRV, but an important one is that science progresses not from the work of a single investigator, but from the collective efforts of many laboratories. XMRV reminds us to trust science, not scientists.
Well said.
The lesson here is rejoice in being wrong – when you are wrong you learn something, more often than when you are right.
 Bring on the Ian Lipkin study…
Lipkin says the
study will continue despite the Blood Working Group’s negative results.
 “Our study designs are different, our power is different, our subjects
are different, and our assays are different,†Lipkin says.  “Whether our
results will differ remains to be seen.â€
 I can’t believe Lipkin says there using different Assays, Its ashame the Blood working group didn’t use the same assays as Lipkin will use?
And I can’t wait to see what retroviruses Dr Ruscetti has discovered, this is very exciting indeed.
He says a whole family of new gammaretroviruses, this will change science for ever.
Thank god for Dr Ruscetti first he helped discover HTLV-1 and now hes gone and done it again and found a whole load of new retroviruses, this man is a genius!
It’s such a shame about the vp62 mistake but I think its time to move on from vp62.
But I can’t help but think thank goodness it happened, if this accident hadn’t happened maybe Dr Ruscetti would not have discovered the new family of Gammaretroviruses. So all things happen for a reason and the Silverman mistake will now lead us on to one of the biggest discoveries of modern medicine.
Lets not waste anymore time, we need to start looking at these gammaretroviruses and find out who’s got them, how it happened and get some treatments for them and try and stop them spreading anymore. I have a bad feeling we probably already have quite a epidemic on our hands.
I look forward to hearing more about these gammaretroviruses Dr Ruscetti, its going to open many doors. God Bless you Dr Frank.
 I agree Lets STOP arguing about this and START treating this as a public health emergency!
We need to look at the retroviruses Dr Francis Ruscetti says he has discovered.
Can make sure that Dr Francis Ruscetti gets all the money, help, resources he needs.
Contact the WHO. We simply can’t go on talking about this another day.
hi, Dr. R, I was wondering if you could comment any further on, “The positive serology reported by WPI and NCI/Ruscetti laboratories
remained unexplained, but are most likely the result of the presence of
cross-reactive epitopes.”
What sort of antigen would give rise to a cross-reactive epitope?
I definitely feel that the one great thing that will come out of all of this is highlighting to people (the general public and scientists included) how science should be done. It is just a shame that it took all of this and even still people are not listening. It also shows the difficulties in communicating the scientific method across to the wider public arena.
VP62 was wrong. HGRV’s may still be in the human population. N=15 has very little power.
The tests the BWG used were using were ones that could be done quickly and on a massive scale to detect XMRV in a large poulation. They were not sensitive time consuming tests.
HGRV research has just begun. There is still so much to learn.
Silverman gave the wrong name to the virus. The WPI and NCI/Ruscetti have the same finding as Lo et al and Hanson.
The blood working group must feel very sorry for themselves for all the errors in the paper.
Patients on medications known to cause false negatives.
No Trizol or preservative used for the PBMCs, invalidating the only assay proven to work.
Not all tubes screened with diagnostically validated assays.
Tubes in the same lab as 22Rv1.
Controls not screened by all labs.
Lo’s team using the assay from Lo et al. that failed to detect the positives.
Lo’s patients not determined to be negative by any diagnostically validated assay.
WPI not allowed to complete work with their culture assay.
VP62 assays all looking for virus not never shown to exist in nature.
Silverman gave the wrong name to the virus. The WPI and NCI/Ruscetti have the same finding as Lo et al and Hanson.
The blood working group must feel very sorry for themselves for all the errors in the paper.
Patients on medications known to cause false negatives.
No Trizol or preservative used for the PBMCs, invalidating the only assay proven to work.
Not all tubes screened with diagnostically validated assays.
Tubes in the same lab as 22Rv1.
Controls not screened by all labs.
Lo’s team using the assay from Lo et al. that failed to detect the positives.
Lo’s patients not determined to be negative by any diagnostically validated assay.
WPI not allowed to complete work with their culture assay.
