Abstract: It is hypothesized that the measles N protein component of the measles virus,chronically interferes 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 functions. Critical among these risk factors is extremely low or non-existent secretory IgA. Second, the overall cellular homeostatic environment is then severely effected by Global and Transient Metabolic and Immune Suppressions from the measles vaccination. Third, the combination of severe immune/enzymatic suppressions from the measles virus, severely reduced secretory IgA, and other CMD's, allows opportunistic infections to flourish, which support secondary immune and enzyme suppressions. Finally, all these suppressions produce a severe intracellular messenger-metabolite flux reduction, which allows the measles N protein freedom to interact, and interfere with, the eukaryotic initiation factor eIF3P40. eIF3P40 is joined to the eukaryotic initiation 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, and associated with autistic behavior in animal studies. The severe repressions from reduced secretory IgA and other CMD's, immune repression from opportunistic infections and consequent and continuing 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 human derived measles N protein specific secretory immunoglobulin A, which is capable of neutralizing the interference. Theoretically, such a test/treatment would restore homeostasis, with a gradual improvement of the autistic condition. Second, it is proposed that if measles N protein specific secretory IgA is properly administered concurrent to infant measles vaccination, few if any cases of autism should be observed, while still providing protection against measles. Third, immunization of the mother with MMR vaccine and subsequent immunization of the child during concurrent breastfeeding. Theoretically, children could then receive sufficient 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 an indirect relationship between autism and measles virus/ vaccination.