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JNCI Journal of the National Cancer Institute 2002 94(23):1733-1735; doi:10.1093/jnci/94.23.1733
© 2002 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 94, No. 23, 1733-1735, December 4, 2002
© 2002 Oxford University Press

EDITORIAL

Regulation of Epstein-Barr Virus Lytic Cycle Activation in Malignant and Nonmalignant Disease

I. George Miller, Jr., Ayman El-Guindy

Affiliation of authors: I. G. Miller, Jr. (Departments of Molecular Biophysics and Biochemistry, Pediatrics, and Epidemiology and Public Health), A. El-Guindy (Department of Molecular Biophysics and Biochemistry), Yale University School of Medicine, New Haven, CT.

Correspondence to: I. George Miller, Jr., M.D., Rm. 420 LSOG, 333 Cedar St., P.O. Box 208064, New Haven, CT 06520-8064 (e-mail: George.Miller@yale.edu).

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Like all other herpesviruses, the oncogenic human gammaherpesvirus, Epstein-Barr virus (EBV; human herpesvirus 4) manifests two distinct phases in its life cycle: latency and lytic replication. During latency EBV expresses a limited number of viral genes that are involved in tasks such as stimulating cell proliferation, inhibiting apoptosis, blocking viral lytic replication, and assuring accurate and equal partitioning of the episomal viral genome to daughter cells. Variants of the EBV latent life cycle, which are distinguished by the latent products expressed, are characteristic of each EBV-associated cancer. During the lytic replication phase of the EBV life cycle, many more viral genes, encoding enzymes, and other proteins involved in nucleotide biosynthesis, RNA processing, viral DNA replication, and capsid and viral envelope synthesis, are expressed. Two genes of EBV, BZLF1 and BRLF1, encode transcriptional activator proteins that mediate the switch between latency and . . . [Full Text of this Article]


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