VP62 assays all looking for virus not never shown to exist in nature.
I had blood taken for tests twice in the past year at two different labs in Ottawa. The first time the girl started telling me how tired she felt and it got around to her telling me she and her sister were diagnosed with cfs. The last time i went to another lab, and the girl told me she was so sick from chicken. That rang alarm bells for me because i know what that is all about. She then answered she was sick from cfs and had food sensitivities and fibromyalgia etc. etc.
Now what are the chances of that happening? So yes I have a bad feeling that we likely already have an epidemic on our hands.
Pingback: ‘Trust science, not scientists’, Vincent Racaniello’s Virology Blog, 27 September 2011 | ME Association
I’m sorry Prof. Racaniello, but you appear to have drawn the wrong conclusions from the Blood Working Group study, who’s only objective was to investigate the risk posed by XMRV to the blood supply. Whether it achieved that objective is still open to debate, given the criticisms levelled at the way it was conducted.
The question about whether XMRV causes ME/cfs is still wide open and it appears that the Lipkin study is being specifically designed to address that question.
The scientific method is therefore alive and well, but the reporting of it is both manipulative and dishonest.
9 patients from WPI positives were tested. 1 was not a patient and the other 5 were never tested before the study began, using a diagnostically validated assay, to see if they were negative.
So this blog from a scientist, who he says not to trust, confirms there were major failures of the paper.
So the question is, as VP62 was constructed by Silverman in 06 for the first time, how did that contaminate the cells in Paprotka?
And when is Science going to retract that paper for deliberately omitting from the paper use of an RT-PCR assay that was the only assay in the study used on the later xenografts, which themselves were never proven to be derived from the same tumor or nit contaminated by 293T cells that contain XMRV and dates from 1977. A cell line the PCR assay, which is included in the paper, found negative. Evidence that the PCR, which we know detects at minimum 2000 copies/100 cells, is not sensitive enough.
Busch must be devastate.
And you have definitive proof that these people have been diagnosed with CFS by a legitimate physician? Or meet the ICC ME criteria? How many times have you heard people say “Oh, I had CFS for about a month last year” and that sort of thing? Two personal anecdotes do not an epidemic, or even statistically significant information, make.
You think the paper should be retracted because it’s conclusion, you believe, has been proven wrong. Â I am not a scientist, but papers aren’t retracted unless there’s been fraud or the like, not because some people think the conclusion or title are wrong, right? Â So this seems biased to me. Â There are tons of actually patently fraudulent papers published on ME by insurance lobbyists posing as scientists. Â Why not call for these papers to all be retracted (and the CDC pages on “CFS”) instead?
I have asked you before why you state the conclusions of Coffin’s paper on the origin of XMRV as a fact when this paper’s results have not been replicated yet. Â You and Coffin both act like that the convention that you don’t say something is proven until it’s been confirmed by other labs applies to Lombardi et al, Lo et al, Hansen, etc., but not to Coffin’s work. Â I don’t have an answer from you yet.
Looking for gammaretroviruses in ME detracts from efforts to solve ME? Â What efforts?!
I know what you mean; but it brings to my mind the question, since you know now how little money is spent by NIH on ME and you know now that NIH and CDC have waged a decades-long war on ME science and patients, why not also highlight these much more serious problems; it would do so much good for science!
I’m aware this is quibbling, but as you’d previously commented on the problems caused by scientists being too sure of themselves, I’d prefer ‘There’s no good reason to think XMRV is related to CFS’ to ‘XMRV does not cause CFS’. It’s hard to prove a negative, but that doesn’t mean it’s sensible to go on thinking that XMRV is related to CFS.
“You think the paper should be retracted because it’s conclusion, you believe, has been proven wrong. Â I am not a scientist, but papers aren’t retracted unless there’s been fraud or the like”
While of course I can’t speak for anybody, that is not the way I read the professor’s argument. I read it as follows:
– The authors have retracted part of their data.Â
– the study’s results are not sufficiently carried by the remaining data.
