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      Autism Revisited: (expanded 2022 version)
      Serendipitous Observations and Theory Relevant To Autism

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            Abstract


            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.

            Content

            Author and article information

            Journal
            ScienceOpen Preprints
            ScienceOpen
            15 January 2022
            Affiliations
            [1 ] Broward Health North Hospital
            Author notes
            Article
            10.14293/S2199-1006.1.SOR-.PPVZSLN.v1
            6306bc8a-fa67-4bc8-abbc-48b8a4256873

            This work has been published open access under Creative Commons Attribution License CC BY 4.0 , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Conditions, terms of use and publishing policy can be found at www.scienceopen.com .


            All data generated or analysed during this study are included in this published article (and its supplementary information files).
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