Abstract
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.
Stealth Viruses
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).
Viteria
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.
Significance
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.
References
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 toccidlab@hotmail.com
