W. John Martin, MD, PhD. Summary of Research on Stealth Adapted Viruses in Chronic Fatigue Syndrome (CFS) Patients and the Potential for Therapy of These Viruses via Activation of the ACE Pathway

    SOUTH PASADENA, CA, September 24, 2012 /24-7PressRelease/ -- I began using the polymerase chain reaction (PCR) on blood samples from CFS patients in the late 1980's and reported low-level positive results in approximately a third of the tested samples. A 1990 brain biopsy from a patient whose illness began as CFS, was also PCR positive. Yet microscopic examination of her brain tissue showed no inflammation; the accepted hallmark of an active virus infection. This disparity implied that the brain-infecting virus, which was presumably responsible for the positive PCR, was not capable of activating the cellular immune defense mechanism. Cellular immunity typically targets relatively few of the components coded for by the virus genome. It is possible, therefore, for a virus to lose or mutate small portions of its entire genome as a means of evading effective immune recognition. I termed this immune evasion mechanism "stealth adaptation."

Renewed efforts at culturing cell damaging (cytopathic) viruses from CFS patients and from patients with more severe psychiatric and neurological illnesses, yielded consistent and unmistakable positive results. Cell damage was primarily seen as the formation of foamy vacuolated cells, which tended to fuse into small clusters. The cultures were shown to other CFS researchers, including Dr. Paul Cheney, who was being supported by the CFIDS Association of America. The Centers for Disease Control and Prevention (CDC) was also informed of the results. In 1991, an aliquot of a clearly positive culture derived from the cerebrospinal fluid (CSF) of a comatose patient with a history of bi-polar psychosis, was provided to the Los Angeles County Department of Health, which subsequently sent the culture to the California State Health Department.

The early microscopic appearances of the cultures were somewhat suggestive of foamy viruses. These are retroviruses, which have incorporated an additional gene, which by itself, is responsible for the foamy cell appearance of infected cells. Actual sequence data obtained on two of the early isolates, however, indicated a more probable origin from cytomegalovirus (CMV), a type of herpes virus.

Definitive DNA sequence data were obtained in 1995 on a virus, repeatedly cultured from the blood and CSF of a CFS patient. The data showed an unequivocal origin from African green monkey simian cytomegalovirus (SCMV). So too did the 1991 virus isolate provided to the County Department of Health. Some other cultured viruses appeared to be related to SCMV, while others were more likely derived from human herpes and human adenoviruses. Stealth adaptation was, therefore, viewed as a generic process, which could potentially occur with all viruses.

The SCMV origin of several stealth adapted viruses clearly implicated probable contamination from African green monkeys, which were still routinely being used to produce live polio virus vaccines. In June 1995, I conveyed this important information to the Food and Drug Administration (FDA), CDC, Los Angeles County Health Department, the polio vaccine manufacturer and officials at the University of Southern California, where I was working as a tenured professor of pathology.

In 2002, I proceeded with an approved study with the Blood Bank at the University of California, Irvine. Consistent with other surveys, approximately 10% of the donated blood samples tested positive by culture. This left the CDC with the dilemma of having to accept the results or fabricate deficiency with the testing methodology. Personal from the California Department of Health acting as inspectors for the Centers for Medicare and Medicaid (CMS) and, by their own admission, working in conjunction with CDC, deemed that testing for stealth adapted viruses had placed the Nation's health in "Immediate Jeopardy" and that all further clinical testing or even use of stored blood samples was prohibited. Detailed copies of all procedures were taken by the State Health Department along with my request that they please undertake their own testing.

A disgruntled patient and vindictive CFS patient support group played into the hands of the CDC by making false and malicious assertions regarding stealth adapted viruses. Unfortunately, the assertions are easily viewed on the internet and have discouraged many from either supporting or learning from my research.

With limited resources, the research focus moved to understanding an alternative cellular energy (ACE) pathway. This pathway provides a non-immunological healing mechanism, which is able to suppress and even reverse the cellular damage caused by stealth adapted and other viruses. The ACE pathway can be easily self-monitored using a fluorescence screening method and can be enhanced with various simple interventions, including lifestyle changes. Community based implementation and evaluation of methods of enhancing the ACE pathway in the prevention and suppression of illnesses caused by stealth adapted and other viruses should become major public health goals.

Federal health authorities have been willing to spend millions of dollars in pursuit of obviously flawed prior studies on the possible role of mouse retroviruses in CFS patients. They have been far less willing to publicly acknowledge research on the existence of stealth adapted viruses. This reluctance to do so is explained in part by the unequivocal origin of some of these viruses from the monkeys used to provide live polio virus vaccines. Therapy for stealth adapted viruses, based on activation of an alternative cellular energy (ACE) pathway, appears promising and warrants further evaluation.

# # #