– Therefore, it is unclear why Science agreed to this partial retraction.
So even while the professor or you or I may agree or disagree with retractions without proof of fraud, the professor is just saying that it is strange to choose to (partially) retract an essential part of a paper. When the data in question are essential to the study’s results, authors should fully retract or don’t retract at all, but definitely not “partially retract”.
That is how I read it and it makes sense to me.
Samples from patients with ME were tested at the WPI and NCI and found to have HGRV gag sequences by nested and nested RT PCR.
These samples were independently reanalyzed and were negative for mouse mitochondrial DNA and IAP sequences. Â Just as importantly the gag sequences were not VP-62 and no trace of the VP-62 plasmid was detected. Â Â
Aliquots of these samples were sent to Silvermans lab for sequencing. Â These were never sent back to the WPI or NCI. Â
Silverman used a single round PCR and reported the detection of gag and env sequences of VP-62. Follwing PCR his samples contained the VP-62 plasmid, when the samples sent to him did not. Â Silverman introduced the VP-62 plasmid into his samples and sequenced the introduced VP-62 and not the retrovirus in the samples sent from the NCI and WPI. Â The wpi and NCI were unable to find anything in the portion of the samples that they retained using Silvermans primers and cycling conditions.
This means that the HGRVs in the Lombardi cohort were not VP-62 and that explains the 00 studies and the BWG results.
Frank Ruscetti knows a bit about discovering new retroviruses and has obviously taught Dr Mikovits well.
Trust their science and not the words of  politicians with science degrees.  Racaniello does so much spinning that he should be called professor gyroscope.
“the study’s results are not sufficiently carried by the remaining data.”
Results are intimately connected to data. Â There is more data within Lombardi than Lo et al, that has never been tested by others.
Virologist are however finding it “strange” that Coffin and Pathak have claimed pXMRV was an accident from the 1990s when it first came into the existence in Silvermans lab in 2006.
 Â
“Results are intimately connected to data. Â There is more data within Lombardi than Lo et al, that has never been tested by others.”
Yet, the argument is that the remaining data does not warrent the main conclusion (and title) of the paper, i.e. that XMRV is present in a majority of tested CFS patients (as well as in some controls).
“Virologist are however finding it “strange” that Coffin and Pathak have claimed pXMRV was an accident from the 1990s when it first came into the existence in Silvermans lab in 2006.”
Don’t believe anything you’ve read from the forums. Regardless of the Paprotka study – even if it were completely untrue, consider this: EVERY SINGLE 22Rv1 cell line stored in labs around the world is infected with XMRV. Most of these cell lines have been distributed to all these labs way before 2006. This unfortunate fact alone conclusively disproves the notion that Silverman is responsible for creating the virus in 2006.
Oh, and although I certainly don’t want to resort to authority arguments (especially not with the subject of this blog in mind), since you have made the assertion:
Are you able to name one virologist to back up your pretty wild assertion?
What is the argument? Â
Xenotropic is merely a measure of tropism and many of the viruses may display a xenotropic pattern of host infection.  As you should be aware xenotropic only means can infect some species and not others. It is now known that xenotropic viruses have the widest host range and thus there is a good chance that some of the viruses detected in the Lombardi cohort may well display a xenotropic host range, although they are known to not be VP-62.Silverman and Pathak have already supported that 22Rv1 cannot be claimed to contain the VP62 plasmid since the 1990s.
“EVERY SINGLE 22Rv1 cell line stored in labs around the world is infected with XMRV.” – Where did you hear that? It is an opinion of your own.
Nice of you to post an abstract, but you should really try to argue how that supports your view.
The key argument here is that only the Silverman data really solidified the case for XMRV. While there was quite a lot of supporting data, non of this is really specific to XMRV. The antibody and virus isolation results, for instance, only make sense in support of the finding of XMRV. None of these experiments on their own provide compelling evidence for the notion that there’s XMRV present in those samples.
“Where did you hear that? It is an opinion of your own.”
