The Autism Epidemic is Attributed to Prenatal Infection with Polio Vaccine- Derived Stealth Adapted Viruses

Since 2000, the US Centres for Disease Control and prevention (CDC) sponsored Autism and Developmental Disabilities Monitoring (ADDM) Network has biannually determined autism rates among 8-year-old children in multiple American States. As quoted by Robert F. Kennedy Jr., the rates have steadily increased from an overall value of 1:150 in children born in 1992 to 1:31 in children born in 2014 [1]. Before the 1990s, autism was infrequent, with a 1970 determined incidence in Wisconsin of 0.7 per 10,000. The beginning of an increase was seen in the 1987 recorded incidence of autistic children in Nebraska of 3.3 per 10,000. California is now considered to have the best data collection on autism. The ADDM determined prevalence of autism among Californian children born in 2014 is 1:22 (4.5%) [2]. Among boys, the incidence is 8%. Based on the increases in recent years, the chance of a boy born this year becoming autistic exceeds 10%. IQ testing was conducted in the 2022 survey, including on 81.5% of the autism affected 8-year-olds in California. Of these children, 55.6% had an intellectual disability (IQ<85), with 28.4% scoring below 70 points. Since only 2% of IQ tests in the entire population score <70, the 28.4% value contradicts any assertions that the increasing autism numbers merely reflect changed diagnostic criteria. Inherited genetic factors and realistically rising levels of environmental toxins cannot explain the rapidly increasing incidence of autism. Yet, Public Health authorities and most autismsupportive communities have actively resisted open discussions of an infectious cause of autism. This is despite many attempts by the author to relate autism to atypically structured, cellular immune system-evading stealth adapted viruses, some of which are derivatives of the cytomegaloviruses of the species of monkeys used to produce polio vaccines [3-6].

PCR studies were initially designed to test for Human Herpes Virus-6 (HHV-6) infection in Chronic Fatigue Syndrome (CFS) patients. Patients with other neurological illnesses were included in the testing. Positive PCR results were obtained with several blood samples, but only when using low-stringency amplification and highly sensitive detection methods. The results were not specific for HHV-6 since various additional PCR primer sets were even more reactive. Positive low-stringency PCR results extended to studies on a brain biopsy obtained in 1990 from a patient with progressing dementia [7]. A striking feature of the biopsy was the absence of inflammation. Approximately a third of patients with CFS tested positive using PCR primers reactive with the thenknown human herpesviruses [8]. Even more striking PCR results were obtained based on the fortuitous cross-reactivity with human T cell lymphotropic viruses (HTLV-I and HTLV-II) reactive primers [9].

Multiple blood samples from a PCR-positive CFS patient were consistently cytopathic when cultured with human fibroblasts [9]. PCR on the cultures yielded products that could be cloned and sequenced. Virus particles were isolated from cultures, allowing for the virus-isolated DNA to be cloned. Partial sequencing of over 300 clones identified the originating virus as an African green monkey Simian Cyto Megalo Virus (SCMV) [10-12]. The entirety of the SCMVrelated clones matched in aggregate, yet unevenly, to somewhat less than 50% of the complete SCMV genome. Only three components in human cytomegalovirus are targeted in total by roughly 90% of the evoked cytotoxic T-cell response [13,14]. The comparable genes in the stealth-adapted SCMV are either deleted or mutated. In contrast to the >200kb genome size of SCMV, DNA isolated from the cultured virus migrated in agarose gel as multiple fragments with estimated sizes of 20 kilobases (kb) [9]. Cellular sequences were present in 16 of the clones, while 35 clones had bacterial sequences [15,16]. A comparison of sequences of several clones that match the same region of the originating virus indicated significant genetic instability [17]. Genetic instability was also shown by matching the incorporated cellular sequences [13]. While the cellular sequences in the SCMV-derived virus were of human origin, it can be inferred that these had replaced African green monkey cellular sequences. Thus, in another partially sequenced stealth-adapted virus, four of seven incorporated cellular sequences matched more closely to the rhesus monkey genome, with the other three matched more closely to the human genome [18]. The matching bacterial sequences in the SCMV-derived stealth adapted viruses included those of Mycoplasma fermentans, a suggested co-pathogen for many of the earlier HIV infected patients[19]. Molecular assays have further linked this strain of Mycoplasma to other types of chronic illnesses [20-22]. Another prominent bacterial species for which genetic sequences have been incorporated is Ochrobactrum. The incorporated sequences are referred to as being “renegade” and can potentially contribute to the added pathogenicity of the viruses and lead to misdiagnosis of infections as bacterial rather than viral [16]. Along with additional evidence, acquiring bacterial sequences raises the prospect of stealth adapted virus transmission via infected bacteria.

