Commentary:

Comments on Autism

Posted on TAAP (The Autism Autoimmunity Project) Website April, 2005

Ms. April Oakes, President of TAAP

Dear April,

Some 12 years ago I was trying to explain the concept of stealth-adapted viruses to a keynote speaker at an autism conference. The prominent psychologist responded: "You have to understand John that autism is our anchor. It is a solid rock that establishers who we are. You are trying to tell us that autism is not a disease but only a symptom. That it involves viruses and yet not ordinary viruses but something you call stealth. How can we possibly embrace these concepts and still maintain ourselves as experts? I'm sorry but don't expect much support from us." Little has changed in the past 12 years except for substituting the word business for anchor and the phrase money-making entrepreneurs for experts.

I realize that autism does not fit the model of an acute infection with high fevers, rashes or even inflammation, the accepted hallmark of infection. Neither the psychologist referred to above or many of today's experts are virologists or even insightful biologists. What is disappointing is that they don't want to hear information that might challenge their egos or ambition to make money.

Where can they get their money and ego boosts? The answer is the parents of autistic children. Parents are recruited to conferences hoping to hear what is new. They are the cash cows being presented with pseudo-scientific talks that are somewhat incoherent and occasionally contradictory. Very little hard data are ever presented. Challenging questioning of speakers by other speakers rarely occurs. Rather a series of diagnostically and therapeutically irrelevant tests are promoted and unproven remedies prescribed.

The real price being paid comes not from the pockets of parents but from the lives of autistic children. I would be more sympathetic if I felt the problem was mainly one of ignorance and restricted thinking. All too often I have found a speaker, fresh from
a standing ovation by parents, conferring with colleagues on how to better milk the situation.

If autism is epidemic, why not look for an infectious cause? I have done so and have concluded that autism is an infection caused by viruses that avoid the immune system (stealth-adapted viruses). Fortunately there is a back up defense system in the form of an alternative cellular energy (ACE) pathway. Activation of this pathway is providing dramatic results in patients with conventional herpes virus infections. It holds great promise as an inexpensive, yet effective, method of suppressing stealth-adapted viruses.

Kind regards, John

Posted on TAAP (The Autism Autoimmunity Project) Website and Shaffer report May 2005

A Viral Causation of Autism
By W. John Martin, M.D., Ph.D.

Much effort and resources within the autism community have been misdirected. Consequently, the epidemic continues. I am very confident autism will eventually be recognized as having a viral cause. This delay will be lessened if parents simply consider the facts and sort through the political and economic agendas that bias what they are mainly being presented.


The important facts are:


1. The cellular immune system does not effectively recognize all viruses. Effective immune recognition is generally restricted to only a few viral components. For example cytomegalovirus (a type of herpesvirus) has nearly 200 proteins yet over 90% of the cytotoxic T cell immune response is directed to only 3 viral components. By a process called "stealth-adaptation" a virus can lose these critical components and yet can retain or regain the ability to cause cell damage. I have DNA sequence data confirming this mechanism. More importantly, I have directly observed animals inoculated with stealth adapted viruses. The animals become extremely sick with widespread tissue damage, including extensive damage to the brain. Yet there is no inflammatory response; the usual hallmark of an infectious process. I have seen similar brain damage in several patients from whom I have cultured cell damaging (cytopathic) viruses. Interestingly, the animals largely recover from their illness over time (discussed later).


2. Unlike other organs in the body, the brain is uniquely sensitive to virus induced cell damage. With other organs, there is an overall uniform function. This means that limited localized damage in one area of these organs can be easily compensated by increased activity elsewhere. The brain functions differently with specific functions localized to distinct areas. Damage in one area cannot, therefore, be easily overcome. An exception is when the virus induces an auto-immune response such as in Hasimoto's disease of the thyroid which is not uncommon among stealth virus infected patients. The other exception is cancer which only requires a single cell to go astray.


3. The big political block to my work came when I announced in 1995 that the prototype stealth-adapted cytomegalovirus was not of human origin, but was derived from the monkeys used to make live polio virus vaccines. I immediately notified FDA, CDC and Wyeth the manufacturer of live polio virus vaccine, but received a very cold reception. Adding to this block was the undisclosed study performed by FDA and Industry in 1972 showing that all of the African green monkeys being used for polio vaccine production were infected with simian cytomegalovirus (SCMV). FDA and Industry failed to disclose this finding not contemplating that viruses could cause chronic illnesses.


