Dr. John Martin: Stealth viruses a public menace
carolyn
Dr John Martin: Stealth viruses a public menace
Thu Dec 11 20:49:38 2003
64.140.158.117

TheStealthVirusSupportGroup@yahoogroups.com

Dr John Martin: Stealth viruses a public menace
Statement from W. John Martin, M.D., Ph.D.
http://www.whale.to/v/martin.html

I have generally disregarded the criticisms that have been leveled against
the existence of stealth-adapted viruses. The individuals making or
repeating the criticisms should never have been taken seriously.
Unfortunately, negative comments are accessible on the internet and
undoubtedly have caused considerable confusion and concern. In the interests
of people reading such comments, I have decided to briefly discuss i)
evidence for the existence of stealth-adapted viruses and ii) suspension of
the clinical diagnostic testing for these viruses



The concept of stealth viruses was formulated in 1990 when I had
the opportunity to examine a brain biopsy from a Palm Springs~ school
teacher with an unexplained severe neurological illness. In spite of a
positive signal using a newly developed molecular probe assay (polymerase
chain reaction or PCR), there was no inflammatory reaction (the accepted
hallmark of an infectious process in an immunologically competent patient).
By 1991, I had managed to culture a cell damaging (cytopathic) virus from a
PCR positive patient with chronic fatigue syndrome (CFS). The virus caused
cells to cluster, fuse and become foamy from lipid (fat) accumulation. A
similar cytopathic virus was cultured from the cerebrospinal fluid (CSF) of
a comatose patient with a 4 year history of a bi-polar manic-depressive
illness. The second virus isolate was sent to the Los Angeles County Public
Health Laboratory which subsequently forwarded the virus to the Californian
Department of Health Laboratory.



DNA sequencing of two PCR amplified regions of the virus repeatedly isolated
from the CFS patient was performed and the data published in 1994. One
region showed partial, but highly significant, matching to a known sequence
of human cytomegalovirus (HCMV). The other region could not be matched to
HCMV. Cytopathic (cell damaging) viruses were being cultured from both
blood and CSF of various other patients with neurological, psychiatric and
auto-immune diseases, including autism, amyotrophic lateral sclerosis (ALS),
schizophrenia and systemic lupus erythematosus. While some of these viruses
showed molecular cross-reactivity with the virus isolated from the original
CFS patient, other viruses were seemingly structurally unrelated. This led
to the conclusion that stealth viruses comprise a broad grouping of viruses
whose characteristic feature is the failure to provoke an inflammatory
response in spite of being actively cytopathic in test tube cultures.



This conclusion did not sit well with traditional virologists who were
accustomed to dealing with precisely definable entities with known and
consistent DNA or RNA composition. Moreover, by focusing on the patient with
CFS, I evoked the ire of several prominent investigators who had tried
without success to culture viruses from CFS patients. Others researchers
were more successful but thought that their findings simply reflected the
reactivation of a conventional virus, such as human herpesvirus-6 (HHV-6),
rather than revealing the primary cause of the patients~ illnesses. Nor
could I satisfy those who wanted a laboratory test that would be
specifically diagnostic for CFS and that could readily distinguished
fatigued from non-fatigued patients; or at least would not be positive in
some seemingly healthy individuals.



I was far more impressed with the clearly abnormal findings, especially when
observed in cultures from patients with otherwise unexplained complex
illnesses. Potential infectiousness was also suggested in patients in whom
family members or even household pets had developed equally complex, yet
clinically diverse diseases. Any doubt about the relevance of these findings
was removed when cultured infected cells were shown to cause severe
non-inflammatory illness in animals. In collaboration with Dr. Tom Glass of
the University of Oklahoma, we observed the virus-induced transformation of
healthy cats to reclusive, pained, irritable creatures creating bald spots
on their heads from constant rubbing. Again, there was no inflammation in
the brains or other tissues of these animals, only the foamy, lipid-filled
cells that were being seen in the viral cultures.



Extended DNA sequencing of the original virus isolate revealed a region for
which there were sequence data of the cytomegaloviruses from various other
species, including African green monkeys. The DNA matching to the sequence
of African green monkey simian cytomegalovirus (SCMV) was extremely close,
indicating an unequivocal origin of the patient~s virus from SCMV. Partial
DNA sequencing of the virus from the still comatose patient with a history
of a bi-polar illness showed a similar origin from SCMV.



