Autism

Other Blogs of W John Martin

2004-12-28T08:34:00.000-08:00

Stealth-Adapted Viruses:The Cause of Autism*

2004-10-17T22:07:00.000-07:00

Stealth-Adapted Viruses:The Cause of Autism*
W. John Martin, M.D.,Ph.D. Center for Complex Infectious Diseases Rosemead CA 91770 Telephone (626)616-2868;
e-mail ccidlab@hotmail
Web address: www.ccid.org/www.s3support.com

Introduction
Autism is a diagnostic label applied to neurological disorders of early childhood onset. It manifests as deficits in communication and in other social interactive skills. Considerable variability exists in the severity of disease in autistic patients, with somewhat arbitrary distinctions between autism and childhood disintegration disorder at one end and delayed normal development at the other extreme. Autistic patients will commonly show a wider variety of clinical manifestations than implied by a single diagnostic label.While many millions of dollars have been spent on autism-related research, only a few studies have provided important insights into the underling cause, prevention and treatment of this disease. This talk will provide a brief summary of generally accepted research views on autism and a lengthier discussion of some of the more controversial opinions. The argument will be presented that autism is essentially an encephalopathy of stealth-adapted viral origin. Research findings on a stealth-adapted virus that arose from the species of monkeys used to produce poliovirus vaccine will be summarized. Sequencing of this virus has suggested specific therapeutic approaches to the treatment of patients with autism and other stealth-virus related clinical conditions. Preliminary clinical experience with some of these approaches has been encouraging and indicates the need for formal therapeutic trials. Studies also need to be pursued into the modes of stealth-virus replication and transmission of what may well prove to be a major threat to the survival of mankind.

Generally Accepted Research Views on the Nature of Autism
1. Autism has a Genetic Component: This is apparent from the higher incidence of autism among boys. It is also supported by the relative concordance of disease among monozygotic (genetically identical) twins compared to dizygotic (genetically different) twins. Still there are numerous examples where only one of two genetically identical twins has the disease. Genetics may well be a contributing factor to the expression of autism, but it is clearly not the only component to this (or these) diseases.
2. Brain Abnormalities in Autistic Children: Head circumference has been accepted as a marker of brain size. While normal at birth, the head circumference of 1-2 year old autistic children is reportedly slightly enlarged. Brain imaging has also shown enlargements in certain regions of the brain, most noticeably in parts of the cerebellum. Equally impressive are various functional studies that show deficits in brain activation upon certain types of sensory stimulation and in blood flow patterns in autistic children. The question arises whether these changes are a consequence of autism, rather than its cause. Limited histopathological studies on brain tissue from autistic patients support the view that certain brain cells are damaged and/or do not normally develop.
3.Biochemical Indications of a Prenatal Disorder. As recently reported, elevated levels of one or more neuropeptides are present in neonatal blood samples obtained from children who subsequently were diagnosed as autistic. The source of the elevated neuropeptides was presumed to be the brain but this was not established. The actual levels of various neuropeptides examined differed among autistic children, but as a group the autistic children were readily distinguishable from normal children. Somewhat confounding, however, was that similar elevations were consistently also found in blood samples collected from mentally retarded children. Mental retardation had not previously been linked with autism and clearly differs with respect to the smaller than normal head circumference seen at birth.

Controversial Issues Relating to Autism

1. Autism is the Result of Vaccination. Reports of marked clinical deterioration and even the initial onset of autism within days of receiving a vaccination has prompted the view that the vaccine has caused the illness. Initially the focus was on diphtheria/petussis/tetanus (DPT) vaccine but more recently it has been on live measles/mumps/rubella (MMR) vaccine. In the case of measles, vaccine-derived viral material has been seen using immunohistochemistry and molecular based assays within hyperplastic lymphoid tissue present in the gastrointestinal tract of autistic children.Similar findings were found in non-autistic children with lymphoid hyperplasia. Although there are reasons for concerns with live viral vaccines, including the finding of retroviral related reverse transcriptase activity in MMR vaccines, a primary etiological role of measles vaccine virus is not supported by data indicating prenatal abnormalities. A detrimental effect of MMR vaccine has also been dismissed with results of various epidemiological studies failing to show statistically significant correlation between vaccine usage and disease prevalence.

2. Autism is a Primary Biochemical Disorder. Urine analyses on autistic children have shown markedly elevated levels of various peptides as well as other types of metabolic products.An inference is that the levels of these chemicals would also be increased in the brain and that they somehow interfere with normal brain function. A prime example is the opiate-like peptides resulting from incomplete digestive breakdown of casein and gluten proteins. This view is bolstered by noticeable clinical improvements in some autistic children when placed on a casein and gluten free diet. Peptides from abnormal bacterial and fungal bowel flora may also been suggested as having neuroregulatory activity whose levels may be reduced by antibiotics. A role for cell associated peptidase is suggested by unpublished studies that peptidase IV inhibitory fragments may also be present in the urine of some autistic children.

Autism: A Stealth-Adapted Viral Encephalopathy

I am proposing that autism is primarily a prenatal infection that involves the brain and occurs in a genetically predisposed individual. The infection renders the person susceptible to further brain damage from vaccines and other environmental factors. Several lines of evidence support the stealth virus cause of autism. For example:
Blood samples from autistic children consistently induce a readily identifiable cytopathic effect (CPE) using viral culture methods adapted for the detection of stealth-adapted viruses. Stealth virus testing of blood samples from autistic children has been subjected to formal “double blind” analyses. Furthermore, cerebrospinal fluid (CSF) and gastrointestinal biopsy have similarly yielded positive cultures.
There is good evidence for stealth virus infections among family members of autistic children. Many of the family members will, upon close questioning, reveal symptoms of neurological and/or immunological dysfunction.
Autistic patients will not infrequently display positive results in assays intended to detect conventional virus and bacterial pathogens. As discussed below, such results can be attributed to cross-reactivity with stealth virus components.
When will the stealth virus theory of autism be accepted and supported by i) researches, ii) Public Health authorities, and iii) families with affected children. The answer to the first point is when it is clearly proven that stealth-adapted viruses, as presently defined, do exist as novel pathogens. This challenge, as well as the goal of eliciting official Public Health involvement, will occur when the message gets across that the extensively sequenced prototype stealth-adapted virus is atypically structured and that it arose as a probable contaminant of poliovaccine production. Finally, parents will begin to focus their energies on the stealth-adapted viruses infecting their children once they begin to see real clinical improvements based onanti-stealth virus therapies.

Sequencing Studies on an African Green Monkey Derived Simian Cytomegalovirus (SCMV)

These studies unequivocally establish the origin of an atypically structured cytopathic virus as being from SCMV. For certain regions of the stealth viral genome, there is over 90% identity between the nucleotide sequences of the stealth virus and that of the Colburn strain of SCMV. Yet in other regions, the two viruses differ in a manner that is best explained by genetic instability in viral replication and by the selection of genetic changes that favor viral survival and avoidance of immune recognition. Of particular note is that the virus failed to evoke an inflammatory reaction in either the patient from whom it has been repeatedly cultured, or from the cats in which it induced considerable brain damage. To date, the genes that would otherwise encode the major antigens targeted by anti-CMV cytotoxic T lymphocytes have not been detected. Nor do the viral cultures react with antibodies against several antigens shared by human and simian CMV.

Over 120,000 nucleotide sequence data have been compiled on the stealth-adapted virus. Long regions of contiguous sequences suggests the coding of somewhat truncated proteins in comparison to the coding potential of the comparable region ofthe human CMV genome. To help clarify the extent to which these changes reflect the preexisting SCMV genome, or are part of a mutational process occurring within a genetically unstable stealth-adapted virus, sequencing is underway on an authentic monkey-derived SCMV.

Even at this stage of the work, is abundantly clear that stealth adaptation involves much more than simple deletion/mutation of particular genes targeted by the cellular immune system. For example, there is a striking over representation of certain genes. Of particular interest, is the finding of multiple copies of genes implicated in the production of, and providing receptors for, potent growth factors called chemokines and present within the virus. This observation strongly suggests the potential value of suppressing chemokine production in this particular patient.

Another striking feature of the DNA analysis is the presence of particular cellular genes adjacent to viral genes. A prime example is the three copies of a cellular chemokine-related gene within the viral genome. These virus-incorporated cell-derived genes do not contain normal stretches of non-coding sequences (introns) that are present in the cell DNA. This would indicate that the recombination process allowing cell-derived genes to become incorporated into a replicating stealth virus had occurred at a partially processed RNA, rather than at a DNA level. If so, it would indicate a role for endogenouse reverse transcriptase in stealth virus assembly and replication. Several other cell-derived sequences are more readily amplified using polymerase chain reaction (PCR) based assays performed on the stealth virus culture than when performed on uninfected cultures, suggesting that the sequences may have been incorporated as part of the stealth virus replication process.

Various bacterial-derived sequences have also been extracted from the cultures. The bacterial sequences are of particular interest since, along with additional data, it appears that the virus is able to pass into, and, therefore, be potentially metabolically empower and be transmitted by bacteria. Taken together, the data are consistent with a viral replicative process that allows the assimilation of extraneous sequences of cellular, bacterial and possibly fungal origins. Addressing this situation is particularly urgent since among the potential activities of cell derived genes, including chemokine-inducing and chemokine-receptor genes, are the induction of malignant changes. The prospect of highly infectious bacteria carrying cancer causing genes is a serious concern that, so far, has been brushed aside by those responsible for overseeing the Nation’s health.

Stealth-adapted viruses that have incorporated bacterial sequences are referred to as “viteria.” Work is underway to confirm that such organisms can be mistaken for actual bacteria in conventional assays for such pathogens as Borrelia burgdoferi, Mycoplasma incognitus, Chlamydia pneumonia, etc. Many bacterial proteins have a propensity to evoke allergic reactions offering a possible explanation for such reactions among autistic children.

Stealth Adaptation as a Generic Process

CPE generally similar to that shown with the SCMV-derived stealth-adapted virus has been consistently seen with blood samples from many other patients. Most of these isolates do not react particularly strongly with antibody and molecular based probes that are highly reactive with the prototype SCMV-derived stealth-adapted virus. This finding suggests marked structural variability and probable multiple, diverse origins of stealth-adapted viruses. Limited sequence and antibody staining data on some of these additional isolates are consistent with origins from other herpesviruses, including Epstein-Barr virus and human herpesvirus-6; and also from such diverse viruses as parvovirus, adenovirus and enteroviruses. The addition of various live viruses to positive stealth virus cultures can lead to enhanced CPE, suggesting the possibility of reciprocal viral stimulation and even the recombinant formation of new viral constructs. This potentiating effect has been noted using live measles and other viral vaccines. It is also reasonable to assume that certain stealth viruses may retain some components that would normally not be involved in evoking cellular immunity, but in the presence of a powerful immune stimulant (such as provided by DPT vaccine) could become a target for cell damaging immunity.

A topic of interest is whether stealth-adapted viruses cultured from autistic children will show any distinguishing characteristics from those cultured from patients with other disease manifestations. Given the overall similarity in the CPE seen when tested blood samples from autistic and non-autistic family members, it seems likely that a similar virus is involved and that clinical manifestation relates to sex, other genes and time and location of infection.

Implications for Patients with Autism

Specific testing for cell derived chemokine genes, as are present in cultures of the prototype stealth virus, has yet to be performed on stealth virus cultures from patients with autism. Clinically, however, drugs that are known to down regulate chemokines are finding increasing use in patients with other stealth-virus associated diseases, including depression, attention deficit and hyperactivity disorder (ADHD) andCFS. Of particular interest are many of the disease modifying anti-rheumatic drugs (DMARDS). Some clinicians have also anecdotally noted symptomatic improvement with Acyclovir, an anti-herpesviral drug.

