As Chronic Lyme Disease?
This article reviews the basis for believing that stealth virus infected patients are being inadvertently diagnosed as having chronic Lyme disease. With only a few exceptions, blood samples from patients being treated for chronic Lyme disease have tested positive in an assay designed to detect stealth-adapted cytopathic viruses. It is known that a stealth virus has assimilated bacterial sequences, some of which are related to genes of Borrelia burgdorferi, the causative agent of classical acute Lyme disease. The presence of bacteria-derived sequences, rather than actual Borrelia bacteria, may account for the positive serological and molecular based assays that are often, but not always, seen in patients labeled as having chronic Lyme disease. The partial clinical response seen in response to antibiotic therapy may reflect the known capacity of certain antibiotics to suppress the production of virus-growth-enhancing chemokines. If the hypothesis of this paper is correct, then many patients currently being classified as having chronic Lyme disease, may respond to therapies being developed for stealth virus infections.
Lyme Disease Diagnosis
Laboratory support for a clinical diagnosis of chronic Lyme disease is currently provided by positive results in various antigen, antibody and/or molecular based assays for Borrelia burgdorferi. Inter-laboratory variability in the performance, reading and interpretation of Lyme disease testing has thrown into question the reliability of such assays, even to the extent that the clinical diagnosis is not infrequently sustained even in the face of negative or inconsistent laboratory findings. Conversely, over time, many patients already diagnosed as having Lyme disease on the basis of positive serological tests are now revealing additional positive assays to such diverse infectious agents as Babesia, Ehrlichiosis, Mycoplasma, Chlamydia, human herpesvirus-6, parvo virus, etc.
Chronic Fatigue Syndrome (CFS)
The clinical manifestations of patients currently labeled as having chronic Lyme disease are essentially indistinguishable from those exhibited by patients categorized as having chronic fatigue syndrome (CFS). In turn, a CFS diagnosis merges with vaguely defined conditions such as fibromyalgia, Gulf War syndrome and depression. Relevant to the present discussion, several CFS patients from non-Lyme disease endemic regions, such as Los Angeles, are showing positive serological test for Borrelia. Centers for treating Lyme disease are springing up with no basis beyond a positive Borrelia antigen and/or antibody test.
The Center for Complex Infectious Diseases has focussed on atypically structured viruses that evade the immune system because they no longer possess the major antigenic targets required to evoke effective anti-viral cellular immunity. Their capacity to evade immune defenses led to the use of the term "stealth" to describe such viruses. In spite of the loss of certain viral antigens, stealth viruses are still able to replicate in, and to cause damage to, cells. The mechanisms that allow for stealth viruses to retain and/or regain their cytopathic (cell damaging) activity are not yet understood, but are likely to be related to their capacity to capture additional genes from infected cells (discussed below). Although stealth viruses describe a diverse group of structurally distinct viruses, they share a general property of inducing a foamy vacuolating cytopathic effect (CPE) in cells of multiple species. They are, therefore, most readily detectable using in vitro culture techniques that are based on observing this characteristic CPE.
Stealth viruses were initially detected in patients with CFS. They have since been positively correlated with a wide range of neurological, psychiatric, auto-immune and malignant diseases. An obvious question is whether stealth virus infections could be misdiagnosed as chronic Lyme disease. If so, what is the explanation for the variably positive antigen, antibody and/or molecular probe based assays that use reagents that react with Borrelia bacteria?
In approaching this problem, CCID has been successful in demonstrating positive stealth virus cultures in blood samples from over 90% of patients referred with a diagnosis of chronic Lyme disease. By comparison, the incidence of a positive stealth virus culture among healthy blood donors and healthy non-medical personnel is less than 15%. The high prevalence of stealth virus infections in patients with chronic Lyme diseases matches well with similar high prevalence rates in CFS patients and patients with other forms of stealth virus associated illnesses (discussed below).
An explanation for the positive Borrelia bacteria based assays may lie in the additional capacity of stealth viruses to assimilate bacterial genes. Normally, viruses that are infectious for human or animal cells (eukaryotic cells) will not infect bacteria (prokaryotic cells). Stealth viruses appear to have overcome this phylogenetic barrier. The term "viteria" has been coined to define eukaryotic viruses that have acquired bacteria-derived genetic sequences. The sources of the bacteria sequences include both eubacteria and archaebacteria and both cell wall containing and cell wall deficient bacteria.
Where do stealth viruses capture bacterial genes?
There is increasing evidence for the direct infection of various bacteria by stealth viruses, including the culturing of bacteria with unusual biochemical profiles from stealth virus infected patients. The assimilation could also occur within eukaryotic cells that are dually infected with a stealth-adapted virus and intracellular bacteria. Among the more notable intracellular bacteria are those that lack rigid cell walls. These include spirochetes, of which Borrelia burgdorferi is a prime example; Mycoplasma fermentans and incognitus; and Rickettsiae. Since these bacteria do not have sterol synthesizing capacities, they are entirely dependent on the infected cell to provide their lipid cell walls. As noted above, lipid ladden cells are a hallmark of the CPE induced by stealth viruses. By simply co-culturing stealth viruses and Borrelia burgdorferi, one can observe a marked enhancement in the intracellular growth of the Borrelia (personal observation). To one extent, this could suggest that an underlying stealth virus infection could create an in vivo environment of Borrelia growth promoting cells.
The rich variety of bacterial sources that have seemingly contributed to the prototypic viteria suggests a diverse array of bacterial-related antigens. Very few, if any, of the currently available commercial assays for Borrelia utilize strict criteria for specificity. At this time, it is considered more likely that within the broad scope of assimilated bacterial sequences, some would be found that simply cross react with the reagents commonly used in Borrelia testing.
Response to antibiotics
An argument advanced for Borrelia infection is that many patients show a partial clinical response following the administration of certain antibiotics. This conclusion discounts the various cellular activities mediated by antibiotics outside of their direct effect on bacteria. For example, erythromycin and clarithromycin (Biaxin) are known to suppress the cellular synthesis of chemokines. This observation is relevant, since at least some stealth viruses have multiple genes encoding both chemokine and chemokine receptors.
If the hypothesis of this paper is correct, patients mistakenly being diagnosed as having chronic Lyme disease should benefit from courses of therapy designed to suppress stealth viruses. Ongoing studies are evaluating the use of a combination of anti-oxidant, anti-rheumatic, antibiotics, and other drugs known to down regulate chemokine production. Patients should have their clinicians contact CCID for additional information.
Published articles on stealth viruses and viteria can be found on the web site www.ccid.org Any additional inquiries can be addressed to CCID at 3328 Stevens Avenue, Rosemead CA 91770 or via e-mail email@example.com