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Epstein-Barr virus (EBV) reactivation is regulated by viral long noncoding RNAs (lncRNAs). A pro-lytic lncRNA triggers reactivation, while a pro-latency lncRNA inhibits it by interacting with CTCF.

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Area of Science:

  • Virology
  • Molecular Biology
  • Genetics

Background:

  • Epstein-Barr virus (EBV) exhibits a biphasic lifecycle, alternating between latent and lytic phases.
  • EBV latency is prevalent in EBV-associated cancers, and reactivation is linked to autoimmune diseases like multiple sclerosis.
  • Mechanisms governing EBV reactivation remain incompletely understood.

Purpose of the Study:

  • To investigate the regulatory mechanisms controlling the Epstein-Barr virus (EBV) lytic switch.
  • To identify novel viral factors involved in EBV reactivation and latency.

Main Methods:

  • Multi-omic approaches were employed to analyze EBV lifecycle regulation.
  • Investigated the roles of viral long noncoding RNAs (lncRNAs) in EBV reactivation.
  • Characterized the interaction of lncRNAs with CTCF and viral genomic elements.

Main Results:

  • Identified two counter-regulating viral lncRNAs: one promoting latency and one promoting lytic replication.
  • Reactivation triggers rapidly induce the pro-lytic lncRNA, which forms an RNA G-quadruplex interacting with CTCF.
  • The pro-lytic lncRNA facilitates the looping of replication enhancers to the lytic promoter, initiating reactivation.
  • The pro-latency lncRNA sequesters the pro-lytic lncRNA, preventing CTCF interaction and inhibiting reactivation.

Conclusions:

  • Viral lncRNAs are key regulators of the EBV lytic switch.
  • The interplay between pro-latency and pro-lytic lncRNAs dictates EBV reactivation.
  • These findings provide a foundation for therapeutic strategies targeting EBV reactivation.