Progress in this field will require disciplined clinical trials with close monitoring of patients using both clinical markers and semi-quantitative stealth virus cultures. In the meantime, work needs to be continued on the development of more specific therapies that are based on a more detailed understanding of the mode of stealth virus replication.
Positive blood cultures is a sign of a body wide infection that can potentially cause multi-organ damage (both as the result of direct virus damage and an evoked auto-immune response). Rather than being viewed narrowly as a neuropsychiatric illness confined to the brain, autism should be viewed as a generalized viral infectious process that also involves the brain. Specific testing for endocrine disorders, gastroenteropathy, liver damage, allergies, etc., should be part of the overall medical profile of any stealth virus infected patient. The finding of a positive stealth virus culture in a child is probably sufficient reason to avoid the intense immunological stimulation associated with DPT vaccine and also to not add extraneous infectious viruses in the form of MMR and live poliovirus vaccine. Acceptance of an infectious cause of autism can help explain the occurrence of stealth-virus associated illness among other family members. Certainly other family members should be tested for infection. The socially difficult issue of possible contagion to classmates, schoolteachers, non-infected family members, etc., is better addressed than denied.

Summary

Autism is a clinical label referring to a set of symptoms that can occur as a result of infection with atypically structured, poorly immunogenic (stealth-adapted) viruses. This conclusion should help reorient the clinical approach to the diagnosis, therapy and prevention of this illness.

*Lecture prepared to be given at Catalina Island, June 9, 2001, but unable to do so for family reasons.

The Business of Autism

2004-10-05T20:45:00.000-07:00

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 by viruses that avoid the immune system (stealth-adapted viruses). Fortunately there is a back up denfense 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.

Measles Vaccine and Autism

2004-10-04T19:18:00.000-07:00

Dear Reader,
The recent DAN conference provided an opportunity to hear once again of Dr. Wakefield's finding. I had listened before in Birmingham, San Diego and during a congressional hearing. My reaction was the same as before: First, some children with autism have a marked pan-enteropathy. This is commonly manifested as lymphoid nodular hyperplasia, a condition not uncommonly seen with viral infections, including HIV. Immunochemistry shows measles virus antigens in some of the lymphoid nodules. More from previous photographs than the less detailed photograph shown at this meeting, the measles antigens appeared to associate with dendritic (antigen presenting cells). The important observation that I could discern was the lack of any associated cell damage (cytopathic effect). Low levels of measles virus RNA has apparently been detected in some cerebrospinal fluid samples from autistic children. It was shown to be of measles vaccine origin. A correlation exists between the use of measles vaccine and autism incidence. From these data, it is concluded that measles vaccine virus is the cause of autism. One mechanism is the release of toxic metabolites through the measles virus damaged gut wall. The role of thimerosal may be to cause sufficient immune suppression to allow the measles virus to persist and to continue to cause gut, and possibly brain, damage.
The formulation has several flaws. For example, non-autistic children with lymphoid nodular hyperplasia and other forms of enteropathy, do not necessarily show remarkable brain damage. Second, the immunohistological findings do not support a cytopathic role of measles virus. The hypothesis does not explain evidence of brain damage prior to birth.
Unfortunately, the DAN conference format was not conducive to scientific debate. I have cultured stealth viruses from gastrointestinal biopsies and have also shown that measles vaccine virus can promote stealth virus growth. Suffice to say, nothing presented at the DAN conference argues against autism is essentially one form of a congenital stealth virus encephalopathy that may be accompanied by signs of stealth virus infection elsewhere in the body, including the gut.

Autism, Thimerosal, DAN Conference

2004-10-02T22:06:00.000-07:00

Dear Readers,
I attended some of the sessions of the October 2004 DAN conference in Los Angeles. I was interested in learning whether my message had landed "If autism is epidemic, why not look for an infectious cause."Instead, I heard a lot of questionable claims relating to mercury. Specifically, the speakers argued that: i) Poisoning from thimerosal and its derrivative ethyl mercury is the predominant cause of the increasing incidence of autism. ii) This increase corresponds to the increasing amounts of thimerosal received as a result of additional vaccines being given to young children. iii) That genetic factors limiting the availability of glutathione is a major reason why some children have an impaired ability to excrete mercury. iv) The genetic factors include genes that code for enzymes active in methionine-related methylation pathways with certain alleles of these genes correlating directly with susceptibility to developing autism. v) That the male predominance of autism is explained by the capacity of testosterone or closely related male hormone to potentiate the toxicity of ethyl mercury derived from thimerosal. vi) Conversely, estrogen can protect cultured neural cells from thimerosal induced cellular damage. vii) That antibiotics also potentiate ethyl mercury induced cell damage. viii) That removal of mercury through chelation, including transdermal DMPS, results in complete remission in a high majority of autistic children. ix) That in addition to be directly neurotoxic, thimerosal suppresses the immune system, leaving the individual open to other infections including vaccine derived measles virus. x) Thimerosal also damages the bowel inhibiting disaccharide enzymes from breaking disaccharides into absorbable monosaccharides. xi) The unabsorbed disaccharides promote the overgrowth of yeasts and bacteria. xii) The abnormal bacteria synthesize d-lactic acid that is toxic to the body and adds to the autistic symptoms.
While the argument for removing thimerosal from vaccines is obvious, to attribute the current autism epidemic to thimerosal is far less convincing. To my mind, many of the speakers seemed to be dabbling. A little biochemistry here, a little genetics there, etc. No one seemed truly knowledgeable and the word "possible" was decidedly absent. The speakers strove to appear to be experts: somewhat analogous to political candidates wanting to appear presidential. The theme was "autism is treatable because of them." Not that autism is a different disease than previously recognized and is more variable and responsive to therapies than earlier forms of the disease. Unfortunately, autism is still not being addressed as an infectious disease.
I was able to speak over lunch with one of the organizers of the conference. I enjoyed giving an update of my work including the potential value of energy based medicine. I also pointed out many of the inconsistencies in the thimerosal arguments. "I've learned more in the last 15 minutes than I have over the last year" was his kind acknowledgement. Buoyed by the reception, I suggested I might speak to the attendees for 5 minutes. After a little consideration the answer was no. Seemingly, educating parents is less of a priority that protecting the reputation of the DAN organization.

Clinical Trials

2004-07-11T10:47:00.000-07:00

A placebo-controlled research study to evaluate the safety and effectiveness of natural products for treatment of autism and related childhood disorders

This study lasts for one month and involves the twice daily administration of either material with possible energy-based activity or control material. Participants will be required to make daily entries into a diary and to complete a questionnaire at the end of the study period. The effects, if any, of the administration of the test and control materials will be determined by an independent analysis of the diaries and questionnaires. Your child may be eligible to participate in this research study if he or she has been diagnosed with autism or is manifesting a related learning or behavioral disorder.* If your child is selected to participate in this study, he/she may benefit by showing improvement in symptoms. However, this study may also potentially involve unforeseeable risks and it is possible that your child’s condition may get worse.
* Related disorders include Attention Deficit Hyperactivity Disorder (ADHD), Obsessive Compulsive Disorder (OCD), Oppositional Defiant Disorder (ODD), Conduct Disorder (CD), Panic Disorder and Childhood Depression.
Information to be submitted by parents/guardians potentially interested in participating in the study:
Name of parent/guardian: __________________________________________________________
Contact information: Daytime telephone_____________ E-mail address______________________
Name of child: ___________________________________________________________________
Diagnosis: _______________________________________________________________________
Age: _________
Please rate your child’s capacities in the following broad areas of disabilities. Your ratings will be used to monitor any changes in your child’s performances during the clinical study. You are welcomed to substitute any characteristic that you feel is better suited for this purpose. Your child may wish to provide input into this selection. Each characteristic should be rated on a scale of 1-5, with 1 being relatively mild or minimally disabling and 5 being severe and very disabling.
Description Rating
1 Language problems including inability to speak at all or to form coherent sentences 1 2 3 4 5
2 Social problems including inability or difficulty in sustaining eye contact, playfulness 1 2 3 4 5
3 Repetitive behavioral patterns, inflexibility and/or attention deficits 1 2 3 4 5
4 Emotional disorders, including irritability, sadness, and/or aggression, 1 2 3 4 5
5 Problems with sleeping, eating, bowel movements, tics, or seizures 1 2 3 4 5

Privacy Statement: This information will be used solely for the selection of potential participants in the above study. Any selected participant will be assigned a coded number that will be used in all further contacts and on all records relating to the outcome of the study. Informed Consent forms and study details will be provided to those selected as potential participants. Please return the form via e-mail to s3support@mail.com For telephone enquiries please call 626-616-2868

Informed Consent
TITLE OF PROJECT: A placebo-controlled research study to evaluate the safety and effectiveness of natural products for treatment of autism and related childhood disorders

PRINCIPAL INVESTIGATOR: W. John Martin, M.D., Ph.D.
24-hour telephone number: (626) 616-2868

E-Mail S3Support@mail.com

PURPOSE OF STUDY

You are invited to voluntarily participate in a research study of natural products that have similar properties to materials that have been shown to provide a source of cellular energy that can assist cells in coping with the damaging effects of certain types of viral infections. The types of viruses have been referred to as stealth or stealth-adapted because they are not effectively recognized by the cellular immune system. The protective (reparative) materials that develop in stealth virus cultures have been called “alternative cellular energy pigments” or ACE-pigments. The Principal Investigator has proposed that stealth virus infections contribute to the brain damage that is present in patients with autism and related diseases. The related diseases include, but are not limited to, Attention Deficit Hyperactivity Disorder (ADHD), Obsessive Compulsive Disorder (OCD), Oppositional Defiant Disorder (ODD), Conduct Disorder (CD), Panic Disorder and Childhood Depression. The natural products that share certain characteristics with ACE-pigments and most have been used primarily to promote the growth of plants. They have all been used in humans without any indications of being toxic. Although there have been personal reports (testimonials) of some benefits in patients with brain damaging illnesses, this has not yet been established in controlled clinical trials. The goal of the present study is to see if, in fact, they will work when used in a manner that has been judged to be appropriate given the recent understanding of ACE-pigments. You are invited as a possible participant in this study if you are the parent or legal guardian of a child with autism or a related disorder.).
PROCEDURE
This study lasts for up to one month and involves the twice daily administration of either natural product(s) or an inactive control material (known as a placebo). Participants will be required to make daily observations and to forward this information via e-mail to a study coordinator. The effects, if any, of the administration of the test and control (placebo) materials will be determined by an independent analysis of the information that you provide.
Up to 10 different natural products will be tested either separately or as combinations. A corresponding control placebo will be similarly tested with a 50:50 chance of patients receiving a test or a control product. It is anticipated that only some of the test products will show easily discernable beneficial effects. You will not know the product that is being supplied but can be assured that each product will have no known significant adverse effects when used in other children.

RISKS AND POSSIBLE BENEFITS
No known medical risks are associated with the study. If any damage or adverse effects were to occur, or were to be perceived to have occurred as a result of the study, it is expressly understood that you, and not the Sponsor or Principal Investigator, will be obligated and financially responsible for obtaining any necessary medical care. The Principal Investigator believes that some of the products will achieve noticeable improvement in brain functioning. If this does occur, the Principal Investigator and S3Support will potentially benefit financially from such a finding.
Confidentiality

Your participation in the study will remain confidential to the extent provided by law. Your child will be assigned a code that will be used in the tabulation of results for publication purposes or to communicate with other investigators. Note, if information relating to a successful product is submitted to the Food and Drug Administration (FDA), this Agency has the right to review all relevant information, including the right to contact you for verification.

Questions and Termination

At all times, you are welcome to contact the Principal Investigator by phone or by e-mail. You have the right to terminate from the study at any time.
AGREEMENT:
I have read the information provided above. I have been given the opportunity to ask questions and all of my questions have been answered to my satisfaction. My signature below indicates that I have decided to allow my child to participate in the study.

Signed: Witness:

Date:

Mercury and Autism

2004-07-11T10:20:00.000-07:00

Mercury Accumulation in Autistic Children: A Possible Consequence of Stealth Virus Infection
and an Additional Rationale for the Therapeutic Use of Humic/Fulvic Acids

The prevailing concept that the body's sole source of cellular energy is from the metabolism of foods has been challenged by studies that have identified energy generating materials in virus infected cells. These materials were termed alternative cellular energy pigments. ACE pigments are capable of donating electrons for metabolic reactions and may also generate a type of biophysical force that has yet to be fully understood. ACE pigments generated in stealth virus cultures contain various types of minerals. Both in this regard and in several other shared properties, ACE pigments are comparable to humates. These materials were previously thought to be partial breakdown products of ancient plant materials as they slowly decay towards becoming coal or oil. More recently humates have been viewed as re-synthesized organic materia ls that are rich in aromatic compounds that are bound (coordinated) by different metals. The metals are thought to facilitate the passage of electrons and may also transmit other energies. Humates can both absorb metals from the environment and deliver metals to living cells. They can also function in a buffering-like capacity by reducing the levels of those metals that are in relatively high concentrations within an environment, while at the same time provide those metals for which there is a deficiency. Humates have been extensively used in agriculture and are also available as dietary supplements.

