Abstract
Epstein–Barr virus (EBV) is a gammaherpesvirus with a 172kb genome and many genes encoding enzymes for lytic viral DNA replication. Recent observations indicate that an S-phase-like environment and the activated DNA repair system are required for viral lytic DNA replication. The virally encoded DNA replication-associated enzymes are then expressed in two clusters, suggesting their participation at different stages of replication. Simultaneously, EBV-encoded regulatory proteins may modulate cell-cycle control to enhance virus replication efficiency. The interactions among proteins in the viral replication complex and cellular proteins may either generate structural specificities for replication proteins or stabilize the protein complexes. During infection, EBV has evolved several strategies to overcome the host defense mechanism, such as interfering with innate immunity and withdrawing into a latent state. This review discusses the latest progress in viral control of lytic replication and the interactions among viral lytic replication compartment and cellular machineries. The possible contribution of EBV lytic gene products to human malignancy is also discussed.
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