What are Stealth Viruses?
Viruses
are submicroscopic infectious agents that replicate inside cells. Viral illnesses
are normally controlled by the body’s immune system acting primarily through
white blood cells called lymphocytes. These cells recognize certain viral proteins
that provide the antigens targeted by specific lymphocytes, leading to an anti-viral
inflammatory response. Not all viral proteins, however, can function as antigens
for effective anti-viral immunity. Indeed, for many viruses, only a very few
proteins are involved in lymphocyte recognition of virally infected cells. Loss
of these critical antigenic proteins can allow a virus to essentially go unrecognized
by the cellular immune system. When such viruses have managed to retain the
capacity to damage cells, they can potentially cause a persistent infection
resulting in a prolonged illness. The viral nature of such an illness is usually
overlooked because of the absence of overt inflammation. Atypically-structured
cell-damaging (cytopathic) viruses were initially identified in patients with
the chronic fatigue syndrome and in patients with more severe neurological and
neuropsychiatric illnesses. The term “stealth” was introduced to highlight their
basic property of evading effective immune recognition, and also because they
had gone unrecognized by the medical community.
Detection of Stealth Viruses
Stealth-adapted
viruses can be most readily detected using specialized, semi-quantitative, viral
culture methods developed and refined over the last decade. Using these procedures,
stealth viruses will typically induce a characteristic vacuolating cytopathic
effect (CPE) in cultures of human and animal-derived cells. Stealth
virus infected cultures can be distinguished from cultures of conventional herpesviruses,
adenoviruses, enteroviruses and retroviruses, by the appearance and host range
of the CPE, and also by using selective immunological and molecular probe based
assays, including polymerase chain reaction (PCR) testing methods.
Cytopathic Effects
A
common feature of the CPE-induced, stealth adapted viruses is marked metabolic
disruption. This is expressed as lipid accumulation, cytoplasmic vacuolization,
formation of aberrant protein and lipoprotein inclusions, and abnormally shaped
nuclei. Comparable foamy vacuolating cellular changes with atypical inclusion-like
structures can be seen in detailed examination of brain and other tissues obtained
from stealth virus infected patients and from animals inoculated with these
viruses. Unlike infections caused by conventional cytopathic viruses, the actual
production of readily identifiable viral particles is uncommon. Seemingly, the
infected cells are metabolically impaired because various energy and other resources
are diverted towards an inefficient and unbalanced synthesis of various virus
coded components at the expense of normal cellular functions. Severe defects
in energy-generating metabolic pathways are also apparent from the marked mitochondrial
changes that are prominent in electron micrographs of virus-infected cells.
Center
for Complex Infections Diseases
Both
clinical- and research-based studies on stealth-adapted viruses have been undertaken
at the Center for Complex Infectious Diseases in Rosemead, California. CCID
is a non-profit organization under the National Heritage Foundation dedicated
to understanding the nature, origin, disease associations, modes of transmission,
methods of diagnosis and responses to therapy of stealth virus infections, and
to the dissemination such information to the medical and lay communities. Information
regarding CCID is available from the internet at www.ccid.org. Additional information is available
from www.EmergingWorlds.com. The
following sections provide a brief overview of some of the ongoing research
activities being conducted at CCID.
DNA Sequencing Studies
A stealth virus isolated from a patient with a
chronic fatigue syndrome like illness was originally noted to have limited DNA
sequence homology to human cytomegalovirus (CMV). As additional sequence data
became available, it became obvious that this virus was a derivative, not of
human CMV, but rather of an African green monkey simian CMV (SCMV). Until the
beginning of last year, these monkeys were routinely used to produce live poliovirus
vaccine. Moreover, although not widely revealed, a joint Food and Drug Administration/Industry study in 1972 indicated that control kidney cell cultures from all 12 African green monkeys tested grew out SCMV, and that most of these isolates were not
detectable using standard procedures.