Some parents of autistic children have attributed their child's illness to mercury toxicity. Mercury is included in various vaccines in the form of a preservative called thimerosal. Mercury poisoning can cause neurological damage and conceivably certain children may be uniquely susceptible to its toxic effects. It is unlikely to be the underlying cause of autism, however, since neuropeptide changes are present in cord blood samples of children who subsequently become autistic. Autistic children show lower levels of mercury in hair analyses compared to normal children. This suggests that they may be accumulating mercury, possibly in the formation of ACE pigments. Litigation is underway concerning possible Industry and Government negligence in disregarding the potential toxicity of thimerosal in vaccines. It would be ironic if i ndeed the mercury obtained from the vaccines was actually being used productively by the body in the formation of ACE pigments.

The ingestion of humates and/or the humic and fulvic acids obtained from humates may help provide a substitute for, or at least the building blocks for the formation of ACE pigments. Stealth virus cultures undergo a repair process attributable to ACE pigments. An additional benefit of ingesting humates is the potential capacity to absorb those minerals that may be in abnormally high concentrations. Humates have a high absorptive capacity for mercury and clinical studies documenting the excretion of mercury in patients consuming humates as dietary supplements would be of interest. More important will be a determination of any clinical changes occurring in the patients.

The increasing incidence of autism is consistent with an infectious cause. Stealth-adapted viruses have been regularly cultured from children with autism and related diseases. Several stealth viruses were unequivocally derived from African green monkey simian cytomegalovirus. Infected monkeys were routinely used for the production of live polio virus vaccines. The Food and Drug Administration has confirmed the presence of simian cytomegalovirus DNA in some of the licensed lots of polio vaccines approved for use in the United States . It would be regrettable if unnecessary focusing on thimerosal in vaccines were to delay official efforts to search for infectious agents inadvertently int roduced into humans through vaccines.

The rationale for vaccines and potential inadvertent consequences including autism, AIDS and other epidemics

2004-07-11T10:17:00.000-07:00

The rationale for vaccines and potential inadvertent consequences including autism, AIDS and other epidemics
W. John Martin
Center for Complex Infectious Diseases
A Component of S3Support
Rosemead , California 91770
Email: S3support@email.com

Abstract

Humans and animals can be protected from epidemic infectious diseases by prior intentional stimulation of the immune system. This process is called immunization and has been hailed as the all time greatest contribution of science to human health. Such enthusiastic endorsements, together with compulsory legislation, have helped ensure widespread public acceptance and compliance with immunization programs. Dissenting or cautionary views on potential risks of certain vaccines have been largely ignored. The vaccine industry now has annual sales in excess of $6 billion with significant liability should adverse effects be proven. Society is facing alarming increases in various types of brain damaging and other illnesses consistent with an infectious process. A role for vaccine-derived “stealth-adapted” viruses in these illnesses, as well as in the emergence of the AIDS virus has been proposed. Such issues should be addressed by full disclosure and open participation of the public and independent researchers.

Introduction

A primary function of the immune system is to provide long term protection against many types of infectious agents. Typically, the immune system responds to an initial exposure to a particular type of virus, bacterium or fungus, with a heightened capacity to subsequently respond to any further exposures to the same microorganism. With some types of microorganisms, the initial exposure will manifest as a time limited primary disease. This is seen, for example, with childhood exposure to common viral illnesses including measles and chicken-pox. Once an individual has contracted measles, he or she is essentially immune from any further episodes of measles.

Epidemics of infectious illnesses have historically taken an enormous toll on mankind. Common examples include plague, smallpox and syphilis during the middle ages; polio, influenza and tuberculosis during the early 20 th century; and currently AIDS and hepatitis A, B and C. Explorations of remote areas of the world were severely hindered by diseases such as yellow fever and malaria.

Man has learned to cope with some of these illnesses by harnessing the power of the immune response. Although the mechanism was not understood at the time, Dr. Edward Jenner was able to prevent primary disfiguring infection with smallpox virus by intentional infection with a related virus, termed vaccinia that was infecting cows (vacca in Latin). The process was referred to as vaccination, and from 1796 began to replace the widespread custom of trying to limit the severity of primary infection using minimal exposure to pus collected from a smallpox skin blister.

The concept of germs causing infectious illnesses was jointly developed by Dr. Robert Koch and Louis Pasteur in the 1880's. While Koch failed in his attempts to develop a tuberculosis vaccine, Pasteur was successful with the development of a rabies vaccine. Essentially, he was able to grow the rabies virus in rabbits and to inject dried spinal cord material into patients exposed to the bite of a rabid animal.

Infectious agents responsible for such serious viral illnesses as polio, influenza and yellow fever were discovered in the early 20 th century by Drs. Landsteiner, Shope, and Walter Reed respectively. Bacteria responsible for diphtheria, tetanus, pneumonia and whooping cough (pertussis) were also identified. Unlike viruses, bacteria could be readily cultured away from living cells. Viruses had to be transmitted between living animals. Fortunately, fertile chicken eggs could be used to propagate influenza and yellow fever viruses. In 1948, Dr. John Enders developed the first animal-free tissue culture method to grow polio virus. With each successfully grown microbe, efforts were made to develop material that could be used to immunize individuals (or animals) against challenge with the same disease causing microbe.

The immune system was also becoming better understood. The issue of whether protection was being provided by soluble factors (antibodies) or cells was addressed in the early 1900's without a clear consensus. Foreign material, referred to as an antigen, was initially thought to “instruct” certain cells to make antibodies that selectively bound to and neutralized the antigen. In 1957 MacFarlane Burnet postulated that the body was pre-equipped with cells that collectively could recognize all foreign antigens but that individual immune cells, identified as comprising lymphocytes and plasma cells, were responsive to only one particular antigen. Selective outgrowth of antigen-specific responding cells explained the heightened antibody and cellular reactivity to subsequent exposure to the same antigen. The levels of antibody reactivity correlated with the levels of resistance to many infectious diseases providing a ready assay to determine efficacy of various immunization protocols.

Killed bacteria and bacteria-derived products provided the mainstay for bacteria immunization programs. Infusion of serum antibodies collected from immunized animals could also be used to provide passive immune protection of patients in the early stage of bacterial illnesses. Modified toxins (toxoids) produced by diphtheria and tetanus bacteria were relatively easy targets for vaccination. Crude extracts and more purified subcomponent vaccines are available for pertussis, cholera, typhoid, meningococcus, pneumococcus, hemophilus influnza and a tuberculosis related bacteria (BCG).

Formalin killed egg-grown influenza viruses were successfully developed into clinical vaccines. The transfer of the yellow fever virus from monkeys to mice was shown by Dr. Max Theiler to significantly reduce its capacity to induce disease in humans. This led to the production in fertile eggs of a live yellow fever vaccine that is still in use today. Experience with influenza and yellow fever vaccines provided contrasting models of how to best develop a polio vaccine once it was successfully cultured. Dr. Jonas Salk used formalin to inactivate disease causing polio virus. Drs. Albert Sabin and Hilary Koprowski independently tried to reduce the virulence of polio viruses by extensive tissue culturing. Dr. Sabin was more successful in isolating weakened strains that were still able to induce a protective antibody response. His vaccine replaced that of Dr. Salk in the early 1960's, although in the United States , the use of inactivated polio vaccine was again mandated in 2000.

The introduction of polio immunization was followed by successful efforts to develop live vaccines against measles, mumps and rubella (MMR) viruses and more recently varicella zoster virus. Inactivated and more recently genetically synthesized hepatitis A and B antigenic materials have become available for vaccines. Experimental programs are underway to produce vaccines against many other viruses including herpes simplex viruses, cytomegalovirus, Epstein-Barr virus, human papillomavirus, rotavirus, Japanese B encephalitis virus and human immunodeficiency virus (HIV).

Numerous infectious agents have also been rendered as vaccines for animal use. Prominent examples include Newcastle disease virus in poultry, canine distemper virus in dogs, feline leukemia virus in cats and brucella bacteria in cattle.

Efficacy of Vaccines

The global eradication of smallpox has been attributed to vaccination and has served as a model for other illnesses, including polio. Common childhood infections with measles, mumps and rubella are less frequent in developed countries compared to the developing world. While some of this reduction can be traced to vaccine use, improved sanitation and nutrition were probably more important variables. Influenza mortality among the elderly and infirm is reduced in immunized populations. Because influenza virus can undergo antigenic changes, it is necessary to provide a vaccine that contains the virus responsible for an ongoing outbreak. The detection of a new influenza virus triggers a rapid response for vaccine production in time to provide protection to those not yet exposed to the current strain of influenza. Diphtheria and tetanus are rarely seen today and essentially only in individuals who have not been immunized. Mortality for meningococcus and pneumonia is reduced for those strains for which vaccines have been produced. Similar success stories apply to vaccinated livestock and domestic pets.

Lifelong protection against many infectious diseases is clearly achievable by vaccination. Moreover, the world remains at risk for newly emerging infectious agents, including common viruses with drastically altered antigens. Advances in biotechnology are likely to streamline vaccine manufacturing. Specifically, recombinant DNA technology is allowing the production in bacteria of structurally well defined antigens of viral, bacterial, fungal and parasitic microorganisms. A greater understanding of the immune system should also enable more directed approaches at eliciting the type of immunity that is most appropriate for a given type of infection. Effective vaccines are not yet available for several major illnesses, including tuberculosis, malaria and AIDS. A potential difficulty in the development and use of such vaccines is the growing reluctance of the public to accept the Government's blanket assurance that vaccines are safe and effective.

Adverse Effects of Vaccines

The use of vaccines has been justified as an important Public Health measure to stem the occurrence of epidemic illnesses. To be effective, it has commonly been argued that universal compliance with immunization programs is necessary. Frivolous concerns such as sprouting cow horns from taking vaccinia virus were aggressively countered by common sense. More serious concerns have periodically arisen and afforded less than stellar attention by Public Health authorities. The reluctance is explained in part by a protective reaction of those responsible for apparent oversights and by the considerable exposure of Industry to potential litigation. Historical examples include the probable transmission of syphilis and tetanus as inadvertent contaminants of vaccinia vaccine lots; the transmission of bovine leukemia virus to cattle herds because of contaminated experimental babesia vaccines; and an outbreak of Venezuela equine infectious virus in horses that was due to a contaminated vaccine.

Field testing of vaccines with live viral challenge can potentially explain the out-of-season cases of polio that occurred in the early 1950's in the United States . Actual polio cases developed among some of those receiving initial lots of Dr. Salk's vaccine because of inadequately assessed inactivation protocols. Simian virus 40 (SV-40) was a common contaminant of both live and killed polio vaccines produced in the freshly grown cells from the kidneys of rhesus monkeys. A switch was made to African green monkeys for further production of polio vaccine without the recall of known contaminated vaccine lots. Concerns about using fresh tissues from African green monkeys arose during the 1960's but simple suggestions such as using serum antibodies from the monkeys to test for possible contaminating viruses were disregarded.

