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.

Parents and interested clinicians are asked to review the web site www.ccid.org and to then contact CCID by phone at (626) 572-7288 or by e-mail to ccidlab@hotmail.com, for scheduling stealth virus testing.