Reviews in medical virologyDec 17, 2013

Switching of Epstein-Barr Virus between inactive and active phases

CRISPR Gene Editing Weekly Brief ↗PubMed ↗DOI ↗

Updated Mar 16, 2026

Abstract

The EBV lytic cycle is associated with the secretion of cytokines and growth factors that may play a crucial role in tumor development.

EBV predominantly establishes a latent infection after primary infection, with only a small percentage of infected cells transitioning to the lytic cycle.
The lytic cycle of EBV is expected to influence tumor maintenance due to its role in cytokine and growth factor secretion.
Inducing lytic replication artificially could lead to potential oncolytic therapies for EBV-positive cancers.
Reactivation from latency relies on the expression of the viral BZLF1 protein, which is activated by various chemical and biological inducers.
The regulation of the BZLF1 promoter is influenced by a balance of active and suppressive epigenetic histone marks and multiple transcription factors.

Simplified

The EBV is a human gamma-herpesvirus that is associated with a variety of neoplasms. Upon primary infection, it transiently runs a short lytic program and then predominantly establishes latent infection. Only a small percentage of infected cells switch from the latent stage into the lytic cycle and produce progeny viruses. Although EBV in cancer cells is mostly in the latent state, the lytic cycle of the virus is also expected to play a pivotal role in development and maintenance of tumors because of its association with secretion of cytokines or growth factors. Moreover, if efficient artificial induction of lytic replication could somehow be achieved, development of oncolytic therapy for EBV-positive cancers would be conceivable. Thus, understanding the switching mechanism is of essential importance. Reactivation of the virus from latency is dependent on expression of the viral BZLF1 protein. The BZLF1 promoter (Zp) normally exhibits only low basal activity but is activated in response to chemical or biological inducers, such as 12-O-tetradecanoylphorbol-13-acetate, calcium ionophore, or histone deacetylase inhibitors. Transcription from the Zp is regulated by the balance between active and suppressive epigenetic histone marks, including histone acetylation, histone H3 Lysine 4 trimethylation and histone H3 lysine 27 trimethylation, being mediated by multiple transcription factors, such as myocyte enhancer factor 2, specificity protein 1, and zinc finger E-box binding homeobox. This review will focus on such molecular mechanisms by which the EBV lytic switch is controlled and discuss the physiological significance of the switching for oncogenesis.

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Switching of Epstein-Barr Virus between inactive and active phases

Abstract

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