In 1972 a joint Government-Industry study showed that kidney cell cultures from all eleven African green monkeys tested were contaminated with simian cytomegalovirus. Only 4 of the 11 isolates were detectable using the then mandated screening test. The Industry's contingency plan essentially concluded that the Bureau of Biologics would be unwilling to take the current product off the market in favor of a competing vaccine being produced in England from an established human cell line. African green monkeys continued to be used even after the Director of the Bureau of Biologics was informed in 1977 that licensed polio vaccines contained foreign DNA that was not of monkey cell origin. Of 8 vaccines lots from around this period that were recently tested in-house by the FDA Office of Vaccine Safety, 3 have DNA of simian cytomegalovirus. In a related study, British authorities reported that 32 of 34 polio vaccine lots from one manufacturer alone were contaminated with monkey cytomegalovirus DNA. FDA and British officials state they are unable to culture replicating cytomegalovirus from these vaccines. FDA was unwilling to provide samples of the vaccines for independent testing, ostensibly because of proprietary restrictions imposed by industry. This issue is important for at least two reasons: First, I have reported the definitive isolation of simian cytomegalovirus-derived cell damaging viruses from two patients with brain damaging illnesses, and as yet uncharacterized viruses from numerous additional patients with illnesses ranging from autism and learning disorders in children, chronic fatigue syndrome and fibromyalgia in adults, and various cancers and neurodegenerative illnesses in the elderly. The viruses were termed stealth because they were essentially not being recognized by the cellular immune system. Based on available DNA sequence data, it appears that the lack of effective immune recognition is due to the loss of the few major critical antigens that are targeted by the majority of virus reactive lymphocytes. Parents of stealth virus positive children have occasionally reported exacerbation of symptoms following vaccination. Vaccine viruses can promote the growth of certain stealth viruses in cultures. Furthermore, non-specific stimulation of the immune response could potentially trigger an anti-viral response directed at a few minor antigens retained by the stealth-adapted virus. Arguably, potential vaccine recipients should be screened for stealth virus infection prior to receiving the vaccine.

Cytomegalovirus, whether from African green or rhesus monkey, has multiple copies of the genes that promote cell entry of HIV and its precursor, the simian immunodeficiency virus (SIV) of chimpanzee. Cytomegalovirus contaminated experimental polio vaccines were used in chimpanzees in Central Africa . It is quite reasonable, therefore, that the use of experimental polio vaccine in Africa led to the conversion of SIV to HIV. Chimpanzees from Africa were also used to experiment with hepatitis B vaccine, again suggesting a possible link of vaccines with the spread of HIV in the United States . Requests to CDC to test stored human sera collected from polio vaccine immunized African children or hepatitis B immunized United States citizens have been ignored.

Political and Economic Considerations

These and other politically sensitive issues are seemingly not being addressed by our Public Health agencies. Undoubtedly, there is a reluctance of those in control to challenge the past performance of those entrusted with ensuring the Nation's health. The Pharmaceutical Industry also maintains a privileged position within our society. Not only does its financial strength curry support from Government, but it is likely to be heavily relied upon in the case of biological warfare. Unfortunately, the primary motivation of this industry appears to have shifted from global Public Health concerns to simple profit motivation. An enormous price differential exists between charges for pediatric vaccines in Westernized countries compared to the developing world. Part of this differential is attributed to refinements in vaccine production, for example use of more purified bacteria products, or the use of inactivated versus live but weakened polio virus. Still the differences are staggering, for example US$0.07 versus US$10.65 for diphtheria-tetanus-pertussis (DTP) vaccine and US$0.10 versus US$8.25 for polio vaccine. Far more money is to be made vaccinating children from affluent countries, as well as international travelers from these countries, than addressing the world's health needs. The multi-national Pharmaceutical Industry has essentially withdrawn from servicing the developing world leaving this responsibility and low profit margin to a Developing Country Vaccine Manufacturers Network with facilities in countries such as India , Iran and Thailand .

The public is justifiably skeptical of the willingness of Government officials to request a full accounting of past and present vaccine manufacturing practices. Compulsory polio vaccination was legislated in the late 1950's to help reduce stockpiles of relatively ineffective lots of inactivated polio vaccines. Collusion between Government and vaccine producers may have occurred in the development and testing of agents of biological warfare. Intentional feeding of mentally retarded children with hepatitis B virus contaminated feces was justified as being necessary to protect other children. Possible responsibility for diseases such as AIDS, autism, sudden infant death syndrome, chronic fatigue syndrome and mental illnesses is vehemently denied and those making such suggestions attacked. To a large measure, vaccine and vaccine-related research have become money-driven endeavors with emphasis on perception rather than reality. This unfortunate trend needs to be addressed with forthright discussions that involve both the public and independent researchers.

Selected References:

History of Vaccines

Bazin H. A brief history of the prevention of infectious diseases by immunisations. Comp Immunol Microbiol Infect Dis. 2003; 26:293–308.

Hilleman MR. Vaccines in historic evolution and perspective: a narrative of vaccine discoveries. J Hum Virol, 2000;3(2):63–76.

Horaud F. Albert B. Sabin and the development of oral poliovaccine. Biologicals. 1963; 21:311–6.

Jenner E. An inquiry into the causes and effects of the variolae, a disease discovered in some of the counties of England , particularly Gloucestershire and known by the name of smallpox. London Samson Low. 1796.

Madsen T. Whooping cough: Its bacteriology, diagnosis, prevention and treatment. Bost Med Surg J, 1925; 192:50–60.

Pasteur L, Chamberland C-E, Roux E. [On the vaccination of sheep]. CR Acad Sci Paris; 1881; 92:1378–83.

Parish HJ. A History of Immunization. E & S Livingston, London , 1965.

Plotkin SA, Mortimer EA. Vaccines. WB Saunders, Philadelphia , 1988.

Salmon DE, Smith T. On a new method of producing immunity from contagious diseases. Am Vet Rev, 1886; 10:63–69.

The Public Health Service and the control of biologics. Public Health Rep, 1995; 110:774–5.

Specific Vaccines

Artenstein MS, Gold R, Zimmerly JG, et al. Prevention of meningococcal disease by group C polysaccharide vaccine. N Engl J Med, 1970; 282:417–20.

Austrian R, Douglas RM, Schiffman C, et al. Prevention of pneumococcal pneumonia by vaccination. Trans Assoc Am Phys, 1976; 89:184–92.

Clenny AT, Hopkins BE. Diphtheria toxoid as an immunizing agent. Br J Exp Path, 1923; 4:283–8.

Enders JF, Weller TH, Robbins FC. Cultivation of the Lansing strain of poliomyelitis in cultures of various human embryonic tissues. Science, 1949; 109:85–87.

Horsfall FL Jr., Lannette EH, Rickard ER, Hirst GK. Studies on the efficacy of a complex vaccine against influenza A. Public Health Rep, 1941; 56:1863–75.

Katz SL, Kempe CH, Blaid FL, Lepow ML, Krugman S, Haggerty J, Enders JF. Studies on an attenuated measles vaccine VIII. General summary and evaluation of results of vaccine. N Engl J Med, 1960; 263: 180–4.

Koprowski H, Jervis GA , Norton TW. Immune response in human volunteers upon oral administration of a rodent-adapted strain of poliomyelitis. Am J Hyg, 1952; 55:108–26.

Krugman S. The newly licensed hepatitis B vaccine. Characteristics and indication for use. JAMA, 1982; 247:2012–5.

McAleer WJ, Buynak EB, Margetter RZ, et al. Human hepatitis B vaccine from recombinant yeast. Nature, 1984; 307:178–80.

Provost PJ, Hughes JV, Miller WJ, et al. An inactivated hepatitis A vaccine of cell culture origin. J Med Virol, 1996; 19:23–31.

Sabin AB , Hennessen WA Winsser J. Studies on variants of poliomyelitis virus. I Experimental segregation and properties of virulent variants of three immunological types. J Exp Med, 1954; 99:551–76.

Salk JE, Krech V, Youngner JS, Bennett BL, Lewis LJ, Bazeley PL. Formaldehyde treatment and safety testing of experimental poliomyelitis vaccines. Am J Public Health, 1954; 44:563–70.

Smith W, Andrews CH, Laidlaw PP. A virus obtained from influenza patients. Lancet, 1933; 2:66–68.

Takahashi M, Otsuka T, Okuno Y, et al. Live vaccine used to prevent the spread of varicella in children in hospitals. Lancet, 1974; 2: 1288–90.

Theiler M, Smith HH. The use of yellow fever virus by in vitro cultivation for human immunization. J Exp Med, 1937; 65:787–800.

Immunology

Ada , GL. Vaccines in Fundamental Immunology . 3rd Edition. Ed. W.E. Paul. Raven Press, New York , 1993:1309–52.

Burnet FM. A modification of Jerne's theory of antibody production using the concept of clonal selection. Aust J Sci, 1957; 20:67–9.

Polio Vaccine Contamination

Baylis SA, Shah N, Jenkins A, Berry NJ, Minor PD. Simian cytomegalovirus and contamination of oral poliovirus vaccines. Biologicals, 2003; 31:63–73.

Kops SP. Oral polio vaccine and human cancer: a reassessment of SV40 as a contaminant based upon legal documents. Anticancer Res,2000; 20:4745–9.

Poinar H, Kuch M, Paabo S. Molecular analyses of oral polio vaccine samples. Science, 2001; 292:743–4.

Sierra-Honigmann AM, Krause PR. Live oral poliovirus vaccines and simian cytomegalovirus. Biologicals, 2002; 30:167–74.

Rizzo P, Di Resta I, Powers A, Ratner H, Carbone M. Unique strains of SV40 in commercial poliovaccines from 1955 not readily identifiable with current testing for SV40 infection. Cancer Res. 1999;596103–8.

Stealth-Adapted Viruses

Martin WJ, Zeng LC, Ahmed K, Roy M. Cytomegalovirus-related sequence in an atypical cytopathic virus repeatedly isolated from a patient with chronic fatigue syndrome. Am J Pathol,1994; 145:440–51.

Martin WJ, Ahmed KN, Zeng LC, Olsen J-C, Seward JG, Seehrai JS. African green monkey origin of the atypical cytopathic 'stealth virus' isolated from a patient with chronic fatigue syndrome. Clin. Diag. Virol, 1995; 4:93–103.

Martin WJ, Glass RT. Acute encephalopathy induced in cats with a stealth virus isolated from a patient with chronic fatigue syndrome. Pathobiology, 1995; 63:115–8.

Martin WJ. Stealth virus isolated from an autistic child. J Autism Dev Disord, 1995; 25:223–4.

Martin WJ. Simian cytomegalovirus-related stealth virus isolated from the cerebrospinal fluid of a patient with bipolar psychosis and acute encephalopathy. Pathobiology, 1996; 64:64–6.

Martin WJ. Genetic instability and fragmentation of a stealth viral genome. Pathobiology, 1996; 64:9–17.

Martin WJ. Severe stealth virus encephalopathy following chronic fatigue syndrome-like illness: Clinical and histopathological features. Pathobiology, 1996; 64:1–8.

Martin WJ. Stealth viral encephalopathy: Report of a fatal case complicated by cerebral vasculitis. Pathobiology, 1996; 64:59–63.

Martin WJ, Anderson D. Stealth virus epidemic in the Mohave Valley . Initial report of viral isolation. Pathobiology, 1997; 65:51–6.

Martin WJ. Cellular sequences in stealth viruses. Patobiology, 1998; 66:53–8.

Martin WJ. Bacteria related sequences in a simian cytomegalovirus-derived stealth virus culture. Exp Mol Path, 1999; 66:8–14.

Martin WJ. Melanoma Growth stimulatory activity (MGSA/GRO-alpha) chemokine genes incorporated into an African green monkey simian cytomegalovirus (SCMV)-derived stealth virus. Exp Mol Path, 1999; 66:15–8.

Martin WJ. Stealth adaptation of an African green monkey simian cytomegalovirus. Exp Mol Path, 1999; 66:3–7.

Martin WJ. Chemokine receptor-related genetic sequences in an African green monkey simian cytomegalovirus-derived stealth virus. Exp Mol Path, 2000; 69:10–6.

Martin WJ, Anderson D. Stealth Virus Epidemic in the Mohave Valley : Severe vacuolating encephalopathy in a child presenting with a behavioral disorder. Exp Mol Path, 1999; 66:19–30.

Martin WJ. Complex intracellular inclusions in the brain of a child with a stealth virus encephalopathy. Exp Mol Path, 2003; 74:179–209.

Martin WJ. Stealth Virus Culture Pigments: A Potential Source of Cellular Energy. Exp. Mol. Path, 2003; 74:210–23.

Polio Vaccines and the Possible Origin of AIDS

Elswood BF, Stricker RB. Polio vaccines and the origin of AIDS. Med Hypotheses, 1994; 42:347–54.

Gisselquist D. Emergence of the HIV type 1 epidemic in the twentieth century: comparing hypotheses to evidence. AIDS Res Hum Retroviruses, 2003; 19:1071–8.

