carolynDr John Martin: Stealth viruses a public menaceThu Dec 11 20:49:38 200318.104.22.168
TheStealthVirusSupportGroup@yahoogroups.com Dr John Martin: Stealth viruses a public menaceStatement 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 againstthe existence of stealth-adapted viruses. The individuals making orrepeating the criticisms should never have been taken seriously.Unfortunately, negative comments are accessible on the internet andundoubtedly have caused considerable confusion and concern. In the interestsof people reading such comments, I have decided to briefly discuss i)evidence for the existence of stealth-adapted viruses and ii) suspension ofthe clinical diagnostic testing for these virusesThe concept of stealth viruses was formulated in 1990 when I hadthe opportunity to examine a brain biopsy from a Palm Springs~ schoolteacher with an unexplained severe neurological illness. In spite of apositive signal using a newly developed molecular probe assay (polymerasechain reaction or PCR), there was no inflammatory reaction (the acceptedhallmark of an infectious process in an immunologically competent patient).By 1991, I had managed to culture a cell damaging (cytopathic) virus from aPCR positive patient with chronic fatigue syndrome (CFS). The virus causedcells to cluster, fuse and become foamy from lipid (fat) accumulation. Asimilar cytopathic virus was cultured from the cerebrospinal fluid (CSF) ofa comatose patient with a 4 year history of a bi-polar manic-depressiveillness. The second virus isolate was sent to the Los Angeles County PublicHealth Laboratory which subsequently forwarded the virus to the CalifornianDepartment of Health Laboratory.DNA sequencing of two PCR amplified regions of the virus repeatedly isolatedfrom the CFS patient was performed and the data published in 1994. Oneregion showed partial, but highly significant, matching to a known sequenceof human cytomegalovirus (HCMV). The other region could not be matched toHCMV. Cytopathic (cell damaging) viruses were being cultured from bothblood and CSF of various other patients with neurological, psychiatric andauto-immune diseases, including autism, amyotrophic lateral sclerosis (ALS),schizophrenia and systemic lupus erythematosus. While some of these virusesshowed molecular cross-reactivity with the virus isolated from the originalCFS patient, other viruses were seemingly structurally unrelated. This ledto the conclusion that stealth viruses comprise a broad grouping of viruseswhose characteristic feature is the failure to provoke an inflammatoryresponse in spite of being actively cytopathic in test tube cultures.This conclusion did not sit well with traditional virologists who wereaccustomed to dealing with precisely definable entities with known andconsistent DNA or RNA composition. Moreover, by focusing on the patient withCFS, I evoked the ire of several prominent investigators who had triedwithout success to culture viruses from CFS patients. Others researcherswere more successful but thought that their findings simply reflected thereactivation of a conventional virus, such as human herpesvirus-6 (HHV-6),rather than revealing the primary cause of the patients~ illnesses. Norcould I satisfy those who wanted a laboratory test that would bespecifically diagnostic for CFS and that could readily distinguishedfatigued from non-fatigued patients; or at least would not be positive insome seemingly healthy individuals.I was far more impressed with the clearly abnormal findings, especially whenobserved in cultures from patients with otherwise unexplained complexillnesses. Potential infectiousness was also suggested in patients in whomfamily members or even household pets had developed equally complex, yetclinically diverse diseases. Any doubt about the relevance of these findingswas removed when cultured infected cells were shown to cause severenon-inflammatory illness in animals. In collaboration with Dr. Tom Glass ofthe University of Oklahoma, we observed the virus-induced transformation ofhealthy cats to reclusive, pained, irritable creatures creating bald spotson their heads from constant rubbing. Again, there was no inflammation inthe brains or other tissues of these animals, only the foamy, lipid-filledcells that were being seen in the viral cultures.Extended DNA sequencing of the original virus isolate revealed a region forwhich there were sequence data of the cytomegaloviruses from various otherspecies, including African green monkeys. The DNA matching to the sequenceof African green monkey simian cytomegalovirus (SCMV) was extremely close,indicating an unequivocal origin of the patient~s virus from SCMV. PartialDNA sequencing of the virus from the still comatose patient with a historyof a bi-polar illness showed a similar origin from SCMV.Having worked with the Food and Drug Administration (FDA), Iimmediately realized that the SCMV-derived stealth viruses could haveentered into the human population from monkeys used to produce live poliovirus vaccines. I called the FDA with my results and learned that they werestill using African green monkeys to produce polio vaccines. I spoke of mywork at an FDA meeting