4. FDA recently did locate 8 licensed lots of polio vaccines released to the public in 1976. Three of the 8 lots have DNA of SCMV. FDA investigators say they cannot culture live virus from these lots, nor can they legally provide them for outside testing. in spite of this finding, FDA officials are still reluctant to follow up on my initial reports of stealth-adapted SCMV being isolated both from a patient with chronic fatigue syndrome and from a patient with a bi-polar manic depressive psychiatric illness.


5. It is technically difficult to culture stealth-adapted viruses because of a tendency for the cell damaging effect not to progress. The cultures undergo a repair process because of materials that accumulate in the culture fluids. I now recognize that these materials provide an alternative (non-mitochondria) source of cellular energy.


6. The polymerase chain reaction (PCR) can be used to detect some stealth-adapted viruses providing the small region being targeted by this reaction is conserved. Another difficulty with the PCR assay is that not all stealth-adapted viruses are derived from SCMV. Rather stealth-adaptation is a generic process that presumably can occur with all types of cytopathic viruses, e.g. EBV, HHV-6, HSV, etc.


7. An individual from Florida recently sent his own and his father's blood to an animal testing laboratory. He had the smarts to pretend to be a veterinarian and to request tests on supposedly monkey blood. The result came back PCR positive for SCMV. I visited the testing lab. and assured myself they were able to clearly exclude human, rhesus monkey and baboon CMV and that the result was indeed positive for SCMV. The infected patient notified CDC of the results. CDC simply concluded they could not culture virus from his blood and the issue has seemingly been dropped. I received a "legal request" from the patient to test his blood. It induced the characteristic cytopathic effect caused by stealth-adapted viruses.


8. The Florida example underscores the infectious nature of stealth-adapted viruses. The gentleman became infected during a trip and soon after returning home saw marked behavioral changes in his son. His father visited briefly and he too became sick. There are many examples of "family illnesses of presumptive infectious origin" including many families in which there is an autistic child. The gentleman has markedly improved on ACE products (discussed below).


9. I have previously performed several double blind studies comparing stealth virus cultures from patients with various illnesses, including autism, with blood samples from volunteer donating blood for transfusions. A clear distinction was seen with the vast majority of patients testing positive compared to 10-15% of blood donors. According to the terms of the approved study, I could obtain no information on the health of those blood donors who tested positive. The implication of a contaminated National blood supply was hard for Public Health authorities to accept. In late 2002 I was encouraged (instructed) not to perform any further clinical testing and to ensure my compliance the clinical testing laboratory license was suspended. The only exceptions allowed were for research and, as I have recently learned, if legally requested.


10. The research focus returned to the issue that if there was no effective immune recognition, how does the body cope with stealth-adapted viruses. The answer was in the cultures that showed complete healing if inhibitory materials were allowed to accumulate. I had previously noted unusual complex structures in the brain cells of humans and stealth-virus inoculated animals. The mitochondria which normally supply the cell with energy were markedly disrupted, yet the cells were still surviving. It appeared as if the complex structures, and the materials accumulating in the cultures, were providing an alternative (non-mitochondria) source of cellular energy. I called these structures alternative cellular energy pigments (ACE pigments). ACE pigments were experimentally shown to provide an auxiliary defense mechanism that is particularly relevant in defending against stealth-adapted viruses.


11. The importance of the ACE pathway has been convincingly demonstrated in the ease of therapy for conventional HSV oral and genital lesions. The ACE pathway in these lesions can be easily activated using a dye called neutral red followed by brief exposure to ultraviolet-A light. This approach also works well with shingles and post herpetic neuralgia and with genital warts caused by human papillomavirus. FDA was notified of these findings last October and are still trying to decide if they want to classify neutral red as a drug or as a medical device.


12. The obvious implication for autistic children is to activate and/or support the ACE pathway. I have been impressed with some preliminary responses and now want to see controlled studies. The current format for the herpes treatment is to have patients select a physician of their choice. The physicians are to evaluate the lesions before and the day after therapy. We can compensate the physician up to $100.00 from fees collected from participants willing to join an Institute of Progressive Medicine . I think we should do the same with autistic children.


13. It is clear that the pharmaceutical approach to many chronic illnesses has its limitations. The public needs to be better informed of developments outside the pharmaceutical industry. Good data need to be collected from well designed clinical trials.


14. I hope the foregoing will give a sense of optimism to parents struggling with autism and related illnesses. Research on stealth-adapted viruses has opened up a whole new approach to disease therapy. I would like to encourage individuals to visit the web site www.s3support.com and to consider participating in clinical trials as one of the bonuses of being a member of the Institute of Progressive Medicine . The web site has copies of various publications and supporting information.


