W. John Martin, M.B., B.S., Ph.D.
Center for Complex Infectious Diseases
3328 Stevens Avenue, Rosemead, California USA 91770
Atypically structured, vacuolating cytopathic stealth
viruses exist and can induce multi-system illnesses,
including severe brain disease. DNA sequencing studies on an
African green monkey simian cytomegalovirus (SCMV)-derived
stealth virus has heightened concerns for the potential
devastating effects of stealth viruses on living organisms.
The prototype stealth virus has lost the major antigenic
targets for recognition by cytotoxic T lymphocytes.
More impressively, it has captured, amplified and mutated
both cellular and bacterial genetic sequences. The term "viteria"
has been introduced for viruses containing bacterial
sequences. Stealth viruses have been cultured from babies
born to infected mothers and from children with a variety of
neurological, psychiatric, allergic and neoplastic diseases.
The cytopathic changes seen in stealth virus cultures
correlate well with the vacuolating cellular damage observed
on histological sections of brain tissues obtained on biopsy
and on autopsy. Studies to combat the spread of stealth
viruses and to effectively treat those already infected are
clearly warranted. Additional information is available from
the internet at www.ccid.org
Poliovirus Vaccine Contamination
One of society's highest obligations is the protection of
its children. Vaccine programs provide a proven method for
childhood disease prevention. The safety of such programs
has been entrusted to vaccine manufacturers and to
government regulatory agencies. Although widely touted as
the major medical triumph of the 20th century, the
development of viral vaccines has elements of less than
stellar performance. The discovery in 1960 of live SV-40
virus contamination in formalin-treated poliovirus vaccine,
produced in kidney cells cultures from rhesus monkeys, did
not lead to an immediate recall of the contaminated
Rather, the production method was switched to the use of
kidney cells from the less well characterized African green
monkeys. This switch in monkey species was soon followed by
the decision to forgo formalin inactivation by using a
weakened (attenuated) live strain of poliovirus (1).
Persisting concerns regarding contaminating viruses in the
live poliovaccine led in 1972 to a joint study between the
vaccine manufacturer and the United States Food and Drug
Administration (FDA). Kidney cultures from all 12 monkeys
tested grew African green monkey simian cytomegalovirus (SCMV).
Only 4 of the SCMV isolates were detectable using the
regular methods for virus detection (2).
No changes in testing methodology were imposed, nor was
the scientific community alerted to the findings. An
explanation that was subsequently offered was that
information about the study was deemed to be proprietary.
The results of this earlier study were, however, not even
conveyed to FDA scientists who, in 1977, notified the
Director of the FDA's Bureau of Biologics that certain
poliovaccine lots contained unexplained non-cellular DNA;
and were, therefore, potentially virally contaminated.
The issue of SCMV contamination of poliovirus vaccines
was again raised with the FDA in May 1995. I was then
working as a virologist at the University of Southern
California. I had developed tissue culture methods that
clearly indicated the presence of atypical viruses in
patients with complex neurological diseases (3-7). The
viruses were striking in that they failed to evoke an
inflammatory reaction in the patients from whom they were
isolated. They were termed stealth viruses on this basis,
and seemingly they lacked target antigens for recognition by
the body's cellular immune system.
Sequencing studies on a stealth virus strongly suggested
it had originated from SCMV. Several meetings with FDA and
Center for Disease Control and Prevention (CDC) officials
pointed to their unwillingness to allow any outside review
of vaccine safety procedures. For example, a simple request
to review histological slides of neurological tissue of
monkeys inoculated with poliovaccine was refused, again on
the basis that it was proprietary information. Noteworthy
was the admission that the vaccines were routinely tested in
rhesus monkeys because African green monkeys commonly show
evidence of neurological disease. Moreover, even in rhesus
monkeys, the vaccine was said to induce considerable
neurological damage, although less than that induced by
The actual SCMV-related sequence data were published in a
respected virology journal in July 1995 (8). The article
aroused the interest of anti-vaccine consumer groups.