Continued sequencing on the SCMV-derived stealth-adapted virus has shown
interesting changes compared to a typical CMV. Of special note is the uneven
representation of genes that encode various viral components. As expected, the
genes that code the proteins known to provide major target antigens for anti-CMV
cytotoxic T lymphocytes are either absent or mutated. Other genes are overly
represented, including genes that code for various chemokines and for chemokine
receptors. Interestingly, one of the markedly amplified chemokine receptor coding
genes found in the stealth virus genome can also function as a receptor for
HIV, suggesting a possible potentiating role of stealth viruses in HIV infected
patients.
One set of amplified chemokine-coding genes detected in the stealth-adapted
virus is of cellular, rather than viral, origin. Cellular genes can apparently
be incorporated into stealth virus genomes, presumably during viral replication.
The particular chemokine-coding cellular gene identified within the prototype
SCMV-derived stealth virus was probably assimilated as a partially processed
RNA molecule since it lacks the normal introns present in cellular DNA. This
implies that stealth virus DNA replication is proceeding through RNA intermediates,
and that it may, therefore, be dependent upon reverse transcriptase, as could
be provided by an assimilated endogenous retroviruses. RNA to DNA replication
is much more prone to error than is DNA to DNA replication. This might explain
sequence variability between the three copies of the chemokine-coding cell-derived
gene that have so far been identified within the stealth virus.
Chemokine receptor genes of both viral and cellular origins have been
implicated in the development of several types of malignancies. It is somewhat
worrisome, therefore, that the stealth adapted virus is apparently employing
this type of gene for its survival. On the other hand, many therapeutic agents
that appear to be of some benefit to stealth virus infected patients are known
to inhibit cheomkine production and receptor activity.
Viteria
It has also been determined that stealth viruses have the
ability to acquire genetic sequences of bacterial and even fungal origin. 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 bacterial sequences include microorganisms that are not known
to grow intracellularly within eukaryotic cells. This strongly suggests that
stealth viruses become viteria by infecting bacteria. Judging from the bacterial
sequences so far identified, genes have been captured from a wide variety of
both gram positive and gram negative bacteria. The linear arrangements of many
of the bacterial-derived sequences are quite different from any of the known
major bacteria, suggesting that an active ongoing selection process may be occurring
to assist in stealth virus propagation within bacteria. Genetically empowered
bacteria, carrying potentially oncogenic stealth-adapted viruses, could become
a far more threatening biological weapons program then ever envisioned by military
planners.
Bacterial sequences incorporated within stealth-adapted
viruses may help explain positive findings in stealth virus infected patients
in various tests for known bacteria, including Borrelia burgdoferi (the cause
of authentic Lyme disease), mycoplasma (a suggested cause of CFS and Gulf war
syndrome); chlamydia (implicated in coronary artery disease and Alzheimer’s
disease), etc. None of the commonly used assays for these bacteria actually
detect cultured organisms, but instead rely upon broadly reactive molecular
and/or serological testing that could as easily be explained by the presence
of viteria.
Clinical Conditions Associated with Stealth Virus Infections
Stealth-adapted
viruses have been recovered from the blood, cerebrospinal fluid, urine, throat
swabs, breast milk, brain biopsies and tumor samples from patients with various
neurological, psychiatric, auto-immune, allergic and neoplastic diseases. Examples
of neurological illnesses are autism, attention deficit and behavioral disorders
in children; depression, schizophrenia, amyotrophic lateral sclerosis, multiple
sclerosis, chronic fatigue and fibromyalgia in adults; and neurodegenerative
illnesses in the elderly. It is now known that the stealth viruses can infect
many organs, but that the brain is especially prone to manifest the effects
of even limited localized cellular damage. The varying manifestations of a stealth
virus encephalopathy is probably heavily influenced by the timing of infection,
regions of the brain that are mostly involved, genetic predisposition to particular
symptoms and the additive pathology of any superimposed auto-immune component
triggered by the viral induced cellular damage. CCID's focus is away from strict
clinical categorization of stealth virus infected patients into discrete neurological
and neuropsychiatric illnesses. This viewpoint has been supported by following
individual patients over several years, and also by the not uncommon occurrences
of related, yet diverse, illnesses occurring among other family members and
even among household pets. Community-wide outbreaks of stealth virus infections
have also been observed with individuals showing varying levels of severity
and duration of illness. Neither the reporting of otherwise unexplainable deaths,
nor the apparent “dumbing” of a whole township, as reflected in the excessive
need for special education for its children, appears to provide adequate Public
Health motivation to confirm CCID’s findings of stealth-adapted viruses.