in June 1995 attended by vaccine manufacturers. Ialso wrote to the President of Wyeth about my research. I petitioned bothFDA and CDC with unsolicited proposals to test polio vaccine lots and torequest funding to continue DNA sequencing. Both proposals were dismissed. Ipresented my findings again to an Institute of Medicine meeting in November1995. A lawyer immediately filed a legal suit against Wyeth for me toreceive the polio vaccine lots administered to some of his clients withneurological diseases. He knew of an ongoing challenge by the mother of astricken child who had surprisingly won a court order (resisted by bothWyeth and FDA) to have the vaccine she had received tested for humanimmunodeficiency virus (HIV). The court order specifically excluded anyadditional testing, including testing for monkey viruses. The lawyerinvolved in this case had recently arranged for me to receive a blood samplefrom the child for stealth virus testing. The lawyer could use a positivetest result to seek an expansion of the scope of the court mandated testingon the polio vaccine lot administered to the child.These events were too much for the Establishment. On November15th, I was told by my University Department Chairman that he had closed mylaboratory, dismissed all of the volunteers, and taken the more than $22,000from my research account. The money he said had gone for back pay andpay-in-lieu of notice for the licensed medical technologist. The funds hadbeen in a USC Gift Account specifically earmarked to trace the possible SCMVorigin of cultured stealth viruses. I strongly protested themisappropriation of the patient donated funds and refused to sign a waiverof the University~s action. I knew the Department Chairman had receivedmajor funding from a subsidiary of Wyeth and felt suspicious that his abruptactions were essentially in response to industry pressure. The blood samplefrom the sick child arrived on November 17th. I managed to store it andshowed it was culture positive by temporarily spending time in the LosAngeles County Public Health Laboratory. I subsequently learned that thechild had a brain biopsy. Although a diagnostic quandary to his treatingphysicians, it showed the vacuolated, foamy cells that I had come torecognize from earlier patients and from the virus inoculated cats. Thechild further deteriorated following the surgery and died.I took leave from USC in January 1996 when confronted withdemands for an additional $15,000 before my laboratory would be reopened.This amount was said to reflect the University~s overhead on the moneydisbursed from the Gift Account. It was also made clear that I could notresume any patient related testing. Under considerable duress, I eventuallylocated a laboratory in a closed, bankrupt hospital and moved what equipmentI could claim as my own into this facility. USC held firm to theirinsistence that any equipment I had purchased from prior grants belonged tothe 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 ofstealth-adaptation and focus on how the diseases might best be treated. Thelaboratory was designated the Center for Complex Infectious Diseases orCCID. 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 validatedthe stealth virus testing in double blinded studies. Similar double-blindedvalidations were independently performed by Dr. Robert Gan, Ph.D., RussellCollins, CLS, and on various occasions by myself (with the help of anassistant to code the samples). As we all knew, positive tests were neitherdisease specific nor confined to patients with severe illnesses. Still apositive test was clearly and unmistakably abnormal. As an example, I recallin 1996 showing a positive culture to the technologist in the VirologySection of the Los Angeles County Public Health Laboratory. She immediatelyrecalled seeing a similar cytopathic effect from a much earlier culture. Asshe retrieved her records it turned out to be the sample sent to her in 1991from the comatose patient with the history of a bi-polar manic depressiveillness.DNA sequencing data continued to substantiate the model ofstealth-adaptation as the loss or mutation of the relatively few genes thatcode for components that are recognized by the cellular immune system. Mostvirologists have yet to appreciate that since individual lymphocytesrecognize distinct antigens, effective immune recognition of virallyinfected cells requires multiple copies of a few viral antigens at the cellsurface rather than a plethora of many antigens that would impede effectivelymphocyte binding. For example, approximately 60% of the anti-humancytomegalovirus cytotoxic T lymphocytes recognize the protein coded by theUnique Long segment gene number 83 (referred to as UL83). Twenty-fivepercent recognize UL55 and another 10% the UL123 protein. Deletion ormutation of these three genes and one can arrive at a virus that will not beeffectively recognized by the cellular immune system. Stealth-adaptedviruses show additional properties including the apparent capacity toassimilate other genes that can include genes of bacterial origins andcellular genes that can potentially cause cancer.It is difficult to exaggerate the potential