That is quite right, but it is supported by independent lines of (compelling) evidence.Â
Moreover, it this were untrue and only some of the 22Rv1 cell lines would have gotten contaminated by Silverman’s VP62 in or after 2006, this would be very easy to demonstrate by the proponents of this silly theory. Which, I might add, would lead to much publicity and critical acclaim.
‘She soon enlisted Ruscetti, who had worked in Gallo’s lab when it
discovered HTLV-I, to screen blood samples from Peterson’s
patients for viruses. Intrigued by the RNase L link
to XMRV, Mikovits and Lombardi—who by then had joined WPI as well—met
Silverman in October 2007 at a prostate cancer
conference in Lake Tahoe, where they discussed the possible role of XMRV
in
CFS. Silverman was happy to collaborate and sent
WPI a clone of the virus, known as VP62. The institute could use it as a
reference to start hunting for the virus in CFS
patient blood samples that Peterson had stored.’
http://www.sciencemag.org/content/333/6050/1694.full
Silverman by all accounts went to great lengths to store the samples he received from contamination. But what if those samples were already contaminated?
Xenotropic is merely a measure of tropism. Â That will be how it supports the point. Â HIV was also incorrectly named HTLV-III when that was discovered. Â The data from the NCI and WPI is substantial. Â Again, HIV here is a good example. Â That virus was detected using many of the same experiment as in Lombardi, but was not cloned for at least 10 years after the first paper was published. Â I’m sure you don’t want that paper to be retracted.
Now I am sure you are confused. Â The WPI and NCI detected HGRVs. Â The virus they found is not VP62, that was Silvermans error.
“That is quite right, but it is supported by independent lines of (compelling) evidence.”
You are suggesting that you have evidence that all 22Rv1 is infected with VP62, which has no relationship to the Lombardi findings? Â Are you certain you have your thoughts together.
They were screened by an independent lab and they were VP62 free.
http://3.bp.blogspot.com/-LE3KbJjEN2g/TnzsXvAzL0I/AAAAAAAAAEE/Otc07jeQbFs/s1600/Slide07.jpg
Patient samples tested positive for gag sequences at the NCI and WPI using nested reverse transcriptase PCR. Of these samples a portion was retained from each and the remainder exported to Dr Silvermans lab for sequencing.The retained sample aliqots have since been tested by an independent lab and found negative for any trace of mouse mitochondrial DNA, IAP sequences or the VP62 plasmid. Additionally, gag sequences were detected which were nothing to do with VP-62. Thus when the samples left the WPI and NCI they were not contaminated.Follwing Dr Silvermans single round PCR the VP62 plasmid was detected in several of the samples and the virus he sequenced was VP62. In short he had sequenced the contaminant that he had introduced into some of those samples.VP62 is not correct sequence for the viruses in the samples exported to Dr Silverman by the NCI and the WPI. The WPI and NCI were not able to detect gag or env sequences in retained portion of the samples using silvermans methods and primers.This explains the negative studies and the Blood Working group. In particular it should be noted that J Levy replicated Silvermans methods and not those of the NCI and the WPI. Unsurprisingly he could not find a HGRV in patients testing positive using the methods of the WPI and NCI.
And yet contamination WAS found by Silverman despite his own extreme lengths and several years after those samples were sent by WPI?
I don’t have access to the content used in this analysis so will have to link to the blog:
http://scienceblogs.com/erv/2011/09/xmrv_and_chronic_fatigue_syndr_28.php#more
Yes Ruscetti discovered HTLV-1. Mikovits trained under Ruscetti.
The WPI used VP35 for PCR not 62, read the paper. Cohen hasn’t.
That’s right. Silverman had VP62 contamination in his lab. He failed to sequence the virus in patients.
That isn’t what is being said though:
‘And yet the CFS samples shipped to Bob Silverman in 2009 were contaminated with XMRV PLASMID before his lab touched them, after WPI touched them, after Silverman gave them the VP62 plasmid.’
That’s not a quote. No one has ever said that and the evidence from an independant lab screening the samples shows that it’s wrong. They were not contimated until after they had been in Silvermans lab. The WPI and separately the NCI didn’t use VP62.