Blood samples from many additional CFS patients yielded readily discernible positive Cyto Pathic Effects (CPE) in cultured human and animal cells [9,23]. A characteristic feature of the CPE was the rounding of spindle-shaped fibroblasts with the formation of clusters of foamy cells, often with evidence of cell fusion. The tissue culture medium had to be repeatedly replaced for the CPE to progress to where it could be readily identified. Other features of long-maintained positive cultures include the formation of intracellular and extracellular pigmented materials and the abundant production of lipid materials. The pigmented materials display energy-transducing properties, including being fluorescent, electrostatic, occasionally ferromagnetic, and capable of creating fine vapor bubbles in water [24]. Electron microscopy of the infected cells shows a paucity of mitochondria, leading to the hypothesis that the particles were a source of a non-mitochondrial or Alternative Cellular Energy (ACE) pathway [25]. It is the added cellular energy via the ACE pathway that leads to the suppression of the CPE.

Most virus cultures conducted during the period from early 1991 to mid-2002 were on blood samples from CFS patients. The next most common source of patient samples was from children with autism and related behavioral, learning, and emotional disorders. A low estimate is the testing of five hundred blood samples and several Cerebro Spinal Fluid (CSF) samples of autistic children. Clearly, discernible CPE occurred in approximately 80% of the tested samples. This level of positivity exceeded the approximate 10% positivity seen with blood samples of asymptomatic individuals. The patient samples in which CPE was either not seen or was insufficient to diagnose as positive were from children, where the clinicians favored a major autoimmune component to the illness. More intensive efforts were not undertaken to obtain positive virus cultures from these children. The testing was mainly performed on patients seen by Dr. Jeffrey C. Kopelson, an autism specialist in New York, and in consultation with Dr. George Lewis, a psychiatrist.

The PCR and culture data clearly implied a role of stealth adapted viruses in neurological and psychiatric diseases, including autism. Yet, in mid-2002 my further clinical testing for these viruses was legally prohibited. Government officials concluded that my reporting on stealth adapted viruses had placed the Nation’s Health in “Immediate Jeopardy”! A Centers for Disease Control and prevention (CDC) virologist publicly stated that “stealth viruses do not exist.” of possible concern to officials was my extending the culturing to blood donors, which I had undertaken in an approved study at the University of California, Irvine. Linkage to polio vaccines was also viewed as contrary to the Nation’s interest. A relevant quotation from Alfonse Bertillon, a French criminologist, is that “One can only see what one observes; one observes only things which are already in the mind.” A brain-infecting virus causing autism has not been, nor seemingly is it currently, on the minds of Public Health officials. The difficulty in persuading officials otherwise was illustrated in the disregard of a presentation that I made in 2019 to the Interagency Autism Coordinating Committee (IACC) [26]. The committee chairman went as far as to suggest that he had not heard of stealth adapted viruses before the meeting, despite written comments on the topic having been previously submitted.

Many use the lack of brain inflammation to exclude the notion of an infectious illness. This argument is countered by the stealth adaptation process, which was further confirmed in animal inoculation studies [27]. Stealth adaptation is a generic process that can potentially occur with all viruses. Their earlier existence may explain the rare occurrence of autism before cytomegalovirusinfected monkeys were used to produce polio vaccines. In dismissing an infectious cause of autism, officials may also contend that there is no evidence of autism occurring among those in contact with affected children. Yet, virus spreading is likely to occur among children with possible secondary infection of their parents. Subsequent children born to infected parents would be at risk for autism. So too are children born to autistic parents. Some autism advocacy groups attribute autism to vaccines, but their focus is either on the toxic vaccine components used as preservatives and adjuvants [28] or on the attenuated measles virus in the MMR vaccine [29,30]. It has been proposed that the measles vaccine virus, especially when used in conjunction with attenuated mumps and rubella viruses, causes damage to the intestinal tracts of children who subsequently become autistic. The damage would allow toxic intestinal compounds to enter the brain via the blood. A more likely interpretation of the clinical linking of vaccine with the development or worsening manifestations of autism is that vaccination provokes immune reactivity against some of the residual, yet normally non-immunogenic components of stealth adapted viruses. Arguably, a reduced willingness of parents to vaccinate their children is justified.