15. Parents can also put political pressure on the system to begin to address autism as an unintended consequence of allowing cytomegaloviruses to contaminate polio vaccines. Infected parents are at risk of having autistic children. Such parents can be identified, but not if the Public Health system will not allow stealth virus testing or acquire the know-how to do this type of testing within their own facilities.





Posted on TAAP (The Autism Autoimmunity Project) Website May 15, 2005

Ms. April Oakes, President of TAAP

Dear April,

Thanks for your expression of concern about the very limited research support I am receiving. The real concern ought to be for autistic children and their families. It is disappointing to me that very few so called advocates for these children are willing to acknowledge the potential role of stealth-adapted viruses in causing autism. I used to think it was my responsibility to convince others of what appeared to me to be pretty obvious. That is, if autism is epidemic one should suspect an infectious cause. A role for stealth-adapted viruses was established in double blind culture studies attested to by well qualified individuals. Yet the data were not acted upon. When I offered to speak at a local meeting in Los Angeles, I was bluntly told "You are off message John;" meaning that I was not supporting mercury as the cause of autism and not advocating expensive laboratory tests or therapies with kick-backs to those willing to wheel and deal.

As I mentioned in an earlier letter, it is truly disappointing when a speaker fresh from receiving a standing ovation by appreciative parents is seen conversing with colleagues on how to franchise a lucrative scheme for generating exorbitant incomes. I rarely receive requests from other investigators or patient advocates to help explain stealth-adaptation or the concept of an alternative (non-mitochondria) pathway of cellular energy. Conversely my requests for an overview of laboratory results to better understand how they influence therapy are met with resistance. Similarly, the actual response rates to the various therapies in terms of hard clinical data are rarely provided.

I would like to see a vigorous movement among parents of autistic children to demand that their children and other family members be tested in Public Health facilities for infectious viruses. Whether they are called stealth-adapted or something else, it is not difficult to demonstrate their presence using methods that were published over a decade ago. Some of the viruses will undoubtedly be shown to have arisen from African green monkey simian cytomegalovirus. This is consistent with FDA's own data of DNA of this virus being present in 3 of 8 licensed polio vaccine lots released in the mid 1970s. It also follows the 1972 realization that the monkeys being used to produce live polio virus vaccine were uniformly infected with simian cytomegalovirus. In retrospect, the use of freshly cultured monkey kidney cells to produce polio vaccines may turn out to be the biggest Public Health blunder of the last century.

Stealth-adaptation of cytomegalovirus and other viruses is based on the simple concept that the cellular immune system only recognizes and reacts to relatively few viral components. In the case of human cytomegalovirus, over 90% of the anti-virus cytotoxic T cells are directed at only 3 of the nearly 200 different components. Loss or mutation of these critical components can allow a virus to evade effective immune recognition. A present day analogy is that of a terrorist who has no insignia or other means of identification. Like a terrorist, stealth-adapted viruses can still cause a lot of damage. It is mostly reflected by impaired functioning of the brain which is especially vulnerable to even limited localized cell damage.

Fortunately, the immune system is not the only defense humans and animals have against virus infections. From the beginning of the research, it was apparent that if cultures of stealth-adapted viruses were left undisturbed, the damaged cells would recover. The recovery process was attributed to the accumulation of what I termed alternative cellular energy pigments (ACE pigments). Validation of this approach has come from recently published studies showing expedited healing of conventional herpes simplex and herpes zoster viruses and also papillomavirus induced skin lesions by activating the ACE pathway. I firmly believe that autism will also be amenable to this type of approach.

ACE related therapies are not dependent upon there being an underlying virus infection. On the other hand, mobilization of Public Health resources in support of preventing and treating autism will be more forthcoming to counter an infectious process. I am open to suggestions and to offers of help to move the process forward. This has been a productive year in terms of publications with five peer reviewed articles, four of which are on the web site www.s3support.com. The article that I look forward to seeing published this year will be one showing marked clinical benefits in autistic and other stealth-adapted virus infected children in response to activation of the ACE pathway. With sufficient support and public awareness, I feel this goal can be achieved.

Kind regards,
W. John Martin, M.D., Ph.D.

Posted on TAAP (The Autism Autoimmunity Project) Website May 15, 2005

Dr. Martin's Conflict with CDC on Stealth-Adapted Viruses

I received several enquiries in response to your posting a letter that I had recently sent. Among the questions being asked is why does CDC not believe in stealth-adapted viruses and why was I prohibited from continuing to perform stealth virus testing within the Center for Complex Infectious Diseases. The CDC has plenty of justification to test for stealth-adapted viruses but not the political will (meaning direction from Congress) to do so. The basic challenge "If autism is epidemic, why not look for an infectious cause?" has never been vigorously pursued by public health authorities. Your readers may be interested in the following vignette.