Through the efforts of one of these groups, I was invited to
attend a vaccine safety meeting of the Institute of
Medicine, National Academy of Sciences (9). The open meeting
held on November 6, 1995 was followed the next day by an
"executive session." I was later informed that several
Industry-connected individuals at this meeting were
"furious" that I was allowed to speak. A "watered down"
account of what I said subsequently appeared in the official
report of the meeting.
Some insight into the lack luster nature of the existing
regulatory system was provided by several brief interchanges
with Government and other officials during the last several
years. For example, I was asked whether formalin treatment
would inactivate stealth viruses. My response was that I did
not know. The chairman of the National Immunization Advisory
Committee suggested the advocacy of a split protocol in
which both formalin inactivated and live attenuated
poliovaccine would provide the necessary time window for the
manufacturer of the inactivated vaccine to develop the
stocks required for a complete switch.
True to his suggestion, the official switch to
inactivated vaccine is scheduled for January 2000. Of
course, those "in the know" would have already switched to
the inactivated vaccine. An FDA reform bill was being
considered by Congress in 1997. I suggested that the bill
include the provision that "If a safety issue is identified
in the regulation of a biological product, then Industry
would waive its proprietary protection so that the
information could be made available to the scientific
community." The suggestion was well received by the counsel
for the House Commerce Committee. It was soon dropped,
however, when support was not forthcoming from Industry, FDA
or the American Medical Association (AMA).
In speaking with an AMA lobbyist, I understood they
"would not want the public to know that their doctors were
not in the knowledge loop." I once asked industry personnel
involved in poliovaccine production whether they were still
encountering SCMV in poliovaccine production lots. After
some hesitation that disappeared as we all identified
ourselves as parents, the straightforward answer was "not
infrequently." Armed with this information I again requested
an FDA official to please use modern techniques, such as the
polymerase chain reaction (PCR), to screen poliovaccine lots
for SCMV. "We would not know what to do with a positive
result" was his answer.
Sequencing Studies on the SCMV-Derived Stealth Virus
Continued sequencing of the prototype SCMV-derived
stealth virus have helped substantiate the original
suggestion that stealth adapted viruses lack the critical
target antigens for cellular immune recognition (10-11). The
virus has a fragmented viral genome (11). While the various
fragments cover extensive regions of a typical
cytomegalovirus, it is missing sequences that correspond to
the known major viral antigens targeted by
anti-cytomegalovirus cytotoxic T lymphocytes. Other regions
of the cytomegaloviral genome are unevenly distributed, with
certain viral genes being markedly over represented. When
multiple copies of a gene were identified, it was not
uncommon to see minor sequence differences indicating an
"error-prone" replication process (10-11).
An overview of the viral sequence data is that
approximately two-thirds of the clones contain sequences
that correspond to cytomegaloviral genes (10). Where direct
comparisons could be made, the genetic sequences matched
more closely to rhesus monkey cytomegalovirus than to human
cytomegalovirus. Even closer homology could be shown between
the stealth virus and the limited known sequences of SCMV.
The data are unequivocal that the virus had originated from
an SCMV and hence from a poliovaccine (8,10-11).
The question that arose was how could such a fragmented
viral genome, lacking certain viral genes while over
expressing other viral genes, retain and/or regain its
ability to be cytopathic for cells. A partial answer to this
question came from analyses of the genes that did not
correspond to those of a cytomegalovirus. Several genes were
apparently directly incorporated from infected cells. These
genes frequently contained short stretches of highly
reiterated cellular sequences (12). One set of cellular
genes was particularly noteworthy. They corresponded to
three copies of a gene that encode a chemokine (13).
While the cellular DNA for this gene contain introns, the
assimilated genes were lacking introns and had, therefore,
been 'captured" as RNA sequences. This finding provided
direct evidence for reverse transcription (that is RNA to
DNA) in the reconstruction of cytopathic stealth viruses.