It is important to obtain sequence data of both the originating viral and subsequently acquired renegade sequences of viruses cultured from children with autism. Then, the sequences of viruses cultured from patients with other types of neurological and psychiatric illnesses can be compared. On a further positive note, studies on stealth-adapted viruses have led to the understanding of a non-mitochondrial source of cellular energy. It can be conveyed to cells via activated water [24]. The ACE pathway has specific favorable comparisons with the immune system in the defense against infectious diseases [31]. It can also have health-restoring benefits for many other illnesses. Alleviation of symptoms was seen in a clinical study on children with autism using UV illumination of fluorescing neutral red dye in activated water [32]. Positive virus cultures can provide an effective means for screening and enhancing the ACE pathway.

Based on positive virus cultures, autism is viewed as a stealth adapted virus encephalopathy that begins before birth. The increasing incidence of autism over the last several decades is explained by prenatal infection with stealth adapted viruses. Many and possibly most of these viruses originated from cytomegaloviruses of the types of monkeys used to produce poliovirus vaccines, specifically African green and rhesus monkeys. Although typically avoiding effective immune recognition, stealth adapted viral infections can be suppressed via the Alternative Cellular Energy (ACE) pathway.

The Institute of Progressive Medicine is a component of MI Hope Inc., a public charity.

1. https://www.c-span.org/program/news-conference/health-and-human-services-secretary-kennedy-news-conference-on-autism-rates/658669.
2. https://www.rescuepost.com/files/embargoed-cdc-addm-community-report-sy2022-final.pdf.
3. Martin WJ (1994) Stealth viruses as neuropathogens. CAP Today 8: 67-70.
4. Martin WJ (1995) Stealth virus isolated from an autistic child. J Aut Dev Dis 25(2): 223-224.
5. Martin WJ (2004) The rationale for vaccines and the potential inadvertent consequences including autism, AIDS and other epidemics. Med Veritas 1: 81-85.
6. Martin WJ (2008) Autism vaccines stealth adapted viruses and mitochondria dysfunction. Best Syndication pp. 4-9.
7. Martin WJ (1996) Severe stealth virus encephalopathy following chronic fatigue syndrome-like illness: Clinical and histopathological features. Pathobiology 64(1): 1-8.
8. Martin WJ (1992) Detection of viral related sequences in CFS patients using the polymerase chain reaction. In: Hyde BM (Ed), In the Clinical and Scientific Basis of Myalgic Encephalomyelitis Chronic Fatigue Syndrome. Nightingdale Research Foundation Press, Ottawa, Canada, pp. 278-283.
9. Martin WJ, Zeng LC, Ahmed K, Roy M (1994) Cytomegalovirus-related sequences in an atypical cytopathic virus repeatedly isolated from a patient with the chronic fatigue syndrome. Am J Path 145(2): 440-451.
10. Martin WJ, Ahmed KN, Zeng LC, Olsen JC, Seward JG, et al. (1995) African green monkey origin of the atypical cytopathic 'stealth virus' isolated from a patient with chronic fatigue syndrome. Clin Diag Virol 4(1): 93-103.
11. Martin WJ (1996) Simian cytomegalovirus-related stealth virus isolated from the cerebrospinal fluid of a patient with bipolar psychosis and acute encephalopathy. Pathobiology 64(2): 64-66.
12. Martin WJ (1999) Stealth adaptation of an African green monkey simian cytomegalovirus. Exp Mol Pathol 66(1): 3-7.
13. Gyulai Z, Endresz V, Burian K, Pincus S, Toldy J, et al. (2000) Cytotoxic T lymphocyte (CTL) responses to human cytomegalovirus pp65, IE1-Exon4, gB, pp150, and pp28 in healthy individuals: Reevaluation of prevalence of IE1-specific CTLs. J Infect Dis 181(5): 1537-1546.
