The authors "have recently discovered that the cell lines used in their paper were inadvertently misidentified. The cell lines utilized in the paper have now been found to contain the bcr/abl translocation and most likely represent the K562 CML cell line, instead of MMS1 and RPM1 myeloma cell lines. Due to this issue, the relevance of the findings to myeloma and thus, the conclusions of the paper, are not supported by the data."Similarly, if the XMRV study used contaminated, then the conclusions of the paper are presumably not supported by the data.
I have a ton more information about this, some of it far more convincing than what I've shared here, but much of that knowledge has come from Dr. Cheney's postings to his patients via our Yahoo group. Those posts are, unfortunately, confidentialmake me very very skeptical. You obviously have far more of a vested interest in this than a neutral observer, and relying on and appealing to secret evidence makes your case seem weaker instead of stronger.
Most of the negative studies failed to find any evidence of XMRV in any sample type. This would suggest that the methods and materials used in the non-replication studies are insufficient to use when attempting to detect human gammaretrovirus in the blood of human samples. The methods, processes, and materials of Lombardi et al. need to be followed precisely. The Alter and Lo study is the only study which has attempted a partial replication of the methods and materials of the Lombardi study, which confirmed evidence of MLV related viruses. Studies using multiple different methods are not replication studies, and studies optimized to detect murine gammaretroviruses and not human gammaretroviruses must be seriouslyIf the main criticism of the study is that the methodology itself is severely flawed, why would studies be done that replicate the exact methodology? Wouldn't more robust findings result from studies with diverse methodologies that all reach the same conclusion? Wouldn't a need to replicate a study with the exact materials in order to get the same results point even more conclusively to a flawed methodology?
questioned. See, Virulence attachment.
and studies optimized to detect murine gammaretroviruses and not human gammaretroviruses must be seriously questioned.Doesn't the "M" in "XMRV" and "X-MLV" stand for murine?
Bioreagent contamination, however, does not adequately explain the detection of XMRV by Lombardi et. al. (5). We have found that the DNA sequences of 3 XMRV proviruses they described are identical to that of VP62, which is the prototype XMRV cloned from prostate cancer tissue (4). Long-term passage of VP62 led to proviruses with accumulated multiple point mutations (fig. S3). As suggested by others (30), independently derived XMRV DNA sequences should show increased genetic diversity compared to the VP62 clone sequence. Therefore, the remarkable conservation of the WPI-XRMV sequences is most consistent with laboratory contamination with the original infectious VP62.but their response essentially argues that other means of detection are not adequate
We conclude that XMRV was generated as a result of a unique recombination event between two endogenous MLVs that took place around 1993–1996 in a nude mouse carrying the CWR22 PC xenograft. Since the probability that the same recombination event could occur independently by random chance is essentially negligible, any XMRV isolates with the same or nearly the same sequences identified elsewhere originated from this event (23).In other words, if these were legitimate XMRV infections in human hosts, the viral DNA should show significant mutations, both between hosts and compared to the laboratory cloned sample. There is little evidence of mutations in the WPI and VIPDX samples, therefore we can conclude that they all came from the same source.
You expect us to believe that you can nail down the exact years and location where XMRV was created? Then you want us to believe that because CFS and prostate cancer were around before your date, that it can’t possibly be the cause of the illnesses. You also want us to believe that XMRV is not the kind of lab contaminant that would jump into the human population and cause disease. Yeah, OK. I can understand why you may be hesitant to be honest here — the stakes are very high. If the way science is conducted can result in new retroviruses invading the human population then every lab everywhere, from college campuses to drug companies, will have to change the way they do research. You’re right, it’s probably best to just to cover up the dangers. It’s just a couple million whiny women anyway….Otherwise I pretty much agree with everything muddgirl said. I hope for relief of CFS suffering, but bet the major causes will turn out to be way stranger than any of our current suspects. I say this as somebody who has a chronic disease of unknown provenance.
I am writing this Editorial Expression of Concern and asking for the voluntary retraction of this study because it’s too much like a bad sci fi movie .
What Alberts did smacked of science by declaration – even censorship, I thought.I have yet to see a complete response from WPI to the papers published on Science Express last week (although I presume such a response is forthcoming), which present pretty convincing evidence that the Lombardi paper does not show a legitimate connection between XMRV and CFS or prostate cancer (note that the dissenting researchers were very clear in stating that they have not disproven all viral causes of CFS, so papers which indicate some viral cause without specifically identifying XMRF aren't helpful for this issue).
Why, therefore, should a retrovirus, akin to HIV, that may be infecting millions worldwide be subject to a process that has controversy, debate and procrastination in-builtYes, why SHOULD a potentially-dangerous medical treatment be subject to rigorous scientific testing? Why not just dose 'em all up and let God sort the out?
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posted by muddgirl at 8:29 AM on May 31, 2011