Last year an individual developed an apparent infectious disease during a business trip. He initially feared AIDS in spite of there being no close sexual encounters. HIV tests were uniformly negative. His concerns about being infectious increased when he noted marked behavioral changes in his son. His father also started to experience headaches, fatigue and memory loss following a weekend visit. Having read of my work on simian cytomegalovirus (SCMV), he inquired of the Miami Zoo how they test for SCMV. They referred him to a primate testing laboratory that performs polymerase chain reaction (PCR) assays for various viruses. Having the smarts to adopt the name of his neighbor's dog for his own blood sample and a similar monkey sounding name for his father's blood, he requested testing from the primate laboratory. Both results came back positive for SCMV by PCR. I visited the laboratory and was assured of the positive results that excluded human, rhesus monkey or baboon CMV. Using the loophole that forensic testing is exempt from the Clinical Laboratory Improvement Act (CLIA) prohibition against unapproved clinical tests, I confirmed, in response to a formal legal request, that the individual was culture positive for a stealth-adapted virus. CDC was contacted by the individual. They did at least request blood and throat samples but did not avail themselves of my offer to describe how best to culture for stealth-adapted viruses. Not getting a positive culture, CDC readily dropped the ball. The individual has significantly benefited from products that can provide support through the alternative cellular energy (ACE) pathway.

There are many other compelling reasons why CDC should be more
proactive in pursuing the potential of widespread SCMV infection in the
community. FDA has published data showing that 3 of 8 licensed polio vaccines released to the public in the mid 1970's contained DNA of SCMV. Congenital infection with regular human cytomegalovirus is one of the known causes of autism, being all the more reason to look for stealth-adapted cytomegalovirus. SCMV has multiple copies of a gene that enhances the infectivity of HIV. CMV is also implicated in major vascular diseases and in several forms of cancer.

Various autism support organizations have been remiss in disregarding a potential infectious process as a major cause for the autism epidemic. More than once I have heard it argued "We don't want to go there less we give our children a pariah status." More likely, the notion of an infection conjures an image of high fevers, inflammation and person to person transmission of an illness. None of these apply to autism. Nor do these parameters apply to stealth-adapted viruses that avoid effective immune recognition and do not provoke an inflammatory reaction.

I have also been personally criticized by a few individuals who seem to need a focus for their anger. Negative comments, especially when presented on the internet have assuredly discouraged others from supporting my research and have played into the hands of those not wanting to face the reality of stealth-adapted viruses. In response to being asked once again to respond to such criticisms, I provided one of your readers with the following historical account. I thought it might be useful for you to share it with other readers. Kind regards, John.


Dear Mr. ________,

I have become pretty immune to pointless criticisms and feel it is part of the territory of working on a socially complex set of illnesses. An early encounter with patient anger came at a talk I gave at the University of Southern California (USC) in August 1994. I had just published an extensive article in the American Journal of Pathology that was entitled "Cytomegalovirus-related sequences in an atypical cytopathic virus repeatedly isolated from a patient with the chronic fatigue syndrome." A husband and wife team of prominent academics from a major neighboring academic institution were in attendance at my talk. The data were straightforward and worth discussing. Instead the tenor of repeated interruptions from the husband was along the lines, "I have chronic fatigue and I am smarter than you. I do not know what causes it, neither do you." Rather than leaving it at that, he complained to the dean who subsequently lectured me on how the University fund raising efforts could be undermined if I pursued divisive research.

There was also a hostile backlash from some prominent researchers within the chronic fatigue and immune system dysfunction syndrome (CFIDS) community. They had looked for viruses but had either not found any or had dismissed what they saw as reflecting secondary reactivation. Again, I was surprised by their complaints going to the dean at USC. A CFIDS support group had earlier wanted there to be a correlation between a positive virus culture and the symptom of fatigue. When this was not true they also withdrew support in favor of more politically connected supporters.

The research continued and by 1995 I had unequivocally established that at least two of the virus isolates were derived from the cytomegalovirus of African green monkeys. These results were published in an article appearing in July 1995 entitled "African green monkey origin of the atypical cytopathic 'stealth virus' isolated from a patient with chronic fatigue syndrome." The same year I published a research letter "Stealth virus isolated from an autistic child" and a compelling paper along with Dr. Tom Glass entitled "Acute encephalopathy induced in cats with a stealth virus isolated from a patient with chronic fatigue syndrome."