14. Khan N, Best D, Bruton R (2007) T cell recognition patterns of immunodominant cytomegalovirus antigens in primary and persistent infection. J Immunol 178(7): 4455-4465.
15. Martin WJ (2019) Renegade cellular and/or bacterial genetic sequences in stealth adapted viruses. J Human Virol & Retrovirology 7(2): 26-40.
16. Martin WJ (2022) Renegade bacterial genetic sequences in a stealth adapted virus: Biological and diagnostic implications. bioRxiv.
17. Martin WJ (1996) Genetic instability and fragmentation of a stealth viral genome. Pathobiology 64(1): 9-17.
18. Martin WJ (2020) Stealth adapted viruses with genetically unstable rhesus monkey cellular sequences. A possible forerunner of complex human illnesses. Cohesive J Microbiology & Infectious Disease 4(1): 000578
19. Sasaki Y, Honda M, Naitou M, Sasaki T (1994) Detection of Mycoplasma fermentans DNA from lymph nodes of acquired immunodeficiency syndrome patients. Microb Pathog 17(2): 131-135.
20. Haier J, Nasralla M, Franco AR, Nicolson GL (1999) Detection of mycoplasmal infections in blood of patients with rheumatoid arthritis. Rheumatology (Oxford) 38(6): 504-509.
21. Nasralla M, Haier J, Nicolson GL (1999) Multiple mycoplasmal infections detected in blood of patients with chronic fatigue syndrome and/or fibromyalgia syndrome. Eur J Clin Microbiol Infect. Dis 18(12): 859-865.
22. Nicolson GL, Nasralla MY, Haier J, Pomfret J (2002) High frequency of systemic mycoplasmal infections in Gulf War veterans and civilians with Amyotrophic Lateral Sclerosis (ALS). J Clin Neurosci 9(5): 525-529.
23. Martin WJ (1992) Viral infection in CFS patients in the clinical and scientific basis of Myalgic encephalomyelitis chronic fatigue syndrome. In: Hyde BM (Ed), Nightingdale Research Foundation Press, Ottawa, Canada, pp. 325-327.
24. Martin WJ (2003) Stealth virus culture pigments: A potential source of cellular energy. Exp Mol Pathol 74(3): 210-223.
25. Martin WJ (2003) Complex intracellular inclusions in the brain of a child with a stealth virus encephalopathy. Exp Mol Pathol 74(3): 197-209.
26. https://www.google.com/search?q=youtube+martin+iacc+autism+stealth&client=safari&sca_esv=08f9404a665a6878&rls=en&ei=3mEFaPmiA5e5wN4P1aDnsA8&ved=0ahUKEwj5idqEwueMAxWXHNAFHVXQGfYQ4dUDCBA&uact=5&oq=youtube+martin+iacc+autism+stealth&gs_lp=Egxnd3Mtd2l6LXNlcnAiInlvdXR1YmUgbWFydGluIGlhY2MgYXV0aXNtIHN0ZWFsdGgyBRAhGKABMgUQIRigATIFECEYoAEyBRAhGKABMgUQIRigAUj3O1CXBljcNnABeACQAQCYAY0BoAHmDqoBBDAuMTW4AQPIAQD4AQGYAhCgAs8PwgILEAAYgAQYsAMYogTCAggQABiwAxjvBcICCxAAGLADGKIEGIkFwgIFECEYqwLCAgUQIRifBZgDAIgGAZAGBJIHBDEuMTWgB6ZSsgcEMC4xNbgHyA8&sclient=gws-wiz-serp#fpstate=ive&vld=cid:ae263cc9,vid:f1Nz_0a85jo,st:0
27. Martin WJ, Glass RT (1995) Acute encephalopathy induced in cats with a stealth virus isolated from a patient with chronic fatigue syndrome. Pathobiology 63(3): 115-118.
28. Geier DA, King PG, Geier MR (2009) Mitochondrial dysfunction, impaired oxidative-reduction activity, degeneration, and death in human neuronal and fetal cells induced by low-level exposure to thimerosal and other metal compounds. Toxicol Environ Chem 91(3-4): 735-749.
29. Wakefield AJ, Murch SH, Anthony A, Linnell J, Casson DM, et al. (1998) Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet 351(9103): 637-641.
30. Wakefield AJ, Anthony A, Sim R (1998) Persistent measles virus infection immunodeficiency in children with autism ileo-colonic lymphoid nodular hyperplasia and non-specific colitis [suppl]. Gut 42(1): A86.
31. Martin WJ (2016) The ACE pathway in comparison to the immune system in the defense against infectious diseases. J Hum Virol Retrovirol 4(1): 119-122.
32. Martin WJ (2014) Alternative cellular energy (ACE) pathway as natural therapy for autism. In: Stealth Adapted Viruses; Alternative Cellular Energy (ACE) & KELEA Activated Water. Author House IN 87-102.