Hooper E. Experimental oral polio vaccines and acquired immune deficiency syndrome. Philos Trans R Soc Lond B Biol Sci., 2001; 356:803–14.

Hooper E. The River: A Journey to the Source of HIV and AIDS . Little Brown, Boston 1999.

Lena P, Luciw P. Simian immunodeficiency virus in kidney cell cultures from highly infected rhesus macaques (Macaca mulatta). Philos Trans R Soc Lond B Biol Sci., 2001; 356:845–7.

Reinhardt V, Roberts A. The African polio vaccine-acquired immune deficiency syndrome connection. Med Hypotheses, 1997; 48:367–74.

Contamination of Other Vaccines

Bagust TJ, Grimes TM, Dennett DP. Infection studies on a reticuloendotheliosis virus contaminant of a commercial Marek's disease vaccine. Aust Vet J, 1979; 55:153–7.

Barkema HW, Bartels CJ, van Wuijckhuise L, Hesselink JW, Holzhauer M, Weber MF, Franken P, Kock PA, Bruschke CJ, Zimmer GM. [Outbreak of bovine virus diarrhea on Dutch dairy farms induced by a bovine herpesvirus 1 marker vaccine contaminated with bovine virus diarrhea virus type 2.] Tijdschr Diergeneeskd, 2001; 126:158–65.

Böni J, Stalder J, Reigel F, Schüpbach J. Detection of reverse transcriptase activity in live attenuated vaccines. Clin. Diagn. Virol, 1996; 5: 43–55.

Caramelli M, Ru G, Casalone C, Bozzetta E, Acutis PL, Calella A, Forloni G. Evidence for the transmission of scrapie to sheep and goats from a vaccine against Mycoplasma agalactiae. Vet Rec, 2001; 148:531–6.

Falcone E, Cordioli P, Tarantino M, Muscillo M, Sala G, La Rosa G, Archetti IL, Marianelli C, Lombardi G, Tollis M. Experimental infection of calves with bovine viral diarrhoea virus type-2 (BVDV-2) isolated from a contaminated vaccine. Vet Res Commun, 2003; 27:577–89.

Johnson JA, Heneine W. Characterization of endogenous avian leukosis viruses in chicken embryonic fibroblast substrates used in production of measles and mumps vaccines. J Virol, 2001; 75:3605–12.

Kappeler A, Lutz-Wallace C, Sapp T, Sidhu M. Detection of bovine polyomavirus contamination in fetal bovine sera and modified live viral vaccines using polymerase chain reaction. Biologicals, 1996; 24:131–5.

Levings RL, Wilbur LA, Evermann JF, Stoll IR, Starling DE , Spillers CA, Gustafson GA , McKeiman AJ, Rhyan JC, Halverson DH, Rosenbusch RF. Abortion and death in pregnant bitches associated with a canine vaccine contaminated with bluetongue virus. Dev Biol Stand, 1996; 88:219–20.

Rogers RJ, Dimmock CK, de Vos AJ, Rodwell BJ. Bovine leucosis virus contamination of a vaccine produced in vivo against bovine babesiosis and anaplasmosis. Aust Vet J, 1988; 65:285–7.

Senda M, Parrish CR, Harasawa R, Gamoh K, Muramatsu M, Hirayama N, Itoh O. Detection by PCR of wild-type canine parvovirus which contaminates dog vaccines. J Clin Microbiol, 1995; 33:110–3.

Thornton DH. A survey of mycoplasma detection in veterinary vaccines. Vaccine, 1986; 4:237–40.

Weaver SC, Pfeffer M, Marriott K, Kang W, Kinney RM. Genetic evidence for the origins of Venezuelan equine encephalitis virus subtype IAB outbreaks. Am J Trop Med Hyg, 1999; 60:441–8.

Failure of Vaccine Virus Inactivation

Nathanson N, Langmuir AD. The Cutter incident. Poliomyelitis following formaldehyde inactivated poliovirus vaccination in the United States during the spring of 1955. II. Relationship of poliomyelitis to Cutter vaccine. Am J Hyg, 1963; 78:29–60.

Brown F. Review of accidents caused by incomplete inactivation of viruses. Dev Biol Stand, 1993; 81:103–7.

Person-to-Person Transmission of Infection

Watanabe M. [The Tuberculosis outbreak due to whooping cough inoculation at Iwagasaki-machi in 1949] Nippon Ishigaku Zasshi, 2003; 49:479–92.

Montella M, Crispo A, Grimaldi M, Tridente V, Fusco M. Assessment of iatrogenic transmission of HCV in Southern Italy : was the cause the Salk polio vaccination? J Med Virol, 2003; 70:49–50.

Chernin E. Richard Pearson Strong and the iatrogenic plague disaster in Bilibid Prison, Manila , 1906. Rev Infect Dis, 1989; 11:996–1004.

Gisselquist DP. Estimating HIV-1 transmission efficiency through unsafe medical injections. Int J STD AIDS, 2002; 13:152–9.

Marx PA, Alcabes PG, Drucker E. Serial human passage of simian immunodeficiency virus by unsterile injections and the emergence of epidemic human immunodeficiency virus in Africa. Philos Trans R Soc Lond B Biol Sci, 2001; 356:911–20.

Other Complications of Vaccination

Geier MR, Geier DA, Zahalsky AC. Influenza vaccination and Guillain Barre syndrome small star, filled. Clin Immunol, 2003;. 107:116–21.

Communicating Vaccine Risks

Ball LK , Evans G , Bostrom. A . Risky Business: Challenges in Vaccine Risk Communication . Pediatrics, 1998; 101:453–8.

Coulter HL, Fisher BL. A Shot in the Dark . Avery Publishing Group, New York , 1991.

Kilch EW. The vaccine dilemma . Issues Sci Tech, 1986; 2:108.

Zhou W, Pool V, Iskander JK, English-Bullard R, Ball R, Wise RP, Haber P, Pless RP, Mootrey G, Ellenberg SS, Braun MM, Chen RT. Surveillance for safety after immunization: Vaccine Adverse Event Reporting System (VAERS)–United States, 1991–2001 . MMWR Surveill Summ, 2003; 52:1–24.

Lanctot, L. The Medical Mafia . Here's the Key Inc., Miami , 1995.

Martin B. The burden of proof and the origin of acquired immune deficiency syndrome . Philos Trans R Soc Lond B Biol Sci, 2001; 356:939–43.

Scheibner V. Vaccination . Published by Australian Print Group, Maryborough, 1993.

Do Stealth Viruses Cause Brain Damaging Illnesses?

2004-07-11T10:15:00.000-07:00

Do Stealth Viruses Cause Brain Damaging Illnesses?

There are growing health problems being faced by many Americans. Autism has doubled in California over the last 4 years and special educational needs of school children are soaring. Severe childhood behavioral problems necessitating residential care are financially forcing many parents to relinquish custody of their children to the State. In a year 2001 sampling of only 19 mid-sized States, the astounding number of voluntary State-orphaned children was 12,700. This heart rendering loss of custody does not even ensure therapy for the children, merely protective restraint. Nearly half of our elderly will experience the memory loss and emotional fragility of Alzheimer's disease. Published figures from the CDC confirm that nearly 20,000 patients are hospitalized each year with a diagnosis of encephalitis. Yet in the majority of these patients, no cause of the illness can be found. Many more individuals experience an alarming decline in brain function that can lead to such tragedies as suicide or mindless criminal behaviors. We know too often of friends with chronic fatigue syndrome, diabetes, arthritis and debilitating mental illnesses.

Individually, any of these increasingly prevalent diseases ought to trigger a serious investigation for the possibility of an infectious cause. When lumped together, and with the added knowledge of virus contaminated vaccines, it is difficult to comprehend the apparent indifference those entrusted with protecting the Public Health.

Unfortunately, our medical system has become somewhat of a puppet of the pharmaceutical industry. It is now largely a game of monopoly with rewards for those who participate and who follow these rules: No accusations of complacency, neglect or cover-up by those making or enforcing the laws governing medical practice; no recognition of illnesses for which pharmaceutical drugs cannot be prescribed; and definitely no criticisms of vaccines.

Yet there is overwhelming evidence for past contamination of polio vaccines. (Incidentally, a plausible explanation also exists for how polio vaccine studies in Africa probably led to the formation of the AIDS virus.) It is also clear that current medical practice is failing to address community-wide and family-centered outbreaks of diseases. Adding to this problem are the competing patient support groups led by individuals failing to see the relationship among the various diseases entities and/or ascribing their particular chronic disease entity to known microbes such as Borrelia burgdorferi, Mycoplasma fermentans, human herpesvirus-6 and others, in the face of clearly contradictory and inconsistent evidence. The short term argument of pushing for a medically reimbursable diagnosis caused by a known microbe has simply led to fruitless debates. Moreover, it has drawn Public Health attention away from the need to seek unconventional infectious agents.

The explanation that best addresses the explosive increase in many chronic debilitating illnesses is the underlying presence of what have been called "stealth-adapted" viruses. These viruses go unrecognized by our immune system, and unfortunately, also ignored by our Public Health authorities. Some were unequivocally derived from polio vaccines. The reality is that infectious illnesses caused by these and other stealth-adapted viruses are rampant in our community. They are certainly a potential cause of many of the diseases afflicting our country.

This web site was inspired by the desire to address the scientific, social and spiritual needs of individual with brain damaging illnesses. Through a series of events (coincidences?), new research findings and close teamwork, we can now begin to realize the aspirations of a group of parents who originally established MI Hope, Inc., as a non-profit foundation for their children (MI stands for mental illness). This organization has blossomed during the last several months and is now ready to be the catalyst of a nationwide movement.

What can you do to become involved and to support these efforts? Becoming a member of S3Support will help lead to an increased awareness of the scientific, social and spiritual issues that need urgently to be addressed. Though various membership benefits, such as automatic enrollment in cost saving plans, out of pocket costs are likely to be returned many times over. Regularly updated, useful scientific information will become readily accessible with moderated input from members. More important, your continuing contributions will help expand the present scientific, social and spiritual programs of S3Support.

Stealth virus isolated from an autistic child.

2004-07-11T10:12:00.000-07:00

Article published by WJ Martin in J Autism Dev Disord. 1995 Apr;25(2):223-4

What are Stealth-Adapted Viruses and Do They Exist

2004-07-11T10:09:00.000-07:00

What are Stealth-Adapted Viruses and Do They Exist

The accompanying article provides a recent review of stealth viruses. Viruses are submicroscopic infectious agents that replicate only within cells. They are comprised of an essential nucleic acid polymer consisting of a linear string of correctly ordered nucleotides that attaches to, and is protected by, viral proteins whose amino acid sequences are coded by the nucleic acid polymer.While viruses are generally much smaller than bacteria, the major distinction between these life forms is that at particular stages of their life cycle, viruses will consist of either an RNA or a DNA nucleic acid polymer. By contrast, bacteria will consistently contain both DNA and RNA and usually many more additional components involved in metabolic functions, including protein synthesis, energy generation, formation of a protective cell wall, etc. While some bacteria are still dependent on human and/or animal cells for their replication, most bacteria can function as free living microorganisms.

Viruses were initially detected on the basis of the cellular damage they induced when they co-opted cellular metabolic processes to allow for their replication. Essentially, the viruses drained the cells existence as they tended to their own reproduction. The virus induced cell damage was referred to a CPE. Some viruses induce a fairly distinctive CPE in particular cell types. For other viruses, the CPE is more subtle and may, in fact, not be seen in routine microscopic examinations, or may be viewed as simply resulting from unexplained toxicity of the material being tested for viral activity.

Viruses can be further characterized by sequencing all or parts of its nucleic acid polymer, and by using antibodies that that selectively react with the proteins that characterize the different types of viruses. These techniques are more narrowly focussed on the detection of viruses whose DNA or RNA sequences are known and whose proteins have been used to generate specifically reactive antibodies.For broader screening of as yet unknown viruses, the tissue culture methods still provide a very powerful tool. Molecular and immunological methods can then be used to further characterize the cytopathic agent.