Having worked with the Food and Drug Administration (FDA), I
immediately realized that the SCMV-derived stealth viruses could have
entered into the human population from monkeys used to produce live polio
virus vaccines. I called the FDA with my results and learned that they were
still using African green monkeys to produce polio vaccines. I spoke of my
work at an FDA meeting in June 1995 attended by vaccine manufacturers. I
also wrote to the President of Wyeth about my research. I petitioned both
FDA and CDC with unsolicited proposals to test polio vaccine lots and to
request funding to continue DNA sequencing. Both proposals were dismissed. I
presented my findings again to an Institute of Medicine meeting in November
1995. A lawyer immediately filed a legal suit against Wyeth for me to
receive the polio vaccine lots administered to some of his clients with
neurological diseases. He knew of an ongoing challenge by the mother of a
stricken child who had surprisingly won a court order (resisted by both
Wyeth and FDA) to have the vaccine she had received tested for human
immunodeficiency virus (HIV). The court order specifically excluded any
additional testing, including testing for monkey viruses. The lawyer
involved in this case had recently arranged for me to receive a blood sample
from the child for stealth virus testing. The lawyer could use a positive
test result to seek an expansion of the scope of the court mandated testing
on the polio vaccine lot administered to the child.



These events were too much for the Establishment. On November
15th, I was told by my University Department Chairman that he had closed my
laboratory, dismissed all of the volunteers, and taken the more than $22,000
from my research account. The money he said had gone for back pay and
pay-in-lieu of notice for the licensed medical technologist. The funds had
been in a USC Gift Account specifically earmarked to trace the possible SCMV
origin of cultured stealth viruses. I strongly protested the
misappropriation of the patient donated funds and refused to sign a waiver
of the University~s action. I knew the Department Chairman had received
major funding from a subsidiary of Wyeth and felt suspicious that his abrupt
actions were essentially in response to industry pressure. The blood sample
from the sick child arrived on November 17th. I managed to store it and
showed it was culture positive by temporarily spending time in the Los
Angeles County Public Health Laboratory. I subsequently learned that the
child had a brain biopsy. Although a diagnostic quandary to his treating
physicians, it showed the vacuolated, foamy cells that I had come to
recognize from earlier patients and from the virus inoculated cats. The
child further deteriorated following the surgery and died.



I took leave from USC in January 1996 when confronted with
demands for an additional $15,000 before my laboratory would be reopened.
This amount was said to reflect the University~s overhead on the money
disbursed from the Gift Account. It was also made clear that I could not
resume any patient related testing. Under considerable duress, I eventually
located a laboratory in a closed, bankrupt hospital and moved what equipment
I could claim as my own into this facility. USC held firm to their
insistence that any equipment I had purchased from prior grants belonged to
the University.



Assisted by Zaki Saluhuddin, the discoverer of the HHV-6 virus,
and by other volunteers, underpaid technicians, and a medical technologist,
I was able to pursue the task of understanding the nature of
stealth-adaptation and focus on how the diseases might best be treated. The
laboratory was designated the Center for Complex Infectious Diseases or
CCID. It was licensed under the Clinical Laboratory Improvement Act (CLIA)
without any deficiencies cited in inspections held in 1996, 1998 and 2000.



Zaki Saluhuddin left in 1998 but not before he had independently validated
the stealth virus testing in double blinded studies. Similar double-blinded
validations were independently performed by Dr. Robert Gan, Ph.D., Russell
Collins, CLS, and on various occasions by myself (with the help of an
assistant to code the samples). As we all knew, positive tests were neither
disease specific nor confined to patients with severe illnesses. Still a
positive test was clearly and unmistakably abnormal. As an example, I recall
in 1996 showing a positive culture to the technologist in the Virology
Section of the Los Angeles County Public Health Laboratory. She immediately
recalled seeing a similar cytopathic effect from a much earlier culture. As
she retrieved her records it turned out to be the sample sent to her in 1991
from the comatose patient with the history of a bi-polar manic depressive
illness.



DNA sequencing data continued to substantiate the model of
stealth-adaptation as the loss or mutation of the relatively few genes that
code for components that are recognized by the cellular immune system. Most
virologists have yet to appreciate that since individual lymphocytes
recognize distinct antigens, effective immune recognition of virally
infected cells requires multiple copies of a few viral antigens at the cell
surface rather than a plethora of many antigens that would impede effective
lymphocyte binding. For example, approximately 60% of the anti-human
cytomegalovirus cytotoxic T lymphocytes recognize the protein coded by the
Unique Long segment gene number 83 (referred to as UL83). Twenty-five
percent recognize UL55 and another 10% the UL123 protein. Deletion or
mutation of these three genes and one can arrive at a virus that will not be
effectively recognized by the cellular immune system. Stealth-adapted
viruses show additional properties including the apparent capacity to
assimilate other genes that can include genes of bacterial origins and
cellular genes that can potentially cause cancer.