It is a quote from ERV’s blog as linked previously: http://scienceblogs.com/erv/2011/09/xmrv_and_chronic_fatigue_syndr_28.php#more
Mikovits refuses to share her data with Science.Â
I think it would be VERY easy to set up a simple experiment that gives Silverman the chance to show that WPI contaminated their samples and for WPI to show that they didn’t. Let both Silverman and Mikovits send their positive samples of the patients in question to an independent lab, blind them and see if Mikovits (or the unnamed independent lab of her choice) can discriminate between her samples and Silverman’s samples.
Yet Mikovits does a test without any proven sensitivity, sends her samples to an unnamed, supposedly independent lab with another assay unproven to work at the desired sensitivity, and you believe that this provides any convincing evidence for the idea that she didn’t contaminate her samples? You see, “absence of evidence is not evidence of absence”, really works both ways…
Mikovits refuses to share the data in question with Science.
The source of contamination came from the artificial clone VP62 from Robert Silverman’s Cleveland Clinic, which was erroneously coined “XMRV”. The VP62 clone was then shipped around globally to numerous labs to locate the same specimen that the WPI Lombardi et al discovered in their 2009 Science journal study. What the WPI found was a family of Human Gamma Retroviruses (HGRVs), as did Alter/Lo et al in their 2010 PNAS publication. Â
Â
VP62 being a lab artefact, does not exist in nature, so every study that used this as a positive control to find HGRVs, were never going to find the same HGRV as WPI and Alter/Lo. In essence, every study that used the VP62 clone was ultimately flawed from the outset, and it is those that should really be retracted by the relevant publications. XMRV/VP62 does not exist in nature, and this is what the negative studies searched for. Naturally they were never going locate a match, and this fully explains their 0/0 results. Â Â
Â
The WPI never used VP62, and what they discovered was isolated and using next generation Deep Sequencing and has now proven their HGRV discovery is not VP62/XMRV. XMRV still exists as a term, but it really accounts for a family of HGRVs which are currently unnamed, and require sequencing to fully identify them. Â
If the Lombardi et al paper is in need of retraction, then the same has to be said for the Lo et al PNAS paper. The fact we now understand VP62 was the source of the contamination, and that the WPI did indeed discover a family of HGRVs, means Lo et al was a full successful validation of their work.
Continuing to use “XMRV†to describe the VP62 clone is a false indictment against the WPI, and confusing facts by called two very different things by the same name is the making of a foolish act, and nothing more than slight of hand in order to prove an opinion.Â
Â
Based upon this, the Silverman partial retraction of the Lombardi et al paper is fully understood. Therefore much credit must go to Dr. Silverman and his team from the Cleveland Clinic whom confirmed this error to hopefully move the HGRV research forward. It was an act of great honesty and integrity, and I do hope they will continue to work with the WPI to isolate and sequence all of the HGRV variants. Â
The moral of this story is, nearly two years of research as been wasted because all the negatives study choose to use a clone as their positive control, rather than a HGRV isolated sample from the WPI, or even Alter/Lo. The fact these 0/0 studies continued to repeatedly refuse to perform a full replication of the Lombardi at el meant that understanding HGRVs has stalled. What is more worrying, some chose to perform more than one negative paper, making the same mistake again. This comes across as mischievous and meddlesome, and the bullying tactics against the WPI deserve a full apology from these so called balanced researchers. Their professionalism if a disgrace.Â
If this is how science works, I may have to start believing in God again.Â
Yet, if you believe that the data does not longer support the notion that XMRV was in those patients but another, related virus, a HGRV that was mistaken for XMRV because of Silverman’s sequencing, than you must actually agree with the notion that a full retraction should have been preferred over a partial retraction.
I mean, you do realize that the title and conclusions of the paper state that XMRV was found and not a HGRV that is not quite XMRV? And this is exactly what the professor was arguing (IMO), the fact that the paper still states that XMRV was found but that the data do not support that conclusion anymore.Â
You made that up. There is no source for such a comment. What kind of a person are you?
