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The above notion could reconcile the paradox of EBV exposure being a strict requirement for subsequent development of MS, and on the other hand the recent failure of an EBV-specific T-cell therapy (Giovannoni et al., 2024): if early EBV infection triggers a molecular cascade driving MS pathogenesis that no longer requires replication of virus, anti-viral therapies begun once MS is clinically evident may be doomed to failure

The correlation between genotype and phenotype in PWS remains unclear, as none of the genes in the PWS region have been specifically implicated in the syndrome on their own ( SNORD116

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