Cancer can now be added to the list of potential stealth
virus-associated diseases. Positive stealth virus cultures have been seen in
virtually all of the multiple myeloma patients tested, and in several patients
presenting with other types of tumors. A previous history of a fatiguing illness
and clinical indications of impairments in normal brain functions are suggestive
of an underlying stealth adapted virus infection in a cancer patient. It will
be interesting to determine the effect of stealth-virus suppressive therapy
in such patients.
Infection Among Blood Donors
An indication
of the probable prevalence of infection among apparently healthy individuals
has come from studies conducted on student blood donors attending a college
campus. Slightly less than 10% of the units tested gave a positive result. As
a requirement of the study, it was not possible to determine the actual health
status of these students. Nor were efforts allowed to follow recipients of the
stealth virus positive blood units. Even if culture-positive individuals are
presently asymptomatic, this would not preclude their being at risk for subsequent
development of a stealth-virus associated illness. This concern is underscored
by the apparent capacity of stealth-adapted viruses to “capture, amplify and
mutate” various additional genes of viral, cellular and bacterial origins.
Role of Other Infectious
Agents in Chronic Illnesses.
Much of the debate over a potential
infectious cause for many of the illnesses that are increasingly being seen
within our society has centered upon conventional microorganisms. Patient support
groups and their affiliating clinicians have championed alternative explanations
for these illnesses. Human herpesvirus-6 (HHV-6), human herpesvirus-8 (HHV-8),
enteroviruses and parvoviruses feature among the viral causes for these illnesses,
while Borrelia burgdoferi, Mycoplasma incognitos and Ehlichiosis are
being promoted as the bacterial causes for a wide spectrum of illnesses. As
is the case for HHV-6 in CFS, HHV-8 in multiple myeloma, enterovirus in ALS
and Borrelia in chronic Lyme disease, when looked at critically, the actual
findings are generally inconsistent with a true etiological relationship. None
of these negative studies exclude the role atypically structured microorganisms;
indeed, if anything they strongly support their presence. As alluded to above,
stealth-adapted viruses can easily be mistaken in diagnostic tests for conventional
viral and bacterial pathogens.
Additional
complex associations between stealth adapted viruses and conventional microorganisms
may exist. For example, the lipid-laden cells infected with a stealth virus
appear especially favorable to the growth of intracellular bacteria, including
Borrelia, the causative agent of Lyme disease. CCID has demonstrated
positive stealth virus cultures in blood samples from over 90% of patients referred
with a diagnosis of chronic Lyme disease. Whether the patients are actually
infected with Borrelia remains unproven, but if so, their growth may
be dependent upon an accompanying stealth virus infection. Synergistic growth
patterns between stealth adapted viruses and the viruses present in several
live viral vaccine preparations, have also been observed. The potential role
of stealth virus encoded chemokine receptors in the evolution and the present
day expression of HIV, is also under consideration.