Using a combination of molecular, immunological and tissue culture techniques, I was able to repeatedly culture a cytopathic virus from a patient with an acute onset neurological illness that has resulted in long term chronic fatigue syndrome (CFS). Having seen the CPE caused by this virus, it was possible to continually adapt the culture method to shortened the period required for its appearance and to promote its development within the cultures. It soon became apparent that generally similar types of CPE could be seen in cultures obtained from patients with other neurological illnesses, including autism and behavioral problems in children, depression and schizophrenia in adults and neurodegenerative diseases in the elderly. Healthy medical students, used as controls, were negative for the marked changes being seen with patients’ samples.

Unfortunately, the work fell into the nationwide controversy regarding the very existence of CFS as an illness. Moreover, whereas the description of a CPE occurring in cultured cells are understandable to those who work directly with viral cultures, most physicians and other healthcare workers are basically unfamiliar with virus culturing techniques. Patient support groups also wanted an assay that would differentiate patient with their particular clinical illness from patients with other diseases. The finding of positive cultures in “non-fatigued” patients, yet not in all patients with CFS, was a blow to the initial support received from a CFS patient group.

2004-07-11T10:05:00.000-07:00

Stealth-Adapted Viruses:
The Cause of Autism*
W. John Martin, M.D.,Ph.D.
Center for Complex Infectious Diseases
Rosemead CA 91770

Introduction

Autism is a diagnostic label applied to neurological disorders of early childhood onset. It manifests as deficits in communication and in other social interactive skills. Considerable variability exists in the severity of disease in autistic patients, with somewhat arbitrary distinctions between autism and childhood disintegration disorder at one end and delayed normal development at the other extreme. Autistic patients will commonly show a wider variety of clinical manifestations than implied by a single diagnostic label.While many millions of dollars have been spent on autism-related research, only a few studies have provided important insights into the underling cause, prevention and treatment of this disease. This talk will provide a brief summary of generally accepted research views on autism and a lengthier discussion of some of the more controversial opinions. The argument will be presented that autism is essentially an encephalopathy of stealth-adapted viral origin. Research findings on a stealth-adapted virus that arose from the species of monkeys used to produce poliovirus vaccine will be summarized. Sequencing of this virus has suggested specific therapeutic approaches to the treatment of patients with autism and other stealth-virus related clinical conditions. Preliminary clinical experience with some of these approaches has been encouraging and indicates the need for formal therapeutic trials. Studies also need to be pursued into the modes of stealth-virus replication and transmission of what may well prove to be a major threat to the survival of mankind.

Generally Accepted Research Views on the Nature of Autism

1. Autism has a Genetic Component: This is apparent from the higher incidence of autism among boys. It is also supported by the relative concordance of disease among monozygotic (genetically identical) twins compared to dizygotic (genetically different) twins. Still there are numerous examples where only one of two genetically identical twins has the disease. Genetics may well be a contributing factor to the expression of autism, but it is clearly not the only component to this (or these) diseases.

2. Brain Abnormalities in Autistic Children: Head circumference has been accepted as a marker of brain size. While normal at birth, the head circumference of 1-2 year old autistic children is reportedly slightly enlarged. Brain imaging has also shown enlargements in certain regions of the brain, most noticeably in parts of the cerebellum. Equally impressive are various functional studies that show deficits in brain activation upon certain types of sensory stimulation and in blood flow patterns in autistic children. The question arises whether these changes are a consequence of autism, rather than its cause. Limited histopathological studies on brain tissue from autistic patients support the view that certain brain cells are damaged and/or do not normally develop.

3.Biochemical Indications of a Prenatal Disorder. As recently reported, elevated levels of one or more neuropeptides are present in neonatal blood samples obtained from children who subsequently were diagnosed as autistic. The source of the elevated neuropeptides was presumed to be the brain but this was not established. The actual levels of various neuropeptides examined differed among autistic children, but as a group the autistic children were readily distinguishable from normal children. Somewhat confounding, however, was that similar elevations were consistently also found in blood samples collected from mentally retarded children. Mental retardation had not previously been linked with autism and clearly differs with respect to the smaller than normal head circumference seen at birth.

Controversial Issues Relating to Autism

1. Autism is the Result of Vaccination. Reports of marked clinical deterioration and even the initial onset of autism within days of receiving a vaccination has prompted the view that the vaccine has caused the illness. Initially the focus was on diphtheria/petussis/tetanus (DPT) vaccine but more recently it has been on live measles/mumps/rubella (MMR) vaccine. In the case of measles, vaccine-derived viral material has been seen using immunohistochemistry and molecular based assays within hyperplastic lymphoid tissue present in the gastrointestinal tract of autistic children.Similar findings were found in non-autistic children with lymphoid hyperplasia. Although there are reasons for concerns with live viral vaccines, including the finding of retroviral related reverse transcriptase activity in MMR vaccines, a primary etiological role of measles vaccine virus is not supported by data indicating prenatal abnormalities. A detrimental effect of MMR vaccine has also been dismissed with results of various epidemiological studies failing to show statistically significant correlation between vaccine usage and disease prevalence.

2. Autism is a Primary Biochemical Disorder. Urine analyses on autistic children have shown markedly elevated levels of various peptides as well as other types of metabolic products.An inference is that the levels of these chemicals would also be increased in the brain and that they somehow interfere with normal brain function. A prime example is the opiate-like peptides resulting from incomplete digestive breakdown of casein and gluten proteins. This view is bolstered by noticeable clinical improvements in some autistic children when placed on a casein and gluten free diet. Peptides from abnormal bacterial and fungal bowel flora may also been suggested as having neuroregulatory activity whose levels may be reduced by antibiotics. A role for cell associated peptidase is suggested by unpublished studies that peptidase IV inhibitory fragments may also be present in the urine of some autistic children.

Autism: A Stealth-Adapted Viral Encephalopathy

I am proposing that autism is primarily a prenatal infection that involves the brain and occurs in a genetically predisposed individual. The infection renders the person susceptible to further brain damage from vaccines and other environmental factors. Several lines of evidence support the stealth virus cause of autism. For example:

Blood samples from autistic children consistently induce a readily identifiable cytopathic effect (CPE) using viral culture methods adapted for the detection of stealth-adapted viruses. Stealth virus testing of blood samples from autistic children has been subjected to formal “double blind” analyses. Furthermore, cerebrospinal fluid (CSF) and gastrointestinal biopsy have similarly yielded positive cultures.

There is good evidence for stealth virus infections among family members of autistic children. Many of the family members will, upon close questioning, reveal symptoms of neurological and/or immunological dysfunction.

Autistic patients will not infrequently display positive results in assays intended to detect conventional virus and bacterial pathogens. As discussed below, such results can be attributed to cross-reactivity with stealth virus components.

When will the stealth virus theory of autism be accepted and supported by i) researches, ii) Public Health authorities, and iii) families with affected children. The answer to the first point is when it is clearly proven that stealth-adapted viruses, as presently defined, do exist as novel pathogens. This challenge, as well as the goal of eliciting official Public Health involvement, will occur when the message gets across that the extensively sequenced prototype stealth-adapted virus is atypically structured and that it arose as a probable contaminant of poliovaccine production. Finally, parents will begin to focus their energies on the stealth-adapted viruses infecting their children once they begin to see real clinical improvements based onanti-stealth virus therapies.

Sequencing Studies on an African Green Monkey Derived Simian Cytomegalovirus (SCMV)

These studies unequivocally establish the origin of an atypically structured cytopathic virus as being from SCMV. For certain regions of the stealth viral genome, there is over 90% identity between the nucleotide sequences of the stealth virus and that of the Colburn strain of SCMV. Yet in other regions, the two viruses differ in a manner that is best explained by genetic instability in viral replication and by the selection of genetic changes that favor viral survival and avoidance of immune recognition. Of particular note is that the virus failed to evoke an inflammatory reaction in either the patient from whom it has been repeatedly cultured, or from the cats in which it induced considerable brain damage. To date, the genes that would otherwise encode the major antigens targeted by anti-CMV cytotoxic T lymphocytes have not been detected. Nor do the viral cultures react with antibodies against several antigens shared by human and simian CMV.

Over 120,000 nucleotide sequence data have been compiled on the stealth-adapted virus. Long regions of contiguous sequences suggests the coding of somewhat truncated proteins in comparison to the coding potential of the comparable region ofthe human CMV genome. To help clarify the extent to which these changes reflect the preexisting SCMV genome, or are part of a mutational process occurring within a genetically unstable stealth-adapted virus, sequencing is underway on an authentic monkey-derived SCMV.

Even at this stage of the work, is abundantly clear that stealth adaptation involves much more than simple deletion/mutation of particular genes targeted by the cellular immune system. For example, there is a striking over representation of certain genes. Of particular interest, is the finding of multiple copies of genes implicated in the production of, and providing receptors for, potent growth factors called chemokines and present within the virus. This observation strongly suggests the potential value of suppressing chemokine production in this particular patient.

Another striking feature of the DNA analysis is the presence of particular cellular genes adjacent to viral genes. A prime example is the three copies of a cellular chemokine-related gene within the viral genome. These virus-incorporated cell-derived genes do not contain normal stretches of non-coding sequences (introns) that are present in the cell DNA. This would indicate that the recombination process allowing cell-derived genes to become incorporated into a replicating stealth virus had occurred at a partially processed RNA, rather than at a DNA level. If so, it would indicate a role for endogenouse reverse transcriptase in stealth virus assembly and replication. Several other cell-derived sequences are more readily amplified using polymerase chain reaction (PCR) based assays performed on the stealth virus culture than when performed on uninfected cultures, suggesting that the sequences may have been incorporated as part of the stealth virus replication process.

Various bacterial-derived sequences have also been extracted from the cultures. The bacterial sequences are of particular interest since, along with additional data, it appears that the virus is able to pass into, and, therefore, be potentially metabolically empower and be transmitted by bacteria. Taken together, the data are consistent with a viral replicative process that allows the assimilation of extraneous sequences of cellular, bacterial and possibly fungal origins. Addressing this situation is particularly urgent since among the potential activities of cell derived genes, including chemokine-inducing and chemokine-receptor genes, are the induction of malignant changes. The prospect of highly infectious bacteria carrying cancer causing genes is a serious concern that, so far, has been brushed aside by those responsible for overseeing the Nation’s health.

Stealth-adapted viruses that have incorporated bacterial sequences are referred to as “viteria.” Work is underway to confirm that such organisms can be mistaken for actual bacteria in conventional assays for such pathogens as Borrelia burgdoferi, Mycoplasma incognitus, Chlamydia pneumonia, etc. Many bacterial proteins have a propensity to evoke allergic reactions offering a possible explanation for such reactions among autistic children.

Stealth Adaptation as a Generic Process

CPE generally similar to that shown with the SCMV-derived stealth-adapted virus has been consistently seen with blood samples from many other patients. Most of these isolates do not react particularly strongly with antibody and molecular based probes that are highly reactive with the prototype SCMV-derived stealth-adapted virus. This finding suggests marked structural variability and probable multiple, diverse origins of stealth-adapted viruses. Limited sequence and antibody staining data on some of these additional isolates are consistent with origins from other herpesviruses, including Epstein-Barr virus and human herpesvirus-6; and also from such diverse viruses as parvovirus, adenovirus and enteroviruses. The addition of various live viruses to positive stealth virus cultures can lead to enhanced CPE, suggesting the possibility of reciprocal viral stimulation and even the recombinant formation of new viral constructs. This potentiating effect has been noted using live measles and other viral vaccines. It is also reasonable to assume that certain stealth viruses may retain some components that would normally not be involved in evoking cellular immunity, but in the presence of a powerful immune stimulant (such as provided by DPT vaccine) could become a target for cell damaging immunity.

A topic of interest is whether stealth-adapted viruses cultured from autistic children will show any distinguishing characteristics from those cultured from patients with other disease manifestations. Given the overall similarity in the CPE seen when tested blood samples from autistic and non-autistic family members, it seems likely that a similar virus is involved and that clinical manifestation relates to sex, other genes and time and location of infection.

Implications for Patients with Autism

Specific testing for cell derived chemokine genes, as are present in cultures of the prototype stealth virus, has yet to be performed on stealth virus cultures from patients with autism. Clinically, however, drugs that are known to down regulate chemokines are finding increasing use in patients with other stealth-virus associated diseases, including depression, attention deficit and hyperactivity disorder (ADHD) andCFS. Of particular interest are many of the disease modifying anti-rheumatic drugs (DMARDS). Some clinicians have also anecdotally noted symptomatic improvement with Acyclovir, an anti-herpesviral drug.

