As per editorial request: 

1. the abstract was placed ahead of the introduction. 

   An additional sentence was added to the conclusion of the abstract section:

    "If this theory is demonstrated, routine correction of secretory IgA deficiency at birth

     with periodic monitoring, could allow for standard MMR immunization or exposure to

     the attenuated virus without fear of autism."

2. the original experimental section was divided into experimental and results sections respectively

3. An additional  (very brief) discussion section was added prior to the history section, which backed

    up the change in the abstract section.

4. To reflect on the  small change in the abstract and additional discussion section, an additional

   sentence was added to the conclusions section.

It is hypothesized that the messles N protein component of the attenuated (vaccine derived) measles virus, chronically interfers with a specific homeostatic mechanism that provides balance between metabolic and immune function, resulting in autism. First, congenital metabolic diseases or risk factors, produce primary LOCAL and CONTINUING SUPPRESSIONS of enzymatic and immune fnctions. Critical among these risk factors is extremely low or non-existant secretory IgA. Second, the overall cellular homeostatic environment is then severely affected by GLOBAL and TRANSIENT metabolic and immune SUPPRESSIONS from the attenuated measles vaccination. Third, the combined effects of severe immune/enzymatic suppresions from the attenuated measles virus, severely reuced IgA, and other CMD's allows opportunistic infections to flourish, which support secodary immune and enzyme suppressions. Finally, all these suppressions produce a severe intracellular messenger-metabolite flux reduction, which allows the attenuated measles N protein freedom to interact and interfere with, the eukarotic initiation factor eIF3P40. eIF3P40 is joined to the eukaryotic inition factor eIF4E through an eIF4G linkage. Theoretically, this would create a severe dysregulation in the eukaryotic initiation factor eIF4E, which has been observed in autistic children, andassociated with autistic behavior in animal studies. This severe messenger-metabolite flux reduction from reduced secretory IgA and other CMD's, immune repression from opportunistic infections and consequent and continuing attenuated measles virus latency, results in an ongoing inability to achieve homeostasis between metabolic functions and immune functions. This manifests as autism. Three tests of this theory are possible. First, treatment with vaccine derived (attenuated) measles N protein specific secretory immunoglobulin A, which is capable of neurtralizing the interference. Theoretically, such a test/treatment would restore homeostasis, with a gradual improvement of the autistic condition. Second, it is proposed that if (vaccine derived) attenuated measles N protein specific IgA is properly administered concurrent to infant measlesvaccination, few if any cases of autismshould be observed, while still providing protection against measles. Third,immunization of the mother with MMR vaccine and subsequent immunization of the child durring concurrent breast feeding. Theoretically, children could then receive sufficentattenuated measles specific secretory IgA via breast milk, with few if any cases of autism (or measles) observed. If correct, these tests could provide empirical evidence of anindirect relationship between autism and attenuated measles virus/vaccination. If this theory is demonstrated, routine correction of secretory IgA deficiency at birth, with pewriodic monitoring, could allow for standard MMR immunization or exposure to the attenuated virus without fear of autism. ​​​​​