Why are you using a quote from a person not involved in the research? VP62 was never in the WPI or NCI labs in question.
“You are suggesting that you have evidence that all 22Rv1 is infected with VP62, which has no relationship to the Lombardi findings? Â Are you certain you have your thoughts together.”
Sorry, didn’t see this part. I am certain that I have my thoughts together.
Incidentally, the gag sequences that WPI reported on in the Lombardi study, are identical or almost identical to VP62. Of course, you could always hypothesize that the sequence is ACCIDENTALLY the same for that part an different for other parts, but that would be an incredible coincidence.
I Â mean, if I have my thought together, this is your line of thinking (please correct me if/where I’m wrong): A scienctist contaminates his samples, another scientists finds the exact same sequence as the contaminant in samples from the same patients, as well as multiple sequences that are almost identical to the contaminant, but the other scientist argues that she has found something different than the contaminant.
What is the basis of such a claim about Mikovits? There was no problem presenting this at the Canadian conference last Friday to a room full of scientists, researchers and doctors. Â The slides are also on the web.
The WPI has already sent their positive HGRV samples to an independent laboratory who confirmed they do not contain VP62. Â There are many labs who have assays that have demonstrated they can detect contamination from a clone, but only the WPI, NCI and Lo labs have data for integrated virus in patients.
“On the contrary, pursuing the CFS-gammaretrovirus
hypothesis is a disservice to those with CFS, and detracts from efforts to
solve the disease.”
Â
Vincent, I find the
above statement both highly bizarre and insulting. How does looking for the
cause of a disease do a “disservice” to the victims of that disease?
Perhaps you should ask the patients what they think.
Â
You then claim:
“There are no data to support such an
association.”
Â
This is false.
Â
Indeed you yourself
reference say in the previous paragraph:
“The remaining experiments show detection of a
retrovirus by cell culture experiments, and the presence of viral proteins or
antibodies to the virus in clinical specimens. None of these findings prove
that what is being studied is XMRV.”
Â
On the one hand you
admit a retrovirus is at play (though not necessarily “XMRV”). On the
other hand you claim there is no data supporting a retrovirus in CFS! So which
is it Vincent? You can’t have it both ways.
Â
Also you say that:
“The FDA/Lo laboratory did not detect any positives by
PCR, using the same nested assay that they had previously reported in their
published study.”
Â
This is misleading.
Although the FDA/Lo had previously used their BWG assay in their published
study, that assay had actually failed to detect any positives in the published
study. So the FDA/Lo results stand. There is most definitely data to suggest a
retroviral association with CFS. We need to find out what that retrovirus is as
a matter of urgency. Making glib statements about supposed
“disservice” does not help that effort one bit.
Â
If anything should
be retracted, it is your article.
“On the
contrary, pursuing the CFS-gammaretrovirus hypothesis is a disservice to those
with CFS, and detracts from efforts to solve the disease.”
Â
Vincent, I find the
above statement both highly bizarre and insulting. How does looking for the
cause of a disease do a “disservice” to the victims of that disease?
Perhaps you should ask the patients what they think.
Â
You then claim:
“There are no data to support such an association.”
Â
This is false.
Â
Indeed you yourself
reference say in the previous paragraph:
“The remaining
experiments show detection of a retrovirus by cell culture experiments, and the
presence of viral proteins or antibodies to the virus in clinical specimens.
None of these findings prove that what is being studied is XMRV.”
Â
On the one hand you
admit a retrovirus is at play (though not necessarily “XMRV”). On the
other hand you claim there is no data supporting a retrovirus in CFS! So which
is it Vincent? You can’t have it both ways.
Â
Also you say that:
“The FDA/Lo
laboratory did not detect any positives by PCR, using the same nested assay
that they had previously reported in their published study.”
Â
This is misleading.
Although the FDA/Lo had previously used their BWG assay in their published
study, that assay had actually failed to detect any positives in the published
study. So the FDA/Lo results stand. There is most definitely data to suggest a
retroviral association with CFS. We need to find out what that retrovirus is as
a matter of urgency. Making glib statements about supposed
“disservice” does not help that effort one bit.
