The pathogenesis of Epstein-Barr virus persistent infection

David A. Thorley-Lawson, Jared B. Hawkins, Sean I. Tracy, Michael Shapiro

Research output: Contribution to journalReview articlepeer-review

120 Scopus citations

Abstract

Epstein-Barr virus (EBV) maintains a lifelong infection. According to the germinal center model (GCM), latently infected B cells transit the germinal center (GC) to become resting memory cells. Here, the virus resides quiescently, occasionally reactivating to infect new B cells, completing the cycle of infection. The GCM remains the only model that explains EBV biology and the pathogenesis of lymphoma. Recent work suggests modifications to the model notably that the virus contributes only modestly to the GC process and predictions from mathematical models that quiescence within memory B cells shapes the overall structure of viral infection but is not essential for persistence. Rather, it is the cycle of infection which allows viral persistence at the very low levels observed.

Original languageEnglish (US)
Pages (from-to)227-232
Number of pages6
JournalCurrent Opinion in Virology
Volume3
Issue number3
DOIs
StatePublished - Jun 2013

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