Progress in this field will require disciplined clinical trials with close monitoring of patients using both clinical markers and semi-quantitative stealth virus cultures. In the meantime, work needs to be continued on the development of more specific therapies that are based on a more detailed understanding of the mode of stealth virus replication.

Positive blood cultures is a sign of a body wide infection that can potentially cause multi-organ damage (both as the result of direct virus damage and an evoked auto-immune response). Rather than being viewed narrowly as a neuropsychiatric illness confined to the brain, autism should be viewed as a generalized viral infectious process that also involves the brain. Specific testing for endocrine disorders, gastroenteropathy, liver damage, allergies, etc., should be part of the overall medical profile of any stealth virus infected patient. The finding of a positive stealth virus culture in a child is probably sufficient reason to avoid the intense immunological stimulation associated with DPT vaccine and also to not add extraneous infectious viruses in the form of MMR and live poliovirus vaccine. Acceptance of an infectious cause of autism can help explain the occurrence of stealth-virus associated illness among other family members. Certainly other family members should be tested for infection. The socially difficult issue of possible contagion to classmates, schoolteachers, non-infected family members, etc., is better addressed than denied.

Summary

Autism is a clinical label referring to a set of symptoms that can occur as a result of infection with atypically structured, poorly immunogenic (stealth-adapted) viruses. This conclusion should help reorient the clinical approach to the diagnosis, therapy and prevention of this illness.

*Lecture prepared to be given at Catalina Island, June 9, 2001, but unable to do so for family reasons.

STEALTH VIRUS INFECTION AND AUTISM

2004-07-11T10:00:00.000-07:00

STEALTH VIRUS INFECTION AND AUTISM

Autism is often mistakenly viewed as a precise clinical entity, rather than as variable sets of symptoms resulting in abnormal social behaviors among young children. Clinical emphasis is given to an early onset (generally before the third year of life); a failure to express empathy for others; poor development, and even regression, of meaningful speech; hypersensitivity to various stimuli; and an apparent need for repetitive self-stimulated sensations.

Discussions concerning a possible infectious cause for autism have met with little interest, especially since the vast majority of those providing medical care for autistic children are not well versed in microbiology. Such discussions also raise disturbing inferences regarding possible sources of infection and modes of disease transmission. This is especially true for any suggestions that live viral vaccines might either cause or exacerbate autistic illnesses.

CCID has performed viral cultures on blood samples from well over 100 autistic children. In greater than 80% of the samples, a marked cytopathic effect (CPE) has occurred. The strongly positive CPE is similar to that induced by "stealth-adapted" viruses. The term stealth was chosen because certain cytopathic viruses seemingly lacked components targeted by the cellular immune defense mechanisms. This conclusion has been substantiated in detailed DNA sequencing studies conducted on a prototype stealth virus. This particular stealth virus originated from an African green monkey simian cytomegalovirus (SCMV), and presumably was derived from an SCMV-contaminated batch of poliovaccine. While the virus lacks genetic sequences coding for the major target antigens for anti-cytomegalovirus cell mediated immunity, it has acquired many additional genes of both cellular and bacterial origins.

Among the viral sequences, a notable finding is the expansion of a viral gene that provides a receptor for cell migration regulatory molecules termed "chemokines". Rather than a single copy of this gene, the virus has at least five copies in a linear array. There is sufficient indirect evidence for chemokines driving the replication of other stealth-adapted viruses to consider therapeutic trials with chemokine regulatory medicines in stealth virus infected individuals.

In preparation for such trials, CCID has tabulated many of the herbal and proprietary medicines reported to suppress various stages of the complex processes leading to chemokine production. Interestingly, a number of these medications have been used individually, with some apparent success, in patients with stealth virus-associated diseases. Following the lead of rheumatologists, there may be advantages to using lower doses of various combinations of differently acting chemokine regulatory agents, rather than relying upon a single medication. Especially for children, the initial priority should be given to those medications without appreciable risks of significant toxicity.

CCID has also standardized the viral cultures to provide a semi-quantitative measure of stealth virus activity. What is now required is the co-operation of parents and knowledgeable prescribing clinicians. Stealth virus cultures should be performed before, and at the end of, a 7-10 day trial of various treatment protocols. If significant suppression of viral activity is observed, the treatment would be continued along with detailed clinical assessments. If no effect was seen, the protocol could be adjusted by adding additional drugs and/or substituting medicines.

Note: Unfortunately, CCID was denied Federal permission to provide stealth virus testing. Correspondence relating to this denial is posted at www.s3support.com

Copy of Petition Available at www.s3support.com

2004-07-11T09:54:00.000-07:00

Please consider signing the following petition that is accessible at www.s3support.com

Autism An Epidemic out of control

There are growing health problems being faced by many
Americans. Autism has doubled in California over the last
5 years and special educational needs of school children
are soaring. Severe childhood behavioral problems
necessitating residential care are financially forcing
many parents to relinquish custody of their children to
the State. In a year 2001 sampling of only 19 mid-sized
States, the astounding number of voluntary State-orphaned
children was 12,700. This heart rendering loss of custody
does not even ensure therapy for the children, merely
protective restraint. Nearly half of our elderly will
experience the memory loss and emotional fragility of
Alzheimer's disease. Published figures from the CDC
confirm that nearly 20,000 patients are hospitalized each
year with a diagnosis of encephalitis. Yet in the majority
of these patients, no cause of the illness can be found.
Many more individuals experience an alarming decline in
brain function that can lead to such tragedies as suicide
or mindless criminal behaviors. Many of us have friends
with chronic fatigue syndrome, diabetes, arthritis and/or
debilitating mental illnesses.

Individually, any of these increasingly prevalent
diseases ought to trigger a serious investigation for the
possibility of an infectious cause. When lumped together
the prospect that our Nation is in the midst of an
infectious epidemic that can manifest itself as various
clinical syndromes is indeed alarming.

We would like to bring to your attention published
reports of simian (monkey) cytomegalovirus DNA
contamination of licensed polio vaccines. The studies were
conducted by the United States Food and Drug
Administration and the United Kingdom National Institute
for Biological Standards and Control. Although the
Government researchers were unable to culture viruses from
the contaminated polio vaccine lots, they have refused to
provide the lots for independent testing. The reason cited
is proprietary protection of the vaccine manufacturer. The
Government studies were prompted by the reported isolation
of viruses related to simian cytomegalovirus from patients
by an independent investigator Dr. W. John Martin, M.D.,
Ph.D.

We, hereby, petition that the Congress of the United
States conduct an immediate review of the evidence for
human illnesses resulting from the use of simian
cytomegalovirus contaminated polio vaccines. Furthermore,
we request that samples of licensed contaminated polio
vaccines by made available to Dr. Martin and other
independent researchers for specialized virus culturing.
We further request that the Federal and State Public
Health Laboratories be provided the resources to conduct
specialized virus cultures in patients with unexplained
brain damaging illnesses, including autism. Additional
information is available at www.s3support.com and
www.rhinoed.com

Comments on Mercury Poisoning Article Cited by Dr. Geier

2004-07-11T09:48:00.000-07:00

I should like to comment on the article by Dr. Chrysochoou and colleagues (Eur J Ped 162: 559-561, 2003) cited by Dr. Mark Geier on presumptive mercury toxicity in a child. Most of the clinical and laboratory features reported for this child are highly atypical for children with autism. For example, the intoxicated child exhibited an acute onset of swollen, tender hands and feet, skin desquamation with a persisting rash, profuse sweating, elevated heart rate and hypertension, and muscle weakness and wasting yet brisk neurological reflexes. Serum lactic dehydrogenase and creatinine levels were elevated, as were urinary epinephrine, norepinephrine, dopamine and HMA. The child showed a complete remission within 13 months.
The clear distinction between signs of acute poisoning and typical autism is only one of several solid arguments against mercury intoxication causing autism. Other arguments include parallel increases in autism rates in the United States and both Sweden and Denmark; countries that did not expand the use of thimerosal containing vaccines. An article by Dr. Stehr-Green and colleagues on this subject was published last year (Am J Prevent Med. 25: 101-106, 2003). Elevated neuropeptides were also found in cord blood of 99% of children who subsequently became autistic (Nelson et al. Neuropeptides and neurotrophins in neonatal blood of children with autism or mental retardation. Ann Neurol. 2001;49:597-606), clearly suggesting prenatal brain damage.
I recently expressed to Ray Gallup reasons why autism should be viewed as part of a larger epidemic of non-inflammatory viral diseases affecting the brain. Sadly a lot of time and resources have been spent pursuing mercury intoxication, measles vaccine virus, genetic disorders, etc., rather than addressing compelling evidence for a congenital viral illness. My e-mail to Ray Gallup is copied below. Kind regards, W. John Martin.

Dear Ray,
I appreciate being included in your e-mail list as it provides useful insight into the enormous toll borne by parents of autistic children. I cannot help but believe that the various autism support groups have gone astray with regards to truly helping those afflicted with autism and related diseases. I attended a CASD meeting in Long Beach recently only to see parents having to pay to be bombarded with incoherent and inconsistent data from supposed experts. I enjoyed presenting the concept of an epidemic of viral illnesses sweeping the country. I further suggested the opportunity for immediate clinical trials, supported by contrasting pre- and post-therapy photographs of a child named Cody. His mother was diagnosed as having cytomegalovirus infection as a young adult. I feel certain this infection persisted and was passed onto Cody causing his autism. He really improves with therapy and regresses if he goes off therapy. Still the double blind clinical trials have not been started, nor championed by any of the conference participants. Kazuko is possibly considering a modest proposal to reestablish stealth viral cultures. This will be helpful but why not go directly to a clinical trial. Public Health laboratories should be doing stealth virus cultures. This was the message behind the petition on the www.s3support.com web site that you kindly signed. Surprisingly, the petition could not even garner 1,000 signatures. I hope other members of your e-mail list will take an interest in the viral cause of autism. I would be happy to answer any of their questions. Kind regards, John Martin.

Stealth Viruses

2004-06-29T20:27:00.000-07:00

What are Stealth Viruses?

Viruses are submicroscopic infectious agents that replicate inside cells. Viral illnesses are normally controlled by the body’s immune system acting primarily through white blood cells called lymphocytes. These cells recognize certain viral proteins that provide the antigens targeted by specific lymphocytes, leading to an anti-viral inflammatory response. Not all viral proteins, however, can function as antigens for effective anti-viral immunity. Indeed, for many viruses, only a very few proteins are involved in lymphocyte recognition of virally infected cells. Loss of these critical antigenic proteins can allow a virus to essentially go unrecognized by the cellular immune system. When such viruses have managed to retain the capacity to damage cells, they can potentially cause a persistent infection resulting in a prolonged illness. The viral nature of such an illness is usually overlooked because of the absence of overt inflammation. Atypically-structured cell-damaging (cytopathic) viruses were initially identified in patients with the chronic fatigue syndrome and in patients with more severe neurological and neuropsychiatric illnesses. The term “stealth” was introduced to highlight their basic property of evading effective immune recognition, and also because they had gone unrecognized by the medical community.

Detection of Stealth Viruses

Stealth-adapted viruses can be most readily detected using specialized, semi-quantitative, viral culture methods developed and refined over the last decade. Using these procedures, stealth viruses will typically induce a characteristic vacuolating cytopathic effect (CPE) in cultures of human and animal-derived cells. Stealth virus infected cultures can be distinguished from cultures of conventional herpesviruses, adenoviruses, enteroviruses and retroviruses, by the appearance and host range of the CPE, and also by using selective immunological and molecular probe based assays, including polymerase chain reaction (PCR) testing methods.

Cytopathic Effects

A common feature of the CPE-induced, stealth adapted viruses is marked metabolic disruption. This is expressed as lipid accumulation, cytoplasmic vacuolization, formation of aberrant protein and lipoprotein inclusions, and abnormally shaped nuclei. Comparable foamy vacuolating cellular changes with atypical inclusion-like structures can be seen in detailed examination of brain and other tissues obtained from stealth virus infected patients and from animals inoculated with these viruses. Unlike infections caused by conventional cytopathic viruses, the actual production of readily identifiable viral particles is uncommon. Seemingly, the infected cells are metabolically impaired because various energy and other resources are diverted towards an inefficient and unbalanced synthesis of various virus coded components at the expense of normal cellular functions. Severe defects in energy-generating metabolic pathways are also apparent from the marked mitochondrial changes that are prominent in electron micrographs of virus-infected cells.