This process was consistent with the error-prone replication
of the stealth virus. Among the cellular genes identified
within the stealth virus, were also genes with potential
oncogenic (cancer causing) activity (13). This finding
highlighted ongoing observations that stealth adapted
viruses were being repeatedly detected in both children and
adults with various cancers (14 and unpublished
An additional challenging observation was the finding
that some of the incorporated sequences had clearly been
captured from bacteria (15). The bacterial genes covered a
wide range of metabolic functions that could enhance
bacterial growth (16). This observation was soon followed by
the detection of atypical bacteria within the flora of
stealth virus infected patients. Moreover, infectious agents
could be released from such bacteria and cause cytopathic
effects when transferred to human and to animal cells. The
presence of bacterial sequences within viruses infectious
for human and animal cells represents a novel life form that
has been termed viteria.
The prospect exists for metabolically empowered bacteria
to establish an increasing presence within nature with
potentially devastating biological consequences. The notion
that viteria represents "Nature's biological weapons
program" is not too far fetched. Information concerning the
existence of viteria and their potential Public health
consequences was conveyed to CDC, FDA, NIH and the US
Congress. Responses are still being awaited from these
Viteria: An Explanation for Serological and Molecular
Findings of Multiple Pathogens in Adults and Children with
Chronic Fatigue and Related Illnesses
The recombination of viral, bacterial and cellular genes
within broadly infectious viteria could help explain much of
the confusion surrounding the cause of chronic fatigue like
illnesses in adults, children and household pets. Depending
upon the focus of the research, various investigators have
ascribed these illnesses to different types of pathogens.
Some of the early reports relied upon high antibody titers
to Epstein-Barr virus (a type of herpesvirus). Others have
noted antibodies reactive with human herpesvirus-6, human
herpesvirus-7, human T lymphotropic virus, parvovirus, Borna
virus, modified endogenous retroviruses, enteroviruses,
including poliovirus, and hepatitis C viruses (17-25). Using
molecular techniques, data have been obtained suggesting the
presence of mycoplasma species, Chlamydia, Rickettsiae,
Brucella and even Borrelia bacteria (26-30).
These data are consistent a broad family of viteria that
have, and are continuing to, capture, amplify and mutate
viral, cellular, bacterial and even fungal genes. Among the
cellular/viral genes are likely to be genes encoding the
reverse transcriptase of endogenous retroviruses. Although,
infection can pass between individuals, including human:
animal transmissions, via infected bacteria, the primary
brain associated illness is viral not bacterial. The
apparent clinical benefits that may occur following
antibiotic therapy are potentially explainable by the known
capacity of certain antibiotics to modulate chemokine
mediated viral activation and replication.
Viteria Detection Systems
The molecular diversity of viteria has helped underscore
the value of tissue culture as a primary detection assay. In
a relatively straightforward procedure, cells from patients
are incubated with normal human and/or animal fibroblasts.
The cultures are observed for the development of a
vacuolating cytopathgic effect (CPE). For controls, blood
samples are obtained from healthy blood donors. None of the
controls are expected to yield a positive CPE. In contrast,
stealth virus infected patients will typically yield a
clearly positive culture.
Once established, the cultures can be screened using
various immunological and molecular based assays. In
particular, cells undergoing CPE will typically stain with
polyclonal antisera reactive with various herpesviruses.
Similarly, low stringency polymerase chain reaction (PCR)
will typically yield multiple products that can be isolated,
cloned and sequenced. Semi-quantitative cultures can also be
used to assess efficacy of various therapies including
chemokine modulating agents and anti-viral drugs. It is also
appropriate to screen the bacterial flora of infected
individuals for atypical bacteria. If necessary, these can
be treated directly using antibiotics and probiotics.
