April 12, 2010: Whittemore Peterson Publicly Challenges UK Researchers to Collaborate on XMRV & ME/CFS Research
Annette Whittemore, Founder & CEO of the Whittemore-Peterson Institute, issued the following public letter to ME/CFS researchers in the UK – essentially challenging them to collaborate in studies of the ME/CFS and the XMRV retrovirus, so as to move the science forward.
The open letter is addressed to Myra McClure, co-author with Simon Wessely of the editorial “Chronic fatigue syndrome and human retrovirus XMRV - Three studies now refute the original study reporting the link” published Feb 25, 2020 in the BMJ (British Medical Journal). It states, in part, “In January 2010, our own group found no evidence of XMRV in a well characterised cohort of 186 patients with chronic fatigue syndrome in the United Kingdom.” Dr. McClure is professor of retrovirology at Imperial College London. Dr. Wessely is professor of psychological medicine at Kings College, London.
The following letter may be reproduced by permission of the WPI.
Whittemore Peterson
Institute for Neuro-Immune Disease
Annette.Whittemore@WPInstitute.org
April 12, 2010
Dear Dr. McClure:
On behalf of the Whittemore Peterson Institute in Reno, Nevada (“WPI”), I am writing you today to ensure that there is direct communication between WPI and your research team.
You may share this letter with others that you deem appropriate, and I will do the same by sharing this letter with other interested parties in both the United States and the United Kingdom.
On January 6, 2010, you reported in PloS One that you failed to detect xenotropic murine leukemia virus-related virus (“XMRV”) in ME/CFS patient samples.
In that publication you reported the following conclusion, “based on our molecular data, we do not share the conviction that XMRV may be a contributory factor in the pathogenesis of ME/CFS, at least in the U.K.”
You subsequently made the following statement in your commentary regarding the Netherlands study in the BMJ, “….van Kuppeveld and colleagues provide the additional information reported at a conference last year that the patients in question came from an outbreak of chronic fatigue syndrome at Incline Village on the northern border of Lake Tahoe in the mid-1980s.”
This statement about the origin of the 101 patient samples is untrue. The patients in the Science study were well defined in the paper as having CFS by the Fukuda and Canadian consensus definitions of ME/CFS.
More importantly the patient samples did not come from the “Lake Tahoe outbreak” as you assert, but rather from patients who had become ill while living in various parts of the United States.
We would also like to report that WPI researchers have previously detected XMRV in patient samples from both Dr. Kerr’s and Dr. van Kuppeveld’s cohorts prior to the completion of their own studies, as they requested.
We have email communication that confirms both doctors were aware of these findings before publishing their negative papers.
In addition, Dr. van Kuppeveld asked for and received reagents and a positive patient sample to determine if his testing procedures could in fact detect XMRV in a positive blood sample before he published his paper. We wonder why these materials were not used in his study which also failed to detect XMRV.
One might begin to suspect that the discrepancy between our findings of XMRV in our patient population and patients outside of the United States, from several separate laboratories, are in part due to technical aspects of the testing procedures.
To help identify the possible reasons for the discrepancies in detection of XMRV, WPI would like to send you known positive patient samples with controls, from the United States in an appropriate number, along with WPI reagents, so that we can help you determine whether your testing methodologies will accurately detect XMRV in a clinical sample of blood.
In addition, WPI would be willing to test a like number of samples from your patient cohort to see if our researchers can detect XMRV in those samples.
This critical exercise would help resolve the question of whether you are using all of the appropriate techniques necessary to detect XMRV in a patient’s sample.
If your tests are able to detect XMRV correctly in the known positives, then the debate can appropriately center on whether we can identify the differences in the patient cohorts which have been the subject of
various studies.
It is in this systematic manner that we all may help to move the science forward; instead of continuing to debate whether or not ME/CFS patients in Europe are infected with XMRV.
It is also important to note that our initial study was not intended to prove causality of ME/CFS, but to report a significant association between patients who had been diagnosed with ME/CFS and XMRV.
We believe that there exists compelling evidence to spur additional scientific review, especially in light of the fact that our team of researchers also discovered XMRV in the blood of 3.7% of our non contact controls.
I look forward to your timely reply.
Sincerely,
Annette Whittemore
Founder and CEO
Whittemore Peterson Institute
posted by Ingrid J. Jones at Tuesday, April 13, 2010
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