E' dal lontano 2002 che lo scienziato Singh mette in correlazione la esacerbata risposta immunitaria nei confrnti del virus del morbillo, nei bambini autistici, e la forte correlazione con anticorpi contro la proteina basica della mielina, in assenza di infezione normale da morbillo.

Ho capito una cosa molto importante nelle ricerche e cioè che quando si studiano ricerche non sull'autismo e troviasmo scritte concetti molti simili allora significa che siamo sulla strada della verità

In questa ricerca infatti che potete trovare qui od in allegato


http://cdn.intechopen.com/pdfs-wm/41738.pdf

si esprime il concetto che una persistente penetrazione del virus del morbillo nel sistema nervoso centrale può provocare una demielinizzazione ed encefalite

Stessa cosa detta da Singh nelle ricerche del 2002 e 2009

Ma come il soggetto contrae il virus del morbillo selvaggio senza segni clinici apparenti ?

Forse dal MMR? o per opera divina?

Inoltre è provata la presenza di mutazioni genetiche del virus del morbillo


"

Demyelinating encephalitis is a type of encephalitis in which the insulating myelin sheath sur‐
rounding nerve fibers is damaged. Most types of demyelinating encephalitis are known to be
caused by viral infection, and therefore the nature of viral persistence in the central nervous sys‐
tem (CNS) has become crucial to understanding the pathogenesis of associated diseases. Suba‐
cute sclerosing panencephalitis (SSPE) is a progressive fatal demyelinating disease caused by
infection with high levels of neuronal measles virus (MV) in the CNS. Thus, MV infection pro‐
vides one of the main paradigms of persistent viral infection that causes encephalitis. Many re‐
views have been published explaining how MV establishes a persistent infection in the CNS [1,
2, 3].

A number of studies on SSPE using cDNA cloning and sequencing techniques have re‐
vealed that MV genomes are present in samples obtained from SSPE patients. This demon‐
strates the presence of mutations that may lead to MV persistence in the CNS.

However, no
study has been able to explain how persistent MV is reactivated and results in subsequent
pathogenesis of the CNS. In this review, we describe a brief overview of MV and SSPE. We will
attempt to focus on host cell modifications related to MV persistence, and on reactivation mech‐
anisms of MV during persistent infections. We will then discuss the pathogenesis of persistent
MV infections in patients to highlight molecular events that lead to the manifestation of SSPE
symptoms. These key advances in the understanding of MV persistence will provide novel in‐
sights into the elucidation of SSPE pathogenesis."