The clinical and microscopic observations made in the cats paralleled those I had seen in severely ill patients with undiagnosed neurological diseases. There was subtle but extensive cell damage without any inflammation, the accepted hallmark of an infectious process. As far back as 1990, I had seen brain biopsies with no inflammation yet microscopic indications of the same type of cellular damage as was occurring in cultures from the blood and cerebrospinal fluids from chronic fatigue syndrome patients as well as from several children with autism and related illnesses. Moreover, the brain tissue yielded evidence for a virus infection using the polymerase chain reaction (PCR) assay.

Several of the cultures showed electron micrographic evidence of virus activity along with peculiar material that I had initially discounted as cellular debris. I soon came to realize that this material was actually helping the cultures overcome the cell damaging effects caused by the viruses and knew that it might provide a clue on how to eventually treat patients infected with these viruses. I called these materials Epione after the wife of Asclepius, the father of Greek medicine.

The African green monkey origin of some of isolated stealth-adapted viruses implicated live polio virus vaccine produced in kidney cell cultures from these monkeys as the probable source. Having worked at the FDA Bureau of Biologics, I was well aware of the vaccine production method and the continuing concerns about virus contaminants. My notifications to FDA, CDC and the vaccine manufacturer were not kindly received. Moreover, my offers to test chronic fatigue syndrome patients for evidence of monkey virus infection exceeded the threshold at USC. My laboratory was closed within a week of a lawyer filing a suit against the polio vaccine manufacturer for me to test some of the bulk lots of vaccines received by his ill clients.

Having seen numerous examples of virus culture positive patients struggling with their illnesses, I was unwilling and indeed unable to sign an agreement with USC not to test any additional patient samples. The research proceeded quietly and at a slow pace in a private largely self-supported laboratory. At critical times an occasional person appeared who helped bridge a critical financial gap. I once called a Japanese donor who had provided some steady support to express my deep appreciation. His simple answer "It is my duty," reinforced my own conviction that I was obligated to proceed with the research.

In 2003 I again crossed a threshold by stating that up to ten percent of students donating blood to the UC Irvine Blood Bank were stealth virus positive. This brought into question the safety of the nation's blood supply.

Of several hundred patient contacts, all but a few have been very rewarding and have more than encouraged my continuing efforts on their behalf. I have encountered the occasional hostile patient with a sense of anger, resentment, self-entitlement and betrayal when I have not endorsed an unjustified demand. One such patient was used by the California Department of Health to carry out the wish of the Centers for Disease Control and Prevention (CDC) to stop patient testing for stealth-adapted viruses. This was achieved by suspending a Clinical Laboratory Improvement Act (CLIA) laboratory license in September 2002. Copies of my fruitless letters to the Centers for Medicare and Medicaid that issues CLIA licenses are included on the web site www.s3support.com

Fueled by the suspension of the CLIA license, the patient went on to file legal suits and make extraordinarily disparaging claims in a television interview. While I answered many leading and insulting telephone questions from a reporter from NBC, I chose not to grant her a filmed interview. My experience at USC had convinced me that major news organizations were unlikely to fairly air an opinion that polio vaccines were a potential source of many of today's epidemic illnesses. The bad publicity from the television showing was used by a splinter CFIDS group to declare on the internet that all stealth virus-related research was bogus.

I have similarly been criticized for not endorsing various co-infections of patients with pathogens such as mycoplasma, HHV-6, Borrelia (the bacterium that causes Lyme disease) or with toxins, such as mercury in the case of autism. The criticisms have only come after an overture for me to join in and share a piece of their pie. I am more comfortable staying with what I know to be true. Viruses do exist that are not effectively recognized by the immune system. These viruses can be frequently cultured from patients with chronic debilitating neurological illnesses. Some of these viruses were unequivocally derived from the cytomegalovirus of the monkeys used to produce live polio virus vaccines. That the body can use a non-immunological defense mechanism to provide an alternative (non-mitochondria) source of cellular energy; and that this alternative cellular energy (ACE) pathway explains the repair process seen in cultures of stealth-adapted viruses. This pathway offers a promising approach to therapy of
stealth-adapted viruses as well as an adjunct approach to therapy of conventional viruses such as herpes simplex, herpes zoster and human papillomavirus infections.

Five papers have been submitted or published this year with several more in preparation. The research is providing interesting insights into basic biology and has important therapeutic and public health ramifications. It could benefit from more support and less criticism. I trust this answers your concerns. Kind regards, W. John Martin, M.D., Ph.D.