Abstract
Productive replication of DNA viruses elicits host cell DNA damage responses, which cause both beneficial and detrimental effects on viral replication. In response to the viral productive replication, host cells attempt to attenuate the S-phase cyclin-dependent kinase (CDK) activities to inhibit viral replication. However, accumulating evidence regarding interactions between viral factors and cellular signaling molecules indicate that viruses utilize them and selectively block the downstream signaling pathways that lead to attenuation of the high S-phase CDK activities required for viral replication. In this review, we describe the sophisticated strategy of Epstein-Barr virus to cancel such “noisy” host defense signals in order to hijack the cellular environment.
Highlights
Cellular DNA damage responses initiate with activation and rapid recruitment of repair proteins to DNA damage sites [1,2]
We describe the elegant strategies used by Epstein-Barr virus (EBV) to cancel ‘‘noisy’’ cellular signaling in order to manipulate the cellular environment for its own genome replication
We propose that, during the course of lytic replication, BZLF1 protein plays two distinct roles in the regulation of p53-mediated transactivation, which depend on the progression of lytic replication: the early stage and the middle to late stages (Figure 1B)
Summary
Cellular DNA damage responses initiate with activation and rapid recruitment of repair proteins to DNA damage sites [1,2]. Herpesviruses such as HSV, HCMV, and EBV modulate the cell cycle to promote a transition through G1-S phase and achieve the cellular environment with high S-phase CDK activities, called the S-phase-like condition, for virus-productive replication (reviewed in [18]). The EBV-encoding protein kinase (PK) BGLF4 phosphorylates MCM complex to inhibit its replicative helicase activity (Figure 2) [34].
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