The inquiry came from the
mother of a long-time, stealth virus infected boy. Her
father, an elderly retired physician, had multiple myeloma.
He had been depressed for years and probably had the same
virus that had infected her son and herself. Would I do
virus testing?
The result was strikingly positive. Similar strong positive
results were found in numerous other multiple myeloma
patients. About the same time, researchers at UCLA were
suggesting a role for human herpesvirus-8 (HHV-8) in this
illness. Their findings have met with resistance from the
scientific community because standard assays for HHV-8 were
yielding inconsistent and often negative results. I
submitted a paper to Lancet co-authored with Dr. Brian Durie,
the physician who was treating the elderly physician and who
had provided blood samples from other patients. As with some
other attempts at publication, the long drawn-out
communication with an Editor led to a final rejection. Yet,
the data were unmistakable. In a well controlled blinded
study, all ten blood samples from multiple myeloma patients
were scored strongly positive, in contrast to none of the
ten control samples.
The elderly physician went on to receive ganciclovir to
which he seemingly partially responded. His daughter
developed a uterine cancer, while the son has continued to
live only a half-life because of persisting brain
dysfunction. He has remained stealth virus positive for over
10 years.
Dr. Durie confirmed that many of his multiple myeloma
patients had a prior, or co-existing, neuropsychiatric
illness. Moreover, he pointed out that several patients had
family members with complex neurological illnesses,
including a mother with two autistic children.
A bigger lead came when Dr. Durie suggested that a patient
might help support our research on multiple myeloma.
Previous grant applications, including two submissions to a
Foundation managed by Dr. Durie’s wife, had been turned
down. CCID was provided with $5,000.00 and the promise of an
additional $10,000 if he tested positive. Unlike all but one
other multiple myeloma patients tested, his blood did not
show a rapid positive response. On further testing, a
delayed positive result was obtained, but the information
was too late to secure funding.
Why the exceptional result? It turned out the patient was
being treated with thalidomide. Moreover, the UCLA and a
European research team had both noted suppression of the
putative HHV-8 in a patient receiving thalidomide.
Thalidomide was also reducing tumor burden in these and in
larger groups of patients.
This finding fitted well into the overall scheme that
cytokines, including chemokines, were potentially regulating
the levels of stealth virus activity. Thus, the generally
accepted mode of action of thalidomide was considered to be
primarily to suppress the cytokine, tumor necrosis factor (TNF),
a known stimulus for chemokine production.
It also argued that other forms of chemokine reduction, as
being proposed for stealth virus infected patients with
neurological illnesses, should be tried in patients with
multiple myeloma. Efficacy could be assessed not only by a
reduction in stealth virus load, but also by a reduction in
tumor load and improvements in any accompanying
neuropsychiatric symptoms.
In preparation for such a trial, I have tabulated many of
the known herbal and proprietary medicines reported to
suppress various stages in the complex processes leading to
chemokine production. These include thalidomide and
clarithromycin, an antibiotic that Dr. Durie has also found
to be useful in some of his multiple myeloma patients.
Following the lead of rheumatologists, there may be
advantages to using low doses of a combination of
differently acting therapies, rather than relying upon a
sinle agent.
Multiple myeloma patients interested in such an approach to
therapy should relay this information to their clinician.
The clinician should contact CCID for further information
and to schedule stealth virus testing. Repeat testing will
be provided 7-10 days after the initiation of selected
therapy.