Answers are grounded in this paper and cite their sources.
Productive (lytic) replication of DNA viruses elicits host cell DNA damage responses, which cause both beneficial and detrimental effects on viral replication. Viruses utilize them and selectively cancel the 'noisy' downstream signaling pathways, leading to maintain high S-phase CDK activities required for viral replication. To achieve this fine tuning of cellular environment, herpesviruses encode many (>70) genes in their genome, which are expressed in a strictly regulated temporal cascade (immediate-early, early, and late). Here, I introduce and discuss how Epstein-Barr virus, an oncogenic herpesvirus, hijacks the cellular environment and adapt it for the progeny production.
No takes yet. Share an insight, caveat, or question.
Yoshitaka Sato (2020) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: