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
Messaggio modificato da akela, 13 aprile 2010 - 11:16:39
