It is now irrefutable that these viruses exist. The most compelling data comprise the actual sequences identified within a prototype stealth-adapted virus that was unequivocally derived from an African green monkey simian cytomegalovirus (SCMV). This species of monkey was routinely used to produce live polio virus vaccine. Studies dating back to 1972 showed that monkeys were a potential source of cytomegalovirus contamination of polio vaccine lots. These data were never made public because of a flaw in the Government regulatory process that treats data obtained on regulated products as proprietary, and therefore protected, from open disclosure.
Strong supportive data for stealth-adapted viruses, have also come from animal transmission studies; double blind viral culture analyses; and both histological and electron microscopic findings on human brain biopsies (See www.ccid.org for details and copies of peer-reviewed publications).
The notion of "stealth-adaptation" has been difficult for many virologists to accept. There was also understandable reluctance among those supportive of both the pharmaceutical industry and Government agencies to acknowledge potential safety problems with vaccines. Hopefully, these obstacles will yield to an increasing public awareness of the damage being caused by the continued disregard of the existence of such viruses.
Various conclusions have been drawn from the available sequence data on the prototype stealth virus. Specifically, the stealth virus uses a novel strategy for replication. It has the capacity to "capture, amplify and mutate" genetic sequences assimilated from infected cells, other viruses and bacteria. This process can help explain how stealth-adapted viruses could be mistaken for either bacteria, such as mycoplasma, Borrelia, chlamydia and Rickettsia, or for conventional viruses, such as HHV-6, CMV, EBV, parvovirus, enterovirus, etc.
As exemplified in the book, "The Virus Within," it is easier, even if misleading, to ascribe illnesses to a named potential pathogen, in this case HHV-6, than to grasp and effectively present the concept of stealth adaptation. Certain laboratories committed to diagnostic studies on conventional viral and bacterial pathogens also have understandable financial reasons not to acknowledge potential misinterpretation of their assays. Large sums of monies have been applied to misguided tests and clinical studies. Patients infected with stealth viruses have also been unnecessarily segregated into various support groups that have tended to be competitive with each other, rather than present a unified demand for Public Health action.
Instead of pursuing a multiplicity of probably misdiagnosed conventional infectious agents, I feel that individual patients should simply request from Congress, FDA and CDC, an explanation for the published sequence data on the prototype SCMV-derived stealth-adapted virus. Five years ago, both agencies declined to support stealth virus research, essentially stating that it was unrelated to their mission. With fresh leadership, possibly more open minds, and an attentive Congress, it may be difficult for the Government to continue to disregard the Public Health threat posed by atypically structured (stealth-adapted) viruses.
On a more promising note, the marked expansion of chemokine receptor coding genes within the prototype stealth virus, suggests a rational approach to suppressing stealth virus activity. The actual sequence data are available on GenBank and will appear shortly in published form. These data have led to useful considerations regarding therapy. In particular, it explains the potential use of antibiotics, not as anti-bacterial agents, but as a method to suppress chemokine production. As many of you know, the apparent benefit of antibiotics, such as Biaxin, in patients labeled as having chronic Lyme disease, has been used as evidence for an active bacterial infection. A similar argument applies to the postulated role of mycoplasma in the Gulf war and chronic fatigue syndromes. By re-addressing these illnesses as stealth virus infections, one can augment chemokine-suppressing antibiotic therapy, with many other anti-chemokine and anti-viral acting drugs. More importantly, one can directly assess stealth virus activity using sequential viral cultures from blood samples. Similar therapeutic studies can be conducted in stealth virus infected animals. An unpublished article entitled "Chemokines and Stealth Viruses: A Blueprint for Therapy in Infected Humans and Animals" is accessible in the "Therapy Section" of CCID website www.ccid.org Patients may wish to share this information with their physicians.
I trust these comments will be useful to many of you coping with complex multi-system illnesses. Please feel free to contact me via e-mail at ccidlab@hotmail.com
W. John Martin, M.D.,Ph.D.