Â
If anything should
be retracted, it is your article.
The validity of a new human pathogen rests on a sample size of 15? Along with a partial retraction of one part of one study? Whew! Thank you Mr. Racaniello for your pronouncement sparing the world from any further meaningful research.Â
“On the contrary, pursuing the CFS-gammaretrovirus hypothesis is a disservice to those with CFS, and detracts from efforts to solve the disease.”
Vincent, I find the above statement both highly bizarre and insulting. How does looking for the cause of a disease do a “disservice” to the victims of that disease? Perhaps you should ask the patients what they think.
You then claim: “There are no data to support such an association.”
This is false.
Indeed you yourself reference say in the previous paragraph:
“The remaining experiments show detection of a retrovirus by cell culture experiments, and the presence of viral proteins or antibodies to the virus in clinical specimens. None of these findings prove that what is being studied is XMRV.”
On the one hand you admit a retrovirus is at play (though not necessarily “XMRV”). On the other hand you claim there is no data supporting a retrovirus in CFS! So which is it Vincent? You can’t have it both ways.
Also you say that:
“The FDA/Lo laboratory did not detect any positives by PCR, using the same nested assay that they had previously reported in their published study.”
This is misleading. Although the FDA/Lo had previously used their BWG assay in their published study, that assay had actually failed to detect any positives in the published study. So the FDA/Lo results stand. There is most definitely data to suggest a retroviral association with CFS. We need to find out what that retrovirus is as a matter of urgency. Making glib statements about supposed “disservice” does not help that effort one bit.
If anything should be retracted, it is your article.
What about this data is it that you don’t wish to accept? Â VP-62 was not isolated from a single patient and does not exist in nature. Â VP62 was only ever in Silverman’s lab. Â Some viruses do have highly conserved regions within their genome. Â The slides show gag, but no plasmid. Â Â
http://3.bp.blogspot.com/-LE3KbJjEN2g/TnzsXvAzL0I/AAAAAAAAAEE/Otc07jeQbFs/s1600/Slide07.jpg
http://1.bp.blogspot.com/-pCSELs4zkeM/TnzsYR_SI9I/AAAAAAAAAEI/JpeGZc6kkyQ/s1600/Slide08.jpg
See post above. Â Do you realise what has been retracted and why all the other more substantial data has been retrained? Â
Way to go, Pet101, to insult people without giving them the option to back up their statement. How can you know there is no source? Have you checked the entire internet?
Anyway, the source for my factual assertion is the Editor-in-Chief of Science, Bruce Alberts. He stated the following to Retraction Watch:
“While we were aware that other co-authors had tested samples and claimed to not find evidence of plasmid contamination, those co-authors were unwilling to provide their data for examination so we were unable to comment on the validity of the other experiments.”
Oops, forgot to add a link. Before you accuse me of making up the Bruce Albert quote too, here it is:
http://retractionwatch.wordpress.com/2011/09/22/why-did-science-partially-retract-the-xmrv-chronic-fatigue-syndrome-paper/
Editor-in-Chief of Science, Bruce Alberts, is the basis for such a claim:
“While we were aware that other co-authors had tested samples and claimed to not find evidence of plasmid contamination, those co-authors were unwilling to provide their data for examination so we were unable to comment on the validity of the other experiments.”http://retractionwatch.wordpress.com/2011/09/22/why-did-science-partially-retract-the-xmrv-chronic-fatigue-syndrome-paper/
Sorry, forget to reply to the other part of your reply.
While many labs may have assays that they can detect contamination from a clone, but outside of Silverman I know of noone that has shown they were able to detect VP62 plasmid at the necessary sensitivity for these trace contaminations.
Certainly WPI have never shown that, and the independent lab cannot be checked, because the independent lab has to be kept…a secret.Â
Yeah, it all makes perfect sense. I think the scientific world is really stunned by this kind of evidence.