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.