Clinical
Approach to the Diagnosis and Therapy of Stealth Adapted Virus Infections (SAVI)
Diagnosis:
A major challenge in providing medical care for stealth
virus infected patients is the multiple and diverse clinical manifestations
of the patients’ illnesses. Individual patients do not fit comfortably into
a single medical discipline, whether it is psychiatry, neurology, rheumatology,
endocrinology, hematology, or any other. Imprecise diagnostic labels, such as
CFS, fibromyalgia, depression, attention deficit, etc., and even the better
defined diagnostic labels, such as schizophrenia, autism, ALS, multiple sclerosis,
Alzheimer’s disease, etc., tend to obscure the complex multi-system nature of
the patients’ illnesses. Another difficulty is quantitating the severity of
disease processes that can vary widely over time, and can be influenced by such
non-specific factors as stress, environmental exposures to chemicals, placebo
effects, etc.
Disordered brain function can be anticipated in many stealth
virus infected patients. This can be documented using a detailed neurological
examination, with a focus on what are sometimes referred to as “soft” neurological
signs. Ancillary, although expensive, tests such as SPECT scans, quantitative
EEG and formal neurocognitive evaluations, can help substantiate a diagnosis
of stealth adapted virus infection with encephalopathy. Additional syndrome
names can be applied depending on clinical and laboratory findings. Tabulation
of symptoms using a detailed questionnaire can be helpful in identifying clinical
problems and in assessing therapy related improvements.
Therapy: Until the existence of stealth viruses
is accepted by Public Health authorities, there will be no approved standard
of care in providing anti-viral treatments. Several suggestions can be made,
however, from what is currently known about the prototype SCMV-derived stealth
virus. Whether these suggestions are relevant to atypical viruses cultured from
other patients remains to be tested. CCID is now reaching out to clinicians
involved with the care of stealth virus infected patients for assistance with
these clinical trials.
Basically, it seems appropriate to undertake efforts to suppress
stealth virus activation and at the same time to support cellular metabolism,
especially mitochondria function. The remarkable expansion of chemokine and
chemokine-receptor related genes within the prototype SCMV-derived stealth-adapted
virus support the potential use of agents that can down regulate chemokine pathways.
Fortunately, many of the widely used herbal and generally non-toxic allopathic
medicines are known to interfere with chemokine signaling. It is probably more
than a coincidence that many of the compounds have also been reported to benefit
at least a proportion of patients with CFS and related illnesses. Ideally,
patients receiving these relatively simple therapies would be retested for stealth
virus activity. If there were no apparent reduction in stealth virus activity,
and if the patient remained symptomatic, one could more easily justify the
use of potentially more toxic allopathic medicines, including known anti herpesviral
agents.
For patients with major neurological, psychiatric, autoimmune
or malignant diseases, the stealth virus associated treatments will simply be
an aside to the accepted standard care of the patient’s underlying illness.
Once sufficient supportive data are collected, it may be possible to proceed
directly with anti-stealth virus therapy as the primary treatment for these
severe disorders.
Request
for Assistance with Clinical Therapeutic Studies
In
support of these studies, CCID has begun to work with medical specialists treating
major medical neurological, psychiatric, rheumatological and neoplastic illnesses,
and also with orthomolecular clinicians experienced in the uses of alternative
medicines. Stealth virus culture activity will be serially determined and correlated
with the use of various therapeutic modalities and changes in clinical status.
CCID can provide copies of patient questionnaires and an appropriate informed
consent form. A database for integrating laboratory, clinical and pharmaceutical
data, will be established and will be assessable to all participating clinicians.
The type of program is urgently needed to address the major Public Health threat
posed by stealth-adapted viruses and viteria.
Additional
information and copies of various research publications on stealth viruses,
requisition forms, etc, can be viewed at www.ccid.org. Clinicians wishing to
participate in stealth virus research should contact CCID. Stealth virus testing
requires an Acid Citrate Dextrose (ACD) yellow-topped tube of whole blood. While
a $250.00 fee is required for an initial diagnostic assay, a subsequent test
on the patient during or following therapy will be at no charge. Blood samples
should be sent via Federal Express to CCID, accompanied by a physician request
for testing. CCID is located at 3328 Stevens Avenue, Rosemead, CA 91770. Ph.
(626) 572-7288, Fax (626) 572-9288, e-mail ccidlab@hotmail.com.
