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To the Editor:
We read with interest the article by Lousa et al.,1 who reported a case of status epilepticus associated with non-GluR3 reactive antineuronal antibodies in a 14-year-old boy. They raise the intriguing possibility that the development of these autoantibodies may have occurred as a result of an autoimmune response associated with viral infection. The authors excluded infection by herpes simplex virus, HIV, measles, mumps, cytomegalovirus, adenovirus, influenza A and B, echovirus 4, 9, 11, and 30, and coxsackievirus A and B, among other microbial pathogens. One notable omission from this seemingly exhaustive list is Epstein–Barr virus (EBV).
This ubiquitous human herpesvirus infects approximately 90% of the population worldwide.2 That EBV establishes latency in B lymphocytes and is subject to lifelong immune surveillance by the host renders it an attractive candidate as an initiator of …
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