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."
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, confidential
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 seriously
questioned. See, Virulence attachment.
and studies optimized to detect murine gammaretroviruses and not human gammaretroviruses must be seriously questioned.
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.
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).
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….
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.
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-built
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