During the last decade, I have written several clinical
articles describing stealth virus infected patients with
complex illnesses. The patients have included children with
autism, adults with psychotic disease and several
individuals with chronic fatigue/fibromyalgia syndrome. Many
of the articles had been summarily dismissed when submitted
to major medical journals. The suggestion of a linkage to
vaccine use or of community wide epidemics has been
unsettling to many reviewers. Still the work has appeared in
peer reviewed publications and has been presented at various
For example, a recent publication (36) described a
stealth virus infected child whose illness began in 1997 as
a behavioral problem. It took over seven months before the
illness was attributed by his parents, both of whom were
physicians, to brain damage. Even then a qualified
neurologist was unable to detect impaired motor or sensory
functions. Yet magnetic resonance imaging (MRI) confirmed
extensive sub-cortical brain damage. A brain biopsy showed
marked vacuolating/spongiform change. The child's clinical
condition progressively deteriorated. He was examined at
several major medical centers where it was wrongly concluded
that he had a genetic disease from which he would soon die.
He was shown to be stealth virus infected by tissue culture
and significantly improved with ganciclovir therapy,
although he still had major residual deficits. In spite of
several courses of anti-viral therapy, with and without
steroids, he subsequently succumbed to overt cerebral
swelling and herniation.
Other fatal cases have included a young adult initially
diagnosed as having a psychotic illness. Four years into
this illness, she had an acute exacerbation with coma and
massive brain damage (32). Her cerebrospinal fluid grew out
a stealth virus closely related to that of the prototype
SCMV-derived virus. Another patient with a fatal illness and
positive CSF findings died with evidence of a cerebral
Virally infected newborn children have variously
presented with an acute viral-like syndrome with
hepatomegaly, thrombocytopenia, choroid plexus hemorrhage or
with more subtle changes comprising unexplained seizure
activity and/or delayed neurological development. At least
one child, born to a mother with a chronic fatigue like
illness, died from a sudden infant death syndrome, two weeks
following routine vaccination. Young children have presented
with autism, attention deficit and hyperactivity, learning
and other behavioral disorders. The association of stealth
virus with autism was clearly established in controlled
double blind studies. Whereas none of 19 control blood
samples tested positive, 13 of 18 children with autism
yielded repeated positive stealth virus cultures.
Other culture positive clinical groups have included
in-patients in psychiatric institutions, cancer patients,
including essentially 100% of patients diagnosed with
multiple myeloma, auto-immune illnesses, including systemic
lupus erythematosus, rheumatoid arthritis and multiple
children diagnosed as having chronic fatigue syndrome. With
all of these illnesses, stealth viral infection is viewed as
a major contributing factor, complicated by the overlay of
auto-immune, allergic and/or neoplastic processes.
An essential theme of this presentation is the apparent
lack of responsiveness on the part of those entrusted with
the nation's Public Health. While it can be argued that
adults need to compete for allocated resources applied to
various illnesses, it is difficult to understand the
indifference shown to health issues affecting children.
Where is the concern that a biopsy-proven childhood viral
infection was not recognized at major medical centers? Where
is the interest in the many other children who have tested
positive for stealth viruses? Why the lack of discussion
about possible brain damage causing national tragedies such
as school shootings, and the increasing prevalence of
autism, attention deficit, asthma and sudden infant death
Are stealth virus infected patients populating our
psychiatric institutions, allergy clinics and even our
cancer wards? The world and, in particular, its children
appear to be at risk for stealth adapted viruses. The
contribution of vaccines to the formation and dissemination
of these viruses should be an open topic for scientific
discussion. This is not occurring with those presently in
charge of overseeing the safety of the Nation's immunization
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2. Unpublished documentation.
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a stealth virus isolated from the cerebrospinal fluid of a
health care worker with chronic fatigue syndrome. Case
report. Pathobiology. 1997;65:57-60.
32. Martin WJ. Simian cytomegalovirus-related stealth
virus isolated from the cerebrospinal fluid of a patient
with bipolar psychosis and acute encephalopathy.
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fatal case complicated by cerebral vasculitis. Pathobiology.
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35. Martin WJ, Anderson D. Stealth virus epidemic in the
Mohave Valley. I. Initial report of virus isolation.
36. Martin WJ, Anderson D. Stealth virus epidemic in the
Mohave Valley: Severe vacuolating encephalopathy in a child
presenting with a behavioral disorder. Exp Mol Pathol. 1999;