Keywords: Stealth adapted viruses, Stealth adaptation, African green
monkey simian cytomegalovirus, SCMV, KELEA, Kinetic Energy Limiting
Electrostatic Attraction, Alternative Cellular Energy, ACE pigments,
Chronic fatigue syndrome, CFS, chronic Lyme disease, Gulf War Syndrome,
PANDAS, polio vaccine, Mycoplasma fermentans , Ochrobactrumquorumnocens , Borrelia burgdorferi , viteria
Abbreviations: ACE – Alternative Cellular Energy, KELEA - Kinetic
Energy Limiting Electrostatic Attraction, SCMV - African green monkey
simian cytomegalovirus, CFS – chronic fatigue syndrome, CPE –
cytopathic effect, CSF – cerebrospinal fluid, kb – kilobases, MI –
mental illness
Discussion
Research conducted within my laboratory into a viral cause of the
chronic fatigue syndrome (CFS) has faced political difficulties
primarily because the initially identified virus in a CFS patient is
derived from an African green monkey simian cytomegalovirus
(SCMV).1 Kidney cell cultures from cytomegalovirus
infected African green monkeys were routinely used in the production of
live polio virus vaccines.2 Stored bulk lots of
several approved batches of polio vaccines have been shown to contain
SCMV DNA, although Public Health authorities were unable to culture
replicating viruses.3,4 About 10% of the cultures of
polio vaccine viruses were apparently discarded by the manufacturer
because of SCMV contamination (personal communication from an employee).
A relevant FDA official was seemingly unaware of the high incidence of
SCMV contamination, which should have justified the imposition of more
stringent detection methods. The detailed characterization of a
cytomegalovirus-related cytopathic virus cultured from a CFS patient was
reported in 1994 in the American Journal of
Pathology.5 The unequivocal derivation of this virus
from SCMV was described in 1995 and confirmed in several subsequent
publications.1,6-8
Polio vaccine viruses were earlier grown in kidney cell cultures
obtained from rhesus monkeys.9 The switching to the
use of African green monkeys occurred in 1963 following the detection of
simian virus-40 (SV-40) infection in many rhesus
monkeys.10-12 Dr. Albert Sabin had previously cultured
an atypical virus contaminant in the rhesus monkey-derived CHAT
experimental polio vaccine.13 This vaccine was
subsequently shown to contain DNA of rhesus
cytomegalovirus.4 Since the atypical virus was
difficult to culture, it was likely a stealth adapted rhesus
cytomegalovirus. The difficulty in culturing may explain why the
presence of the virus was denied by the CHAT vaccine manufacturer. This
vaccine had been extensively tested in African chimpanzees, as well as
in African children during the late 1950s. As described elsewhere, the
human immunodeficiency virus (HIV) likely arose from chimpanzees
inoculated with the contaminated CHAT polio vaccine.15The ominous transmission of rhesus monkey cellular sequences has
occurred in stealth adapted virus infected
humans.16-18 Certain of the originally transmitted
primate sequences appear to have been subsequently replaced by human
genetic sequences, presumably by homologous
recombination.16,17
There is a notable finding with regards to the detected rhesus cellular
sequences in different stealth adapted virus cultures. It is the close
matching of several of the rhesus sequences detected in the cultures
from three unrelated CFS patients.16,17 This finding
implies that stealth adaptation may be a relatively rare occurrence with
further selection of more highly infectious viruses.
The initially cultured stealth adapted virus consists of genetically
unstable, DNA fragments with a size of approximately 20
kb.5,6 This is less than a tenth of the 226 kb size of
SCMV and more in keeping with the size of large RNA viruses. This
finding along with the significant sequence differences in the clones
matching to the same region of the SCMV genome implies the probability
of RNA to DNA replication presumably involving an endogenous reverse
transcriptase. This would also explain the minor sequence variations
between matching polymerase chain reaction (PCR) amplified products in
other stealth adapted virus cultures.16,17 Direct RNA
to RNA replication may, however, be occurring with certain other
SCMV-derived stealth adapted viruses. For example, a positive PCR
results with a patient’s culture required prior RNA to DNA reverse
transcription.19 Of considerable concern is the
potential of stealth adapted viruses to acquire highly pathogenic,
transmissible cellular sequences.16-18,20,21 These can
arise by either genetic mutation or the acquisition of sequences from
abnormal cells, including cancer cells. Stealth adapted virus infections
can pass reciprocally between humans and animals providing additional
opportunities for the infectious transmission of genetically determined
illnesses.22 Public Health epidemiologists should be
monitoring for unanticipated rises in the incidences of various chronic
illnesses in humans and animals.
