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In Reply: In response to Dr Lily, we have discussed possible explanations for this association elsewhere.¹ In that article, we proposed that molecular mimicry, rather than direct invasion of the central nervous system, is a more likely pathway for the link between EBV and MS. Our analogy between elevated prediagnostic levels of antibodies to EBV in MS and in Burkitt lymphoma or nasopharyngeal carcinoma was not meant to suggest that there are similar mechanisms underlying these diseases; the commonality is that changes in antibodies against EBV are present several years before the diagnosis and are the earliest nongenetic marker of increased risk. Our original hypothesis was based on the epidemiological evidence that individuals who are EBV seronegative have a risk of developing MS that is less than one tenth that of individuals who are infected with EBV,² and that individuals with late age at infection with EBV have an increased . . . [Full Text of this Article]

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