I would like to respond to the recent discussion regarding the label of chronic Lyme disease for the illness affecting many individuals subscribing to this list. My introduction to this illness came from a telephone call from Dr. Burrascano nearly 3 years ago. He wanted to know if some of his patients were virally infected. I began to test blood samples from his patients using a viral culture method developed for atypically structured (stealth-adapted) viruses. Blood samples consistently yielded positive results. This led to a long telephone call one Friday afternoon with a member of Dr. Burrascano’s staff. The description of the patients being seen by Dr. Burrascano matched that of patients being diagnosed elsewhere within the United States with chronic fatigue syndrome (CFS). The similarity extended to the apparent spread of disease to other family members, including children.

I expressed the view that stealth virus infected patients were possibly being misdiagnosed as chronic Lyme disease in a brief internet submission in September 1999 (available at www.ccid.org). My opinion was based on the following observations: The presently used diagnostic tests for Borrelia infection were questionable in their specificity. I soon learned that clinicians had their choice of using a laboratory that would provide mostly positive results, or one that would give mostly negative results. The commonly used test was flawed since it relied on a mixture of polyclonal (broadly-reactive) antibodies, with known false positives from several sources. Similarly, the Borrelia western blots were biased since, unlike HIV western blots, the antigens were predominately those of the pathogen. The PCR assays were not routinely validated by direct sequencing of the amplified products, and even if performed did not necessarily prove the presence of intact bacteria. Discordant results in the various tests were puzzling to both patient and clinician, but commonly overlooked in favor of making a diagnosis. Even patients testing negative in all such tests were still being labeled as having chronic Lyme disease. Similarly, the negative results with a recently introduced, sensitive ELISA based anti-peptide antibody assay, are apparently being disregarded by those promoting the diagnosis of chronic Lyme disease.

Arguments in favor of chronic Lyme disease have included a favorable response in some patients to antibiotics, and a worsening of symptoms soon after the administration of antibiotics (likened to a Herxheimer’s reaction seen in syphilitic patients). Antibiotics can have biological actions apart from their anti-bacterial effects and Herxheimer-like reactions commonly occur in CFS patients receiving various types of new medications. More relevant to the discussion is the influence of support organizations formed to sponsor research and political awareness of chronic Lyme disease, with resulting pressure on medical insurance companies to provide reimbursements for a named entity. "We can accept the idea that Lyme patients may also be infected with a stealth-adapted virus, but we will not forego our interest in maintaining the Lyme disease label" was a typical response.

An argument against persisting with the concept of chronic Lyme disease in stealth virus culture positive patients is that it leads to inadequate and misdirected therapy. More importantly, it removes from the Public Health agenda, the responsibility to face the existence of newly emerging pathogens in the form of atypically structured (stealth-adapted) viruses. It also maintains the artificial separation of many clinical syndromes that may well have a common underlying infectious cause. All too often families come to realize the interconnection between those being labeled with Lyme disease and those with psychiatric, neurological, auto-immune, and malignant illnesses.

The existence of stealth-adapted viruses is clear from the sequence data obtained on a virus derived from an African green monkey simian cytomegalovirus (SCMV). This virus undoubtedly arose from a live polio virus vaccine produced on kidney cells from an African green monkey. It has acquired genes of both cellular and bacterial origins. Among the bacterial genes are sequences that overlap with known genes of Borrelia and other bacteria. The acquisition of bacterial sequences by stealth-adapted viruses (viteria) can, therefore, potentially explain positive findings in low specificity testing for Borrelia seen in a number of stealth virus infected patients.

Of therapeutic interest is the remarkable expansion of chemokine and chemokine-receptor related gene sequences in the prototype stealth-adapted virus. This has led to the trial of various chemokine/cytokine suppressing medicines to treat stealth virus infected patients. Clarithromycin (Biaxin) is one such medicine since, in addition to its anti-bacterial properties, it is able to suppress Activating Protein-1, along the pathway to NFkappaB and chemokine activation. Certain chemokines are also known for their potential oncogenic activity. The SCMV-derived stealth-adapted virus has several copies of a chemokine gene implicated in melanomas, prostate cancers and brain tumors. Such findings underscore the potential major Public Health threat being posed by stealth-adapted viruses.

In summary, attributing the complex illnesses being experienced by an increasing number of patients to Borrelia burgdorferi, may well have the adverse effects of impeding progress in the development of effective therapies, and of delaying Public Health efforts in coming to terms with the existence of atypically structured, stealth-adapted viruses.

W. John Martin, M.D., Ph.D.