CFS and similar chronic illnesses have been attributed to various types
of bacteria. This conclusion has been primarily based on positive
serology but also supported by genetic detection
methods.23-31 Included as a possible causal bacteria
is Mycoplasma fermentans, which is also described as a common
co-pathogen in HIV infected AIDS patients.32-34 The
evidence of infection by Mycoplasma fermentans is not restricted
to CFS and HIV infected individuals.33 Portions of its
DNA have been detected in many patients with other illnesses including
amyotrophic lateral sclerosis, Gulf War syndrome, rheumatoid arthritis,
autism, and chronic Lyme disease.24,35-39 The
identification of M. fermentans derived genetic sequences in the
initially cultured SCMV-derived stealth adapted virus suggests a
different interpretation.21,40-43 Rather than
indicating a bacterial infection, the detected Mycoplasma- related
genetic sequences in a wide range of illnesses may be components of
infecting stealth adapted viruses. Indeed, I was privately informed that
the sequencing studies on CFS and chronic Lyme disease diagnosed
patients revealed unanticipated minor discrepancies from authenticM. fermentans DNA sequences. The other major source of bacterial
sequences in the initially cultured SCMV-derived stealth adapted virus
is closely related but not identical to Ochrobactrumquorumnocens , an alpha proteobacterium.21Somewhat related bacteria have been implicated as a possible cause of
Morgellons disease,44 although there is currently more
emphasis on this illness being potentially due to Borreliaburgdorferi ,45 the bacteria that causes acute
Lyme disease.
So called chronic Lyme disease has many clinical features in common with
CFS and fibromyalgia patients.23,46 Extensive
culturing of blood samples from patients diagnosed as having chronic
Lyme disease showed the consistent presence of stealth adapted viruses.
DNA sequence analysis was not performed on any of the cultured viruses
to check for the presence of Borrelia burgdorferi genetic
sequences. Chronic Lyme disease patients commonly show evidence for
additional infections, which include Bartonella, Ehrlichia,
Mycoplasma, and other bacteria and the Babesiaparasite.47 The evidence is more commonly serological
rather than isolation of organisms. It has led to long-term antibiotic
therapy with questionable benefits. Detailed sequencing of stealth
adapted viruses cultured from diagnosed chronic Lyme disease patients is
indicated.
Another possible example of the mistaken identification of stealth
adapted virus infections as a bacteria-induced illness is PANDAS
(Pediatric Autoimmune Neuropsychiatric Disorders Associated with
Streptococcal Infections).48,49 From personal
experience in reviewing laboratory testing data, it is not uncommon for
there to be either anti-Streptolysin O (ASO) or anti-DNase B antibody
but not both, as would be expected if there were an infection with
viable bacteria. Positive Lyme disease serology has also been reported
in association PANDAS.50 Moreover, stealth adapted
viruses were reliably cultured from children clinically diagnosed as
having PANDAS. The generic term “viteria” has been introduced to help
convey the concept of stealth adapted viruses being potential carriers
of bacteria-derived genetic sequences.21,40
Unlike the cellular sequences, which are derived from non-coding regions
of cellular genes, the bacteria-derived genetic sequences code for
structural components with potential metabolic, enzymatic, and/or
immunogenic activities. 21,40-43 It is also possible
that some of these components have biophysical properties, including the
indirect providing of a non-food source of cellular energy. A feature of
stealth adapted virus cultures is that the virus induced cytopathic
effect (CPE) becomes suppressed in the absence of regular replacement of
the culture medium. The CPE quickly recurs upon the refeeding with fresh
medium.51 The suppression the CPE correlates with the
cellular production of energy transducing materials that form into
self-assembled, pigmented particles in the extracellular fluids. The
materials can further develop into colorful threads and
ribbons51,52 Reactivation of the virus CPE does not
occur if a few of these particles are first added to the refeeding
culture medium.51 The particles are fluorescent,
especially in the presence of certain dyes, electrostatic, electron
donating, and occasionally ferromagnetic. Similar particles develop in
stealth adapted virus infected patients, in whom they can be
misidentified as parasitic insects.52,53
Subsequent research led to the understanding that cells have the
intrinsic capacity to derive cellular energy by means other than through
the metabolism of food. This alternative cellular energy (ACE) pathway
involves the transfer of an environmental energy force into both the
body’s intra- and extracellular fluids. The force is termed KELEA, an
abbreviation for Kinetic Energy Limiting Electrostatic
Attraction.54-58 Many naturally occurring, and cell
synthesized compounds with regional differences in their electrical
charges may continually attract and release KELEA, possibly upon
oscillatory movements. Such compounds, termed ACE
pigments,51,52 can increase the KELEA levels in nearby
fluids, including water. They include the extracellular materials
developing in long-term stealth adapted virus
cultures51 Certain forms of fluctuating electrical
activities in the brain and muscles are likely to be the major ways that
humans and animals normally receive KELEA, which is then transferred to
the body’s fluids.59 Some of the KELEA attracting
brain and muscle mediated activities can presumably be learned.