It is difficult to exaggerate the potential Public Health
significance of the stealth-adaptation process to the microbial threat posed
to mankind. The production of live vaccines, especially in tissues from
foreign species, such as the use of African green monkeys to produce live
polio vaccines, could clearly facilitate stealth-adaptation. Armed with an
insider~s knowledge of the vaccine industry and the influence it can have on
public policy, I continue to believe the message will eventually get
through. On each trip to Washington or Atlanta, I make a point of visiting
FDA or CDC, respectively. The following unanswered e-mail sent August 2000
to the then CDC Head of Herpesvirus Research (Dr. Phil Pellett) following a
herpesvirus conference is typical:



~Dear Phil,

Thank you for the discussion during the last evening of the International
Herpesvirus Workshop. You were willing to talk "bluntly," yet in a
constructive manner, regarding CDC shunning of my research. As you said, CDC
administrators look to you for scientific judgment on matters relating to
herpesviruses. Without your support, there is little chance of any response
to my requests that CDC pursue what I perceive to be a major Public Health
problem. As I recall, the major points of our discussion were as follows:

You spent approximately 45 minutes at my poster and came away with the
impression that some of the sequence data must be incorrect. You were
concerned that sequence homology matching should be more uniform and not
differ along a stretch of nucleotides. You asked if all of the sequencing
had been fully double-stranded and whether I had reviewed all of the primary
data. I indicated that most of the extended sequencing had been performed by
Lark Technologies, at Houston Texas. While there was some internal
overlapping, the sequences were primarily derived from one-way reactions.
While, there is the possibility of an occasional nucleotide error, this
would have had no effect on the conclusions that I was drawing from the
data. I understand that you hold your own sequence-related studies up to a
particularly rigorous standard, but this has more to do with the types of
conclusions that you are trying to draw, rather than justifying dismissing
any sequences that are not verified by double-stranded confirmation. Most of
the sequences have been on GenBank for a long time and can be reviewed
directly by anyone who's interested. The irregular matching that you noted
is indeed interesting and goes along with an earlier publication on the
genetic instability of the virus.

You also suggested that real science ought to be obvious to the intelligent
scientist and that it was my responsibility to present the work so that it
would be more widely accepted. Again I disagree. Most scientists are pretty
fixed in their belief system, and historically any shift in a prevailing
paradigm is met with resistance. The average scientists can not be expected
to plow through loads of someone else's raw data, or as you said "interpret
my data for me." The CDC is something of an exception, however, since its
mission is to be vigilant for possible threats of emerging infections. The
poster provided a good opportunity for a scientific discussion, but you
chose to view it in my absence. I, therefore, do not know if you fully
understood and appreciated the significance of what was being presented.

I was surprised by your suggestion that I sought a chance to discuss my work
at CDC as a "cheap" way of claiming CDC recognition. I view my challenge as
primarily to get CDC to listen and to take some action. I hope you will
continue to provide some assistance by engaging in more meaningful
discussions of actual sequence data and patients' histories. In particular,
I would like to know your responses to the following issues that I have
raised.

1. Do you doubt that the virus for which I have extensive sequence data, was
derived from an African green monkey simian cytomegalovirus.

2. Do you doubt that the virus came from a patient, or that it can induce
severe illness when inoculated into cats.

3. Are you convinced that the virus has some unusual sequences that at least
qualifies it as being an atypically structured virus.

4. Do you feel the apparent absence of UL83 and UL55 related genes could
provide the virus a way of evading recognition by the cellular immune
system.

5. Are you willing to accept that the virus has recombined with cellular
sequences, including the CXC chemokine coding gene, melanoma growth
stimulatory activity, a potential oncogene.

6. Do you see any significance in the apparent amplification of the US28
chemokine receptor coding gene.

7. Do you accept the presence of bacteria-derived sequences within the viral
genome.

8. Are you aware of the high proportion of patients with unexplained
encephalitis-like illnesses, including cases in which brain biopsies have
been submitted to CDC for review.

9. Given our positive tissue culture findings in such patients, can you
dismiss the possibility that these patients are infected with atypically
structured viruses.

10. Don't you think we owe it to those responsible for the Nation's Public
Health


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