proper distribution
Posted with permission:
Mikovits and her colleagues published a paper and accessory materials in
the journal Science, a highly respected journal and have also provided
additional and in some cases more recent information elsewhere. In the
Science publication they report that the XMRV retrovirus occurs in about
2/3rds of CFS/ME patients but only in 3.7% of normal controls. They also
report that subsequently, using a more sensitive assay, XMRV occurs in over
90% of CFS/ME patients - we don't know what the percentage is for normal
controls using that more sensitive assay.
The virus was originally isolated from some aggressive prostate cancer
cells. In addition, in unpublished data, it is also apparently shows high
prevalence in fibromyagia patients and in atypical multiple sclerosis (MS)
patients.
Comment: These data apparently show that XMRV is not specific for CFS/ME
but rather occurs in other disease states, as well as in some normals. My
own view is that this makes it much more likely to be an opportunistic
disease, caused by the changes in immune function and other properties of
these diseases, rather than a primary cause. Specifically, the retrovirus,
based on its DNA sequence, has its replication stimulated by NF-kappaB
activity, an activity that is elevated as part of the NO/ONOO- cycle and
has been reported to be elevated in CFS/ME. Furthermore, the low NK cell
activity and other types of immune dysfunction, that occurs in these
various diseases, may also be expected to stimulate the ability of the
virus to maintain itself in disease sufferers.
In order to show that it is the primary cause of CFS/ME, it is necessary to
show that XMRV follows Koch's postulates, but so far it does not apparently
follow Koch's first postulate, which requires that it always occurs in
people with the disease but does not occur in normals. The other three
Koch's postulates have not been tested.
In contrast to that, we have a good fit to the five principles underlying
the NO/ONOO- cycle for both CFS/ME and fibromyalgia. Because one can argue
that the fit to these five principles serve very much like Koch's
postulates for NO/ONOO- cycle disease, I will argue that we have a
substantially more compelling case for a NO/ONOO- cycle etiology than we do
for an XMRV infectious etiology for either CFS/ME or fibromyalgia.
That does not mean that XMRV is unimportant, however. Even if it turns out
to be an opportunistic infection, like mycoplasma and HHV-6 are, it still
may contribute to the etiology of the disease. And it still raises the
question of whether we can cure cases of CFS/ME and fibromyalgia simply by
normalizing the NO/ONOO- cycle as opposed to normalizing it and also using
antivirals to depress XMRV and/or HHV-6. This is a question and I don't
claim to have the answer to it, although my hope is that normalizing the
cycle will also cure at least some of these infections, that may not be
true.
There have been comments in the media to the effect that this finally shows
that CFS/ME is physiological, not psychological. This is true, but this
should have been obviously true anyway, at least six or seven years ago.
Nevertheless the media coverage of CFS/ME obtained by Mikovits and
her colleagues must be viewed as a true gift to those interested in
extending public knowledge of this disease.
Martin L. (Marty) Pall
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