The ACE pathway provides a non-immunological defense mechanism against
stealth adapted viruses. It can also suppress other types of
infections.51,52,60-63 Moreover, the physiological
functions of the ACE pathway extend well beyond the control of
infectious diseases.64 It can be converted into
chemical energy58 and, thereby, help compensate for
illnesses due to impaired metabolic activity. It may also enhance the
biophysical processes that allow for the detection of changes in the
physical environment. It can support tissue regeneration in the absence
of scarring,65 and help sustain a higher level of
brain activity including conscious awareness. 66
Although CFS was the early focus of research on stealth adapted viruses,
positive cultures were obtained from patients with more widely
recognized major neurological and psychiatric illnesses. Indeed, the
second SCMV-derived stealth adapted virus was cultured from a
23-year-old woman who was initially diagnosed at age 19 with
schizophrenia.67 The diagnosis was changed to bipolar
psychosis largely based on her clinical response to lithium therapy. She
had required residential care since her diagnosis. She acutely
deteriorated into coma prior to admission to the Los Angeles County
Hospital in early 1991. The stealth adapted virus was cultured from an
acellular cerebrospinal fluid (CSF) sample obtained upon her hospital
admission. She remained comatose till her death several years later.
Illnesses among family members of CFS patients also support an
etiological role of stealth adapted viruses in major neurological and
psychiatric diseases.68,69 Prominent examples include
Alzheimer diseases occurring in grandparents, CFS and amyotrophic
lateral sclerosis (ALS) in parents, and severe learning and behavioral
disorders in children. Another example is Parkinson’s disease in a
grandparent, CFS in both parents, and schizophrenia in a teenage son.
Upon inquiry it is not uncommon to learn of CFS-like illness in mothers
of children with autism. Stealth adapted viruses were consistently
cultured from children with autism.70
Stealth adapted viruses were also cultured from all tested patients
diagnosed with multiple myeloma.71 This may explain
the preceding or concurrent neuropsychiatric symptoms that are seemingly
common among patients diagnosed with multiple myeloma. Either direct or
circumstantial evidence also suggests a major role of stealth adapted
viruses in glioblastoma multiforme and in certain leukemias. Potentially
any type of virus can undergo stealth adaptation possibly with a
particular likelihood of occurring with herpesviruses because of their
large size.
It is important that the culturing and detailed sequencing of stealth
adapted viruses be undertaken. Moreover, the testing should not be
restricted to patients with neurological or psychiatric symptoms. Thus,
while relatively few virus-coded components are targeted by the cellular
immune system, a much wider array of components can typically evoke
anti-viral antibodies. Such antibodies may provide a barrier to stealth
adapted viruses from infecting the brain.22 Because of
genetic instability, there can be a range of structurally diverse
antigenic components coded by the viral and acquired bacterial genes.
The resulting antibodies can be reactive with a range of different
viruses and bacteria. They can also lead to antigen-antibody immune
complexes with the potential of inducing renal, joint, and other
diseases. Stealth adapted virus infection can also potentially trigger
common autoimmune diseases, including systemic lupus erythematosus
(SLE), multiple sclerosis Hashimoto’s disease, Addison’s disease, Type 1
diabetes, idiopathic thrombocytopenia (ITP), etc.
Stealth adapted viruses can also be an important cofactor in many common
illnesses in addition to those that have been previously mentioned. The
similarity of symptoms, including fatigue and cognitive deficits,
between CFS patients and many of those with the Long Covid
Syndrome72 warrant the culturing of these patients for
stealth adapted viruses. This possible association is further supported
by the concurrent elevations in anti-herpesvirus antibodies in certain
patients diagnosed with the Long Covid Syndrome.73,74
Public Health authorities prohibited my clinical culturing of stealth
adapted viruses in 1972 stating that I had put the Nation’s Health into
Immediate Jeopardy. Certain CDC, NIH, and FDA officials have repeatedly
shied away from my requests that they confirm the culturing of stealth
adapted viruses. It is time for a more proactive response.
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