Center for Complex Infections Diseases

Both clinical- and research-based studies on stealth-adapted viruses have been undertaken at the Center for Complex Infectious Diseases in Rosemead, California. CCID is a non-profit organization under the National Heritage Foundation dedicated to understanding the nature, origin, disease associations, modes of transmission, methods of diagnosis and responses to therapy of stealth virus infections, and to the dissemination such information to the medical and lay communities. Information regarding CCID is available from the internet at www.ccid.org. Additional information is available from www.EmergingWorlds.com. The following sections provide a brief overview of some of the ongoing research activities being conducted at CCID.

DNA Sequencing Studies

A stealth virus isolated from a patient with a chronic fatigue syndrome like illness was originally noted to have limited DNA sequence homology to human cytomegalovirus (CMV). As additional sequence data became available, it became obvious that this virus was a derivative, not of human CMV, but rather of an African green monkey simian CMV (SCMV). Until the beginning of last year, these monkeys were routinely used to produce live poliovirus vaccine. Moreover, although not widely revealed, a joint Food and Drug Administration/Industry study in 1972 indicated that control kidney cell cultures from all 12 African green monkeys tested grew out SCMV, and that most of these isolates were not detectable using standard procedures.

Continued sequencing on the SCMV-derived stealth-adapted virus has shown interesting changes compared to a typical CMV. Of special note is the uneven representation of genes that encode various viral components. As expected, the genes that code the proteins known to provide major target antigens for anti-CMV cytotoxic T lymphocytes are either absent or mutated. Other genes are overly represented, including genes that code for various chemokines and for chemokine receptors. Interestingly, one of the markedly amplified chemokine receptor coding genes found in the stealth virus genome can also function as a receptor for HIV, suggesting a possible potentiating role of stealth viruses in HIV infected patients.

One set of amplified chemokine-coding genes detected in the stealth-adapted virus is of cellular, rather than viral, origin. Cellular genes can apparently be incorporated into stealth virus genomes, presumably during viral replication. The particular chemokine-coding cellular gene identified within the prototype SCMV-derived stealth virus was probably assimilated as a partially processed RNA molecule since it lacks the normal introns present in cellular DNA. This implies that stealth virus DNA replication is proceeding through RNA intermediates, and that it may, therefore, be dependent upon reverse transcriptase, as could be provided by an assimilated endogenous retroviruses. RNA to DNA replication is much more prone to error than is DNA to DNA replication. This might explain sequence variability between the three copies of the chemokine-coding cell-derived gene that have so far been identified within the stealth virus.

Chemokine receptor genes of both viral and cellular origins have been implicated in the development of several types of malignancies. It is somewhat worrisome, therefore, that the stealth adapted virus is apparently employing this type of gene for its survival. On the other hand, many therapeutic agents that appear to be of some benefit to stealth virus infected patients are known to inhibit cheomkine production and receptor activity.

Viteria

It has also been determined that stealth viruses have the ability to acquire genetic sequences of bacterial and even fungal origin. Normally, viruses that are infectious for human or animal cells (eukaryotic cells) will not infect bacteria (prokaryotic cells). Stealth viruses appear to have overcome this phylogenetic barrier. The term "viteria" has been coined to define eukaryotic viruses that have acquired bacteria-derived genetic sequences. The sources of the bacterial sequences include microorganisms that are not known to grow intracellularly within eukaryotic cells. This strongly suggests that stealth viruses become viteria by infecting bacteria. Judging from the bacterial sequences so far identified, genes have been captured from a wide variety of both gram positive and gram negative bacteria. The linear arrangements of many of the bacterial-derived sequences are quite different from any of the known major bacteria, suggesting that an active ongoing selection process may be occurring to assist in stealth virus propagation within bacteria. Genetically empowered bacteria, carrying potentially oncogenic stealth-adapted viruses, could become a far more threatening biological weapons program then ever envisioned by military planners.

Bacterial sequences incorporated within stealth-adapted viruses may help explain positive findings in stealth virus infected patients in various tests for known bacteria, including Borrelia burgdoferi (the cause of authentic Lyme disease), mycoplasma (a suggested cause of CFS and Gulf war syndrome); chlamydia (implicated in coronary artery disease and Alzheimer’s disease), etc. None of the commonly used assays for these bacteria actually detect cultured organisms, but instead rely upon broadly reactive molecular and/or serological testing that could as easily be explained by the presence of viteria.

Clinical Conditions Associated with Stealth Virus Infections

Stealth-adapted viruses have been recovered from the blood, cerebrospinal fluid, urine, throat swabs, breast milk, brain biopsies and tumor samples from patients with various neurological, psychiatric, auto-immune, allergic and neoplastic diseases. Examples of neurological illnesses are autism, attention deficit and behavioral disorders in children; depression, schizophrenia, amyotrophic lateral sclerosis, multiple sclerosis, chronic fatigue and fibromyalgia in adults; and neurodegenerative illnesses in the elderly. It is now known that the stealth viruses can infect many organs, but that the brain is especially prone to manifest the effects of even limited localized cellular damage. The varying manifestations of a stealth virus encephalopathy is probably heavily influenced by the timing of infection, regions of the brain that are mostly involved, genetic predisposition to particular symptoms and the additive pathology of any superimposed auto-immune component triggered by the viral induced cellular damage. CCID's focus is away from strict clinical categorization of stealth virus infected patients into discrete neurological and neuropsychiatric illnesses. This viewpoint has been supported by following individual patients over several years, and also by the not uncommon occurrences of related, yet diverse, illnesses occurring among other family members and even among household pets. Community-wide outbreaks of stealth virus infections have also been observed with individuals showing varying levels of severity and duration of illness. Neither the reporting of otherwise unexplainable deaths, nor the apparent “dumbing” of a whole township, as reflected in the excessive need for special education for its children, appears to provide adequate Public Health motivation to confirm CCID’s findings of stealth-adapted viruses.

Cancer can now be added to the list of potential stealth virus-associated diseases. Positive stealth virus cultures have been seen in virtually all of the multiple myeloma patients tested, and in several patients presenting with other types of tumors. A previous history of a fatiguing illness and clinical indications of impairments in normal brain functions are suggestive of an underlying stealth adapted virus infection in a cancer patient. It will be interesting to determine the effect of stealth-virus suppressive therapy in such patients.

Infection Among Blood Donors

An indication of the probable prevalence of infection among apparently healthy individuals has come from studies conducted on student blood donors attending a college campus. Slightly less than 10% of the units tested gave a positive result. As a requirement of the study, it was not possible to determine the actual health status of these students. Nor were efforts allowed to follow recipients of the stealth virus positive blood units. Even if culture-positive individuals are presently asymptomatic, this would not preclude their being at risk for subsequent development of a stealth-virus associated illness. This concern is underscored by the apparent capacity of stealth-adapted viruses to “capture, amplify and mutate” various additional genes of viral, cellular and bacterial origins.

Role of Other Infectious Agents in Chronic Illnesses.

Much of the debate over a potential infectious cause for many of the illnesses that are increasingly being seen within our society has centered upon conventional microorganisms. Patient support groups and their affiliating clinicians have championed alternative explanations for these illnesses. Human herpesvirus-6 (HHV-6), human herpesvirus-8 (HHV-8), enteroviruses and parvoviruses feature among the viral causes for these illnesses, while Borrelia burgdoferi, Mycoplasma incognitos and Ehlichiosis are being promoted as the bacterial causes for a wide spectrum of illnesses. As is the case for HHV-6 in CFS, HHV-8 in multiple myeloma, enterovirus in ALS and Borrelia in chronic Lyme disease, when looked at critically, the actual findings are generally inconsistent with a true etiological relationship. None of these negative studies exclude the role atypically structured microorganisms; indeed, if anything they strongly support their presence. As alluded to above, stealth-adapted viruses can easily be mistaken in diagnostic tests for conventional viral and bacterial pathogens.

Additional complex associations between stealth adapted viruses and conventional microorganisms may exist. For example, the lipid-laden cells infected with a stealth virus appear especially favorable to the growth of intracellular bacteria, including Borrelia, the causative agent of Lyme disease. CCID has demonstrated positive stealth virus cultures in blood samples from over 90% of patients referred with a diagnosis of chronic Lyme disease. Whether the patients are actually infected with Borrelia remains unproven, but if so, their growth may be dependent upon an accompanying stealth virus infection. Synergistic growth patterns between stealth adapted viruses and the viruses present in several live viral vaccine preparations, have also been observed. The potential role of stealth virus encoded chemokine receptors in the evolution and the present day expression of HIV, is also under consideration.

Clinical Approach to the Diagnosis and Therapy of Stealth Adapted Virus Infections (SAVI)

Diagnosis: A major challenge in providing medical care for stealth virus infected patients is the multiple and diverse clinical manifestations of the patients’ illnesses. Individual patients do not fit comfortably into a single medical discipline, whether it is psychiatry, neurology, rheumatology, endocrinology, hematology, or any other. Imprecise diagnostic labels, such as CFS, fibromyalgia, depression, attention deficit, etc., and even the better defined diagnostic labels, such as schizophrenia, autism, ALS, multiple sclerosis, Alzheimer’s disease, etc., tend to obscure the complex multi-system nature of the patients’ illnesses. Another difficulty is quantitating the severity of disease processes that can vary widely over time, and can be influenced by such non-specific factors as stress, environmental exposures to chemicals, placebo effects, etc.

Disordered brain function can be anticipated in many stealth virus infected patients. This can be documented using a detailed neurological examination, with a focus on what are sometimes referred to as “soft” neurological signs. Ancillary, although expensive, tests such as SPECT scans, quantitative EEG and formal neurocognitive evaluations, can help substantiate a diagnosis of stealth adapted virus infection with encephalopathy. Additional syndrome names can be applied depending on clinical and laboratory findings. Tabulation of symptoms using a detailed questionnaire can be helpful in identifying clinical problems and in assessing therapy related improvements.

Therapy: Until the existence of stealth viruses is accepted by Public Health authorities, there will be no approved standard of care in providing anti-viral treatments. Several suggestions can be made, however, from what is currently known about the prototype SCMV-derived stealth virus. Whether these suggestions are relevant to atypical viruses cultured from other patients remains to be tested. CCID is now reaching out to clinicians involved with the care of stealth virus infected patients for assistance with these clinical trials.

Basically, it seems appropriate to undertake efforts to suppress stealth virus activation and at the same time to support cellular metabolism, especially mitochondria function. The remarkable expansion of chemokine and chemokine-receptor related genes within the prototype SCMV-derived stealth-adapted virus support the potential use of agents that can down regulate chemokine pathways. Fortunately, many of the widely used herbal and generally non-toxic allopathic medicines are known to interfere with chemokine signaling. It is probably more than a coincidence that many of the compounds have also been reported to benefit at least a proportion of patients with CFS and related illnesses. Ideally, patients receiving these relatively simple therapies would be retested for stealth virus activity. If there were no apparent reduction in stealth virus activity, and if the patient remained symptomatic, one could more easily justify the use of potentially more toxic allopathic medicines, including known anti herpesviral agents.

For patients with major neurological, psychiatric, autoimmune or malignant diseases, the stealth virus associated treatments will simply be an aside to the accepted standard care of the patient’s underlying illness. Once sufficient supportive data are collected, it may be possible to proceed directly with anti-stealth virus therapy as the primary treatment for these severe disorders.

Request for Assistance with Clinical Therapeutic Studies

In support of these studies, CCID has begun to work with medical specialists treating major medical neurological, psychiatric, rheumatological and neoplastic illnesses, and also with orthomolecular clinicians experienced in the uses of alternative medicines. Stealth virus culture activity will be serially determined and correlated with the use of various therapeutic modalities and changes in clinical status. CCID can provide copies of patient questionnaires and an appropriate informed consent form. A database for integrating laboratory, clinical and pharmaceutical data, will be established and will be assessable to all participating clinicians. The type of program is urgently needed to address the major Public Health threat posed by stealth-adapted viruses and viteria.

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