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It is hypothesized that the measles 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 functions. Critical among these risk factors is
extremely low or non-existent 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
suppressions from the attenuated measles virus, severely
reduced 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 attenuated 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. 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 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
(vaccine derived) attenuated measles N protein specific 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
attenuated 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 attenuated measles
virus/vaccination.