Public Healthsignificance of the stealth-adaptation process to the microbial threat posedto mankind. The production of live vaccines, especially in tissues fromforeign species, such as the use of African green monkeys to produce livepolio vaccines, could clearly facilitate stealth-adaptation. Armed with aninsider~s knowledge of the vaccine industry and the influence it can have onpublic policy, I continue to believe the message will eventually getthrough. On each trip to Washington or Atlanta, I make a point of visitingFDA or CDC, respectively. The following unanswered e-mail sent August 2000to the then CDC Head of Herpesvirus Research (Dr. Phil Pellett) following aherpesvirus conference is typical:~Dear Phil,Thank you for the discussion during the last evening of the InternationalHerpesvirus Workshop. You were willing to talk "bluntly," yet in aconstructive manner, regarding CDC shunning of my research. As you said, CDCadministrators look to you for scientific judgment on matters relating toherpesviruses. Without your support, there is little chance of any responseto my requests that CDC pursue what I perceive to be a major Public Healthproblem. As I recall, the major points of our discussion were as follows:You spent approximately 45 minutes at my poster and came away with theimpression that some of the sequence data must be incorrect. You wereconcerned that sequence homology matching should be more uniform and notdiffer along a stretch of nucleotides. You asked if all of the sequencinghad been fully double-stranded and whether I had reviewed all of the primarydata. I indicated that most of the extended sequencing had been performed byLark Technologies, at Houston Texas. While there was some internaloverlapping, the sequences were primarily derived from one-way reactions.While, there is the possibility of an occasional nucleotide error, thiswould have had no effect on the conclusions that I was drawing from thedata. I understand that you hold your own sequence-related studies up to aparticularly rigorous standard, but this has more to do with the types ofconclusions that you are trying to draw, rather than justifying dismissingany sequences that are not verified by double-stranded confirmation. Most ofthe sequences have been on GenBank for a long time and can be revieweddirectly by anyone who's interested. The irregular matching that you notedis indeed interesting and goes along with an earlier publication on thegenetic instability of the virus.You also suggested that real science ought to be obvious to the intelligentscientist and that it was my responsibility to present the work so that itwould be more widely accepted. Again I disagree. Most scientists are prettyfixed in their belief system, and historically any shift in a prevailingparadigm is met with resistance. The average scientists can not be expectedto plow through loads of someone else's raw data, or as you said "interpretmy data for me." The CDC is something of an exception, however, since itsmission is to be vigilant for possible threats of emerging infections. Theposter provided a good opportunity for a scientific discussion, but youchose to view it in my absence. I, therefore, do not know if you fullyunderstood and appreciated the significance of what was being presented.I was surprised by your suggestion that I sought a chance to discuss my workat CDC as a "cheap" way of claiming CDC recognition. I view my challenge asprimarily to get CDC to listen and to take some action. I hope you willcontinue to provide some assistance by engaging in more meaningfuldiscussions of actual sequence data and patients' histories. In particular,I would like to know your responses to the following issues that I haveraised.1. Do you doubt that the virus for which I have extensive sequence data, wasderived from an African green monkey simian cytomegalovirus.2. Do you doubt that the virus came from a patient, or that it can inducesevere illness when inoculated into cats.3. Are you convinced that the virus has some unusual sequences that at leastqualifies it as being an atypically structured virus.4. Do you feel the apparent absence of UL83 and UL55 related genes couldprovide the virus a way of evading recognition by the cellular immunesystem.5. Are you willing to accept that the virus has recombined with cellularsequences, including the CXC chemokine coding gene, melanoma growthstimulatory activity, a potential oncogene.6. Do you see any significance in the apparent amplification of the US28chemokine receptor coding gene.7. Do you accept the presence of bacteria-derived sequences within the viralgenome.8. Are you aware of the high proportion of patients with unexplainedencephalitis-like illnesses, including cases in which brain biopsies havebeen submitted to CDC for review.9. Given our positive tissue culture findings in such patients, can youdismiss the possibility that these patients are infected with atypicallystructured viruses.10. Don't you think we owe it to those responsible for the Nation's PublicHealth
W. John Martin, M.D., Ph.D. quotes W. John Martin, M.D., Ph